Promoting the Calcified Roasting of Vanadium Slag Based on the CeO2-Catalytic Oxidation Mechanism.

Calcification roasting-acid leaching is a clean, efficient, and environmentally friendly process, but in the roasting process, the local temperature is often too high, the heat release is not timely, and the heat transfer is blocked. Furthermore, the material is easy to sinter, which affects the final vanadium extraction effect. In this paper, a small amount of CeO2 was introduced in the roasting process of vanadium slag to promote the calcified roasting. The results showed that the vanadium leaching rate reached 93.17% with the addition of 0.1 wt % CeO2 at a roasting temperature of 750 °C, which was higher than that obtained without CeO2 addition (90.00%). The results of XPS, XRD, and SEM-EDS analyses confirmed that adding CeO2 to the roasted clinker significantly increased the proportion of pentavalent vanadium to the total vanadium by up to 28.64%. O2-TPD analysis revealed an enhanced chemisorbed oxygen with the CeO2-assisted roasting, indicated the activation of oxygen by CeO2, and resulted in an enhanced oxidation of vanadium. The work in this paper establishes an alternative route for catalytic oxidation-enhanced vanadium slag roasting, which can improve the utilization of vanadium slag at relatively lower temperatures under the action of CeO2 and is of positive significance in solving the problems of sintering and energy consumption in the roasting process.

Cyclophilin A/CD147 signaling induces the epithelial-to-mesenchymal transition and renal fibrosis in chronic allograft dysfunction by regulating p38 MAPK signaling.

OBJECTIVE: Our study was designed to explore the role of Cyclophilin A (CyPA)/CD147 signaling in renal allograft fibrosis and chronic allograft dysfunction (CAD). MATERIALS AND METHODS: A rat renal transplant model with significant CAD was successfully achieved. Renal allograft tissues and blood samples were collected. Hematoxylin and eosin, Masson's, and immunohistochemistry staining were performed. Since CD147 is mainly expressed in the renal tubular epithelial cells, human HK-2 cells were used and intervened by specific concentrations of CyPA, and the total protein and mRNA were extracted. Western blot assay and polymerase chain reaction were performed to explore the protein and mRNA expression of CyPA, CD147, and epithelial-to-mesenchymal transition (EMT)-related biomarkers. SiRNA-CD147 and specific inhibitors of p38 MAPK were used to explore the cellular mechanisms involved in the process. RESULTS: We have successfully established and validated a 20-week renal transplant CAD model. We observed significant distributed and expressed CyPA and CD147 in the renal allograft fibrotic tissues. We also found a significant expression of CD147 and EMT-related markers in the HK-2 cells stimulated by CyPA. The CD147 siRNA confirmed the previous in vitro results. The selective inhibition of MAPK suggested the notable role of p38 MAPK signaling pathway in the CyP/CD147 signaling involved in renal allograft fibrosis. CONCLUSIONS: Our study reported the positive relationship of CyPA-CD147 signaling with renal allograft dysfunction. The in vitro study suggested that CyPA-CD147 signaling induce the development of the EMT process by p38 MAPK signaling, thus contributing to renal allograft fibrosis and CAD.

Construction of an individualized clinical prognostic index based on ubiquitination-associated lncRNA in clear cell renal cell carcinoma patients.

BACKGROUND: ccRCC is considered as the main subtype of RCC, which accounted for sixth deadliest cancer worldwide. Recently, ubiquitination has been reported to be closely involved in the progression of tumore. The purpose of this study was to identify the ubiquitination-associated genes and co-expressed lncRNAs on the prognosis of clear cell renal cell carcinoma (ccRCC) patients. METHODS AND PATIENTS: We downloaded 530 cases and the corresponding transcriptome profiling from The Cancer Genome Atlas (TCGA) database. We distinguished mRNA and lncRNA expression data from the transcriptome profiling and then extracted the expression of mRNAs that regulate protein ubiquitination. We obtained lncRNAs associated with protein ubiquitination regulation from the lncRNA data by gene co-expression analysis. Cox regression analysis of survival time, survival status, and lncRNA expression level was carried out, and a prognostic index (PI) was constructed. RESULTS: The PI was established based on 8 prognostic lncRNAs that regulate protein ubiquitination and distinguish the high-risk group patients from all patients. Multivariate analysis indicated that this PI was an individualized clinical prognostic factor for patients with ccRCC. Regarding clinical characteristics, a ubiquitination-associated clinical-prognostic index (UCPI), containing 8 ubiquitination-related lncRNAs and age, was established and tested with AUC of 0.80. CONCLUSION: We established a UCPI containing 8 lncRNAs related to protein ubiquitination. This UCPI may become an appropriate model to predict the prognosis in ccRCC patients and guide clinicians to adjust the follow-up regimen.

Stretchable Capacitive Pressure Sensing Sleeve Deployable onto Catheter Balloons towards Continuous Intra-Abdominal Pressure Monitoring.

Intra-abdominal pressure (IAP) is closely correlated with intra-abdominal hypertension (IAH) and abdominal compartment syndrome (ACS) diagnoses, indicating the need for continuous monitoring. Early intervention for IAH and ACS has been proven to reduce the rate of morbidity. However, the current IAP monitoring method is a tedious process with a long calibration time for a single time point measurement. Thus, there is the need for an efficient and continuous way of measuring IAP. Herein, a stretchable capacitive pressure sensor with controlled microstructures embedded into a cylindrical elastomeric mold, fabricated as a pressure sensing sleeve, is presented. The sensing sleeve can be readily deployed onto intrabody catheter balloons for pressure measurement at the site. The thin and highly conformable nature of the pressure sensing sleeve captures the pressure change without hindering the functionality of the foley catheter balloon.

ZNF433 positively regulates the beta-catenin/ TCF pathway in prostate cancer and enhances the tumorigenicity of cancer cells.

BACKGROUND: Prostate cancer often shows the over-activation of beta-catenin/t-cell factor (TCF) signaling. It remains largely unknown how the beta-catenin/TCF transcriptional machinery is tightly controlled. METHODS: The ZNF433 mRNA and protein levels in the clinical tissues were examined using q-PCR, Western blot and immunohistochemistry. The phenotypes of prostate cancer cells were examined using MTT assay, Boyden chamber assay and anchorage-independent assay. The interaction between ZNF433 and beta-catenin was evaluated by immunoprecipitation. RESULTS: In the present study, ZNF433 was upregulated in prostate cancer samples, and promoted the growth and migration of prostate cancer cells. Furthermore, ZNF433 was the binding partner of beta-catenin and activated beta-catenin/TCF signaling in prostate cancer. Moreover, ZNF433 enhanced the binding between beta-catenin and TCF4. In addition, NC043, small antagonist for beta-catenin/TCF complex, inhibited the malignant behaviors of prostate cancer cells driven by ZNF433. CONCLUSION: In summary, these studies demonstrate the tumor-promoting roles of ZNF433 in prostate cancer, and suggesting that ZNF433 was a potential target for the treatment.

Efficacy and safety of febuxostat for treating hyperuricemia in patients with chronic kidney disease and in renal transplant recipients: A systematic review and meta-analysis.

Febuxostat is potent and well-tolerated in the management of chronic gout. However, its clinical efficacy and safety in the treatment of hyperuricemia in patients with chronic kidney disease (CKD) and in renal transplant recipients have remained to be fully determined. The MEDLINE, EMBASE and Cochrane Library databases were searched for relevant articles. Data were extracted and pooled results were estimated from the standard mean difference (SMD) with 95% confidence intervals (95% CIs). The quality of the studies included was assessed, and their publication bias was examined. Four prospective randomized controlled trials and two retrospective observational studies were included in the systematic review and meta-analysis. Febuxostat administration significantly reduced the serum uric acid concentration in patients with CKD and in renal transplant recipients when compared with allopurinol or placebo in the short-term (1 month: SMD, -2.24; 95% CI, -3.59 to -0.89; P-value of SMD=0.001; I2, 92.4%; 3 months: SMD, -1.20; 95% CI, -2.04 to -0.36; P-value of SMD=0.005; I2, 88.9%; 6 months: SMD, -1.49; 95% CI, -2.68 to -0.30; P-value of SMD=0.014; I2, 92.9%). Furthermore, the increase in the estimated glomerular filtration rate in the febuxostat group was significantly higher than that in the control group (SMD, 0.30; 95% CI, 0.031 to 0.58; P-value of SMD=0.029; I2, 0.0%). No significant difference in the changes in serum creatinine (Scr), low-density lipoprotein (LDL) and high-density lipoprotein (HDL) was identified between the two groups (Scr: SMD, -0.17; 95% CI, -0.97 to 0.63; P-value of SMD=0.67; I2, 79.2%; LDL: SMD, -0.21; 95% CI, -0.49 to 0.07; P-value of SMD=0.13; I2, 34.1%; HDL: SMD, -0.05; 95% CI, -0.70 to 0.61; P-value of SMD=0.89; I2, 69.2%). In conclusion, febuxostat is a potent and well-tolerated agent for the short-term management of hyperuricemia in patients with CKD and in renal transplant recipients. However, these data should be interpreted with caution due to the varied design of the studies included in the present meta-analysis.

NOL8, the binding protein for beta-catenin, promoted the growth and migration of prostate cancer cells.

Overactivation of beta-catenin/TCF signaling in prostate cancer is very common. However, how the beta-catenin/TCF complex is regulated in the nucleus remains largely unknown. In this study, we have shown that NOL8, a binding protein of beta-catenin, enhanced the interaction between beta-catenin and TCF4, and activated beta-catenin/TCF signaling. NOL8 is up-regulated in the prostate cancer, and promoted the growth, migration and colony formation of cancer cells. Knocking down the expression of NOL8 inhibited the growth, migration and colony formation of prostate cancer cells. The molecular mechanism study demonstrated that NOL8 promoted the migration and colony formation of cancer cells by activating beta-catenin/TCF signaling. Taken together, this study demonstrated the oncogenic roles of NOL8 in prostate cancer and suggested that NOL8 might be an important therapeutic target for prostate cancer.

Retracted Article: Long noncoding RNA PCA3 regulates glycolysis, viability and apoptosis by mediating the miR-1/CDK4 axis in prostate cancer.

Prostate cancer is one of the common tumor malignancies in men worldwide. Although long noncoding RNAs (lncRNAs) have been demonstrated to play essential roles in the progression of prostate cancer, the roles and potential mechanism of lncRNA prostate cancer antigen 3 (PCA3) remain poorly understood. In the present study, we investigated the role of PCA3 in aerobic glycolysis, viability and apoptosis in prostate cancer cells and probed the interaction between PCA3 and microRNA-1 (miR-1)/cyclin-dependent kinase 4 (CDK4). Here we found that PCA3 and CDK4 were up-regulated while miR-1 was down-regulated in prostate cancer tissues and cells. Moreover, knockdown of PCA3 inhibited aerobic glycolysis and viability and induced apoptosis in prostate cancer cells. Intriguingly, PCA3 was bound to miR-1 and inhibition of miR-1 reversed the regulatory effect of PCA3 knockdown on aerobic glycolysis, viability and apoptosis in prostate cancer cells. Besides, CDK4 was indicated as a target of miR-1 and it was regulated by PCA3 through functioning as a competing endogenous RNA (ceRNA) of miR-1 in prostate cancer cells. The results indicated that PCA3 might drive aerobic glycolysis, viability and apoptosis by regulating the miR-1/CDK4 axis in prostate cancer cells, providing a promising avenue for treatment of prostate cancer.

Association between TGFB1 genetic polymorphisms and chronic allograft dysfunction: a systematic review and meta-analysis.

BACKGROUND: Epidemiological studies have investigated the role of transforming growth factor-ß1 (TGF-ß1) in chronic allograft dysfunction (CAD) following kidney transplantation. TGFB1 gene polymorphisms (SNP rs1800470 and rs1800471) may be associated with the risk of CAD. In this meta-analysis, the relationship between these two variations and the risk of CAD was explored. MATERIALS AND METHODS: MEDLINE, EMBASE, the Cochrane Central Register of Controlled Trials (CENTRAL), Embase, the Chinese CNKI and WANFANG databases were searched. Data were extracted and pooled results were estimated from odds ratios (ORs) with 95% confidential intervals (95% CIs). Quality assessments were performed, and publication bias of all eligible studies examined. RESULTS: Eight studies with 1038 subjects were included in our analysis. According to the effects on TGF-ß1 secretion, haplotypes were categorized as "HIGH", "INTERMEDIATE" and "LOW". The combined results showed a statistically significant difference of TGFB1 haplotypes between the CAD recipients and control subjects when "HIGH" with "INTERMEDIATE" and "LOW" ("HIGH" vs. "INTERMEDIATE" + "LOW": OR: 3.56, 95% CIs: 2.20, 5.78, P < 0.001) were compared. No significant association was found between the TGFB1 codon 10 or codon 25 and the CAD risk in all five genetic models. CONCLUSIONS: Our meta-analysis has found the haplotype of TGFB1 codon 10/25 T/T G/G and T/C G/G genotypes, associated with increased production of TGF-ß1, was linked with CAD risk following kidney transplantation. Moreover, no significant difference was found between TGFB1 codon 10 or codon 25 and the development of CAD.

The MMP2 rs243865 polymorphism increases the risk of prostate cancer: A meta-analysis.

Prostate cancer is a common cancer in men. However, the association between the rs243865 single-nucleotide polymorphisms in the matrix metalloproteinase 2 gene (MMP2) and the risk for prostate cancer is inconclusive. We searched the PubMed, EMBASE, Cochrane Library, and the Chinese CNKI and WANFANG databases for the relevant literature. Data were extracted and pooled results were estimated from odds ratios (OR) with 95% confidence intervals (95% CIs). The quality of included studies was assessed, and publication bias of all included studies was examined. A total five studies involving 1895 patients with prostate cancer and 1918 controls were included. There was a significant association between rs243865 polymorphisms and higher risk of prostate cancer in the co-dominant model, dominant model, and allele model (CC vs. CT+TT, OR: 1.60, 95% CI: 1.22-2.11, P = 0.001; CC vs. CT, OR: 1.80, 95% CI: 1.34-2.42, P < 0.001; C vs. T, OR: 1.32, 95% CI: 1.05-1.66, P = 0.016, respectively). However, there was no significant difference between the co-recessive model and recessive model. Our meta-analysis results suggest that MMP2 rs243865 polymorphisms are significantly associated with higher risk of prostate cancer.

Upregulation of microRNA-96 and its oncogenic functions by targeting CDKN1A in bladder cancer.

BACKGROUND: Genome-wide miRNA expression profile has identified microRNA (miR)-96 as one of upregulated miRNAs in clinical bladder cancer (BC) tissues compared to normal bladder tissues. The aim of this study was to confirm the expression pattern of miR-96 in BC tissues and to investigate its involvement in carcinogenesis. METHODS: Quantitative real-time PCR was performed to detect the expression levels of miR-96 in 60 BC and 40 normal control tissues. Bioinformatics prediction combined with luciferase reporter assay were used to verify whether the cyclin-dependent kinase inhibitor CDKN1A was a potential target gene of miR-96. Cell counting kit-8 and apoptosis assays were further performed to evaluate the effects of miR-96-CDKN1A axis on cell proliferation and apoptosis of BC cell lines. RESULTS: We validated that miR-96 was significantly increased in both human BC tissues and cell lines. According to the data of miRTarBase, CDKN1A might be a candidate target gene of miR-96. In addition, luciferase reporter and Western blot assays respectively demonstrated that miR-96 could bind to the putative seed region in CDKN1A mRNA 3'UTR, and significantly reduce the expression level of CDKN1A protein. Moreover, we found that the inhibition of miR-96 expression remarkably decreased cell proliferation and promoted cell apoptosis of BC cell lines, which was consistent with the findings observed following the introduction of CDKN1A cDNA without 3'UTR restored miR-96. CONCLUSIONS: Our data reveal that miR-96 may function as an onco-miRNA in BC. Upregulation of miR-96 may contribute to aggressive malignancy partly through suppressing CDKN1A protein expression in BC cells.

[Impact of preoperative nutritional risk on complications after radical cystectomy].

OBJECTIVE: To evaluate whether urological patients at nutritional risk are at higher risk for complications after radical cystectomy than those not at nutritional risk. METHODS: We performed a retrospective observational study in the consecutive patients undergoing radical cystectomy between 2010 and 2013. A total of 147 patients were enrolled in this study. The nutritional risk score was assessed preoperatively by a specialized study nurse. The patients with NRS (nutritional risk screening, NRS2002)scores≥3 were considered to have nutritional deficiency. Postoperative complications were defined using the standardized Clavien-Dindo classification. Univariate and multivariate analyses were performed to identify the predictors of complications. RESULTS: The patients aged ≥70 years(50.57%) were more prone to nutritional risk than those aged <70 years (31.67%, P=0.023). Of the 63 patients at nutritional risk, 39 (61.90%) presented with at least 1 complication compared with 29 of the 84 controls (34.52%, P=0.001). The patients at nutritional risk were at threefold risk for complications on binary Logistic analysis (OR=3.128,95%CI 1.538-6.361,P=0.002). The length of hospital stay of the patients at higher nutritional risk was longer than that of those without nutritional risk [(12.9±5.7) d vs. (10.4±4.3) d, P=0.003]. CONCLUSION: The patients aged ≥70 years are at higher nutritional risk than that of those aged <70 years. Patients at nutritional risk are more prone to complications after radical cystectomy.

[Changes of miRNA-17-5p, miRNA-21 and miRNA-106a level during rat kidney ischemia-reperfusion injury].

OBJECTIVE: Ischemia-reperfusion (I/R) is a main cause of acute kidney injury (AKI). The renal expression profiles of microRNA (miRNA) and time course of their changes after renal I/R were explored to screen acute AKI prognostic-related microRNAs and biomarkers. METHODS: The expression profile of miRNA was analyzed for detecting miRNAs in kidney after renal I/R injury. Real-time polymerase chain reaction (PCR) was performed to validate the results of microarray. And the relationship was examined between kidney injury and time course of changes in selected miRNAs. RESULTS: Twenty-one miRNAs were differentially expressed in kidney of rats with renal I/R injury. And 5 miRNAs had prominent differences. miR-17-5p, miR-21 and miR-106a were selected for further confirmation by quantitative real-time-PCR. And the results were consistent with those of microarry. During early stage (4 h) after I/R, the expression level of miR-17-5p significantly increased (P < 0.05). And it occurred earlier than those of BUN level and plasma concentration of neutrophil gelatinase-associated lipocalin (NGAL). Renal expressions of miR-21 and miR-106a were significantly elevated in ischemia 20 min and 30 min groups at 12 h and 24 h post-reperfusion (P < 0.01). And the trend was in accordance with those of BUN and NGAL. CONCLUSIONS: miR-21, miR-17-5p and miR-106a are differentially expressed during different phases of renal I/R injury. And miR-17-5p is more sensitive than BUN and NGAL so that it is a more ideal biomarker for AKI.

Overexpression of HMGB3 protein promotes cell proliferation, migration and is associated with poor prognosis in urinary bladder cancer patients.

Human urinary bladder cancer (UBC) is the fourth most common cancer and the eighth most common cause of cancer death in the USA. High mobility group box 3 (HMGB3), a member of a family of proteins containing one or more high mobility group DNA binding motifs, was reported to be overexpressed in a variety of human cancers. However, the expression and role of HMGB3 in human UBC remains unclear. Here, we found that UBC patients had upregulated HMGB at both mRNA and protein levels. Immunochemistry (IHC) evaluation of HMGB3 expression in 113 UBC clinical specimens showed that high expression of HMGB3 had positive correlation with UBC tumor size (P = 0.019), tumor WHO grade (P = 0.031), stage (P = 0.028), and lymph node metastasis (P = 0.017). Moreover, patients with higher HMGB3 expression showed a poorer overall survival rate than those with relatively low HMGB3 (P = 0.0079, log-rank test). Multivariate analysis revealed that HMGB3 expression is an independent prognostic marker. The UBC cancer cell proliferation and migration ability were measured by 3-(4, 5-dimethylthiazol-2-yl)-2, 5-diphenyltetrazolium bromide (MTT) and wound healing assays, respectively. RNA interference of HMGB3 in UBC cell lines inhibited cancer cell growth and migration, along with the downregulation of PCNA and MMP2 protein levels. In sum, our data suggests HMGB3 may serve as an important oncoprotein and indicate that overexpression of HMGB3 in UBC could be used as a potential prognostic marker.

Subcutaneous nephrovesical bypass: Treatment for ureteral obstruction in advanced metastatic disease.

The aim of the present study was to explore the value of subcutaneous nephrovesical bypass (SNVB) for the treatment of ureteral obstruction due to pelvic metastatic disease. SNVB stents (n=30) were implanted in 24 patients with advanced metastatic disease between January 2008 and December 2012. Urinalysis, serum creatinine (SCr), glomerular filtration rate (GFR), quality of life (QoL) scores, and renal ultrasonography were evaluated at follow-up. The SNVB procedures were successful in all 24 patients. Patient follow-ups occurred at an average of 10.6 months. Preoperative hydronephrosis was eliminated in 16 cases (53.3%) and reduced in the remaining patients. Following surgery, SCr levels reduced significantly from 256±46 to 124±23 µmol/l (P<0.001). GFRs increased from 25±4.8 to 45±5.3 ml/min (P<0.01). The mean QoL scores were 3.4±1.4 preoperatively and 7.6±1.0 postoperatively (P<0.001). The results showed that SNVB is a minimally invasive, effective and safe procedure for patients with ureteral obstruction resulting from advanced malignant disease. As an alternative procedure to percutaneous nephrostomy, SNVB offers patients a better QoL.

[Antisperm-antibodies induced by testicular torsion and its influence on testicular function].

OBJECTIVE: To investigate the changes of antisperm antibodies (AsAb), sexual hormones, and inhibin B (INH B) in patients before and after testicular torsion, as well as the effects of these factors on testicular function and reproduction. METHODS: Ten patients with single acute testicular torsion (left side 9 and right side 1), aged 16-45 years (19.6 on average), disease course of 3-6 days (averaging 4.7 days), underwent surgical removal of the damaged testis. Before and after the operation, serum AsAb (IgG, IgM, IgA) and INH B were measured by ELISA, and serum follicle-stimulating hormone (FSH), luteotropic hormone (LH), and testosterone (T) determined by chemoluminescence autoanalyzer. RESULTS: After the operation, the AsAb levels rose significantly and remained high for at least 26 weeks. The level of INH B was the lowest in the 3rd week and restored to normal in the 12th week, with significant difference between preoperation and the 3rd or the 6th week after the operation. The levels of LH and INH B in the 26th week were elevated significantly compared with the 6th. CONCLUSION: Testicular injury induced the elevation of AsAb, which would last a very long time. The change of INH B was closely related with the injury of the testis, which reflected the degree of testicular injury and functional restoration of the patients after the operation. Our study showed that AsAb and INH B can be used as useful tools for monitoring testicular function and reproduction.