Chronic prostatitis/chronic pelvic pain syndrome (CP/CPPS) is a prevalent urological condition marked by ongoing pelvic pain, inflammation, and a reduced quality of life. Increasing evidence indicates that dysregulated immune responses and oxidative stress contribute to CP/CPPS pathogenesis. Myricetin (MYR), a natural flavonoid, has been reported to exert anti-inflammatory and antioxidant effects in multiple disease models. However, its role in CP/CPPS remains unclear. The protective effects of MYR were evaluated in an experimental autoimmune prostatitis (EAP) mouse model and in lipopolysaccharide (LPS)-induced RWPE-1 prostate epithelial cells. Prostatic histopathology, pelvic pain behavior, inflammatory cytokine levels, immune cell infiltration, and oxidative stress markers were assessed in vivo. In vitro, inflammatory mediator expression, reactive oxygen species (ROS) production, oxidative stress status, mitochondrial function, and signaling pathway activation were examined using qRT-PCR, Western blotting, immunofluorescence, and biochemical assays. Network pharmacology analysis was used to predict potential targets and pathways associated with the effects of MYR. The involvement of Nrf2 signaling was further examined using the Nrf2 inhibitor ML385. MYR markedly alleviated prostatic inflammation and pelvic pain in EAP mice, accompanied by reduced serum levels of pro-inflammatory cytokines and chemokines, decreased infiltration of CD4-positive T cells and CD68-positive macrophages, and improved oxidative stress status. In LPS-induced RWPE-1 cells, MYR suppressed the expression of inflammatory mediators, reduced ROS accumulation, restored redox balance, and attenuated mitochondrial dysfunction. Mechanistically, MYR inhibited the phosphorylation of ERK, JNK, p38, and STAT3, suppressed NF-κB activation, and promoted Nrf2 signaling. Pharmacological inhibition of Nrf2 largely abolished the anti-inflammatory and antioxidant effects of MYR. MYR attenuated inflammation, oxidative stress, and pain-related changes in experimental prostatitis, and these effects were associated with coordinated modulation of MAPK, STAT3, NF-κB, and Nrf2 signaling pathways. These findings suggest that MYR may represent a potential candidate for further preclinical investigation in CP/CPPS.

LncRNA AL161431.1 is currently known as a factor that can promote epithelial-mesenchymal transition. However, its role in the prognosis, immune infiltration and progression of bladder cancer (BLCA)patients is still unclear. The expression of AL161431.1 is elevated in BLCA tissues compared to normal tissues according to the TCGA database. By combining this data with clinical information, patients with high AL161431.1 expression have more advanced clinicopathological stages and shorter survival periods. Furthermore, AL161431.1 was identified as an independent prognostic factor for bladder cancer. We further analyzed the differences in immune infiltration, tumor mutation burden (TMB), immune checkpoints, and sensitivity to immunotherapy between groups with different levels of AL161431.1 expression. Enrichment analysis demonstrated that AL161431.1 is associated with numerous immune signaling pathways. High expression of AL161431.1 in cancer tissues was confirmed by qRT-PCR. CCK8, transwell, and wound healing demonstrated the oncogenic effects of AL161431.1. In conclusion, AL161431.1 is associated with immune infiltration in bladder cancer and has the potential to become a biomarker for predicting the prognosis of BLCA.

BACKGROUND:This meta-analysis aimed to clarify the connection between six polymorphisms in the FTO gene and susceptibility to cancer. METHODS:The relevant literature on the relationship between FTO variants and cancer susceptibility was comprehensively gathered from PubMed, Scopus, Embase, Medline, and Web of Science prior to May 20, 2024. RESULTS:Our analysis revealed that FTO rs9939609 had a certain correlation with an elevated cancer risk within the Asian demographic q vs. r (OR = 1.22, 95% CI = 1.07-1.39, p = 0.003); rq + qq vs. rr (OR = 1.18, 95% CI = 1.04-1.35, p = 0.011); qq vs. rr + rq (OR = 1.78, 95% CI = 1.39-2.27, p = 0.001). Additionally, FTO rs1477196 was linked to a higher risk of thyroid cancer qq vs. rr + rq (OR = 1.47, 95% CI = 1.13-1.91, p = 0.004) and remarkably relevant to an increased cancer susceptibility for Caucasians (q vs. r (OR = 1.29, 95% CI =1.06-1.57, p = 0.009); rq + qq vs. rr (OR = 1.37, 95% CI = 1.04-1.80, p = 0.024)). In the stratified analysis of rs8047395, the results indicated that rs8047395 had a certain correlation with cancer susceptibility for thyroid cancer q vs. r (OR = 1.23, 95% CI = 1.01-1.51, p = 0.041) and qq vs. rr + rq (OR = 1.53, 95% CI = 1.24-1.91, p < 0.01). CONCLUSION:FTO rs9939609 showed a correlation with cancer risk among individuals of Asian descent. FTO rs1477196 was correlated with an increased risk for thyroid cancer and remarkably relevant to an increased cancer susceptibility for Caucasians. FTO rs8047395 was associated with the risk of thyroid cancer.

BackgroundSeveral previous animal and human studies have found a strong association between asthma and spermatozoa quality, but whether these associations are causal or due to bias remains to be elucidated.MethodsWe performed a two-sample Mendelian randomization (MR) analysis to assess the causal effect of genetically predicted asthma on the risk of abnormal spermatozoa. Asthma, childhood-onset asthma (COA), and adult-onset asthma (AOA) (sample sizes ranging from 327,670 to 408,442) were included as the exposures. Genetic information for abnormal spermatozoa was obtained from a genome-wide association study (GWAS) comprising 209,921 participants. In univariable MR (UVMR) analysis, the inverse variance weighted (IVW) method was conducted as the primary method, with the MR Egger and weighted median used as supplementary methods for causal inference. Sensitivity analyses, including the Cochran Q test, Egger intercept test, MR-PRESSO, and leave-one-out analysis, were performed to verify the robustness of the MR results. Multivariable MR (MVMR) was conducted to evaluate the direct causal effects of asthma on abnormal spermatozoa risk.ResultsUVMR detected causal associations between genetically predicted asthma and an increased risk of abnormal spermatozoa (OR: 1.270, 95% CI: 1.045–1.545, p = 0.017). Moreover, we found that AOA (OR: 1.46, 95% CI: 1.051, 2.018, p = 0.024) has positive causal effects on the risk of abnormal spermatozoa rather than COA (p = 0.558). Sensitivity analysis found little evidence of bias in the current study (p > 0.05). MVMR further confirmed that asthma directly affected the risk of abnormal spermatozoa.ConclusionOur MR study suggested that genetically predicted asthma could be associated with an increased risk of abnormal spermatozoa, and similar results were obtained in AOA. Further studies are warranted to explain the underlying mechanisms of this association and may provide new avenues for prevention and treatment.

Background:Benign prostatic hyperplasia (BPH) is one of the most common causes of lower urinary tract symptoms (LUTS) among the aging male population. Recent studies have shown that histological inflammation (HI) plays a significant role in BPH, with prostatic exosomal protein (PSEP) identified as a potential biomarker for prostate diseases. Therefore, this study aimed to explore the effect of HI on LUTS in patients with BPH, and to further explore the clinical value of PSEP as a diagnostic biomarker of BPH complicated with HI and whether PSEP could be used as an index to predict the improvement of LUTS after operation. Methods:This study was an open-label, cohort study. The study enrolled all patients who were clinical diagnosed as BPH with LUTS and prepared to receive operation of the prostate at the Department of Urology of the Second Hospital of Hebei Medical University. International Prostate Symptom Score (IPSS) were used to evaluate the LUTS of the BPH. And the enrolled patients were divided into four groups, including none, mild HI, moderate HI, and severe HI, based on postoperative pathological results. Then the relationships between HI and IPSS, the National Institutes of Health-Chronic Prostatitis Symptom Index (NIH-CPSI), as well as PSEP were analyzed. Simple and multiple linear regression analyses were performed on the preoperative IPSS and the difference of IPSS before and after surgery was examined. SPSS software version 26 was used for statistical analysis and Prism 9.0 was used to make violin plots. Results:A total of 69 patients were enrolled in the study. The violin plot results indicated IPSS and NIH-CPSI scores exhibited significant increases in correlation with the severity levels of HI (P<0.001; P<0.001). Among BPH patients with total prostate-specific antigen (t-PSA) levels higher than 4.0 ng/mL, a significant correlation was observed between PSEP levels and HI (P=0.04). Besides, simple and multiple linear regression analysis showed that HI (P<0.001) or PSEP (P=0.03) was significantly associated with IPSS and improvement of LUTS, assessed by postoperative and preoperative IPSS differences. Conclusions:The study indicated that IPSS and PSEP (when t-PSA >4 ng/mL) were correlated with the severity of HI in patients with BPH. PSEP was linearly correlated with IPSS and the degree of reduction in IPSS after surgery. Consequently, PSEP may serve as a promising predictor for assessing surgical efficacy and diagnosing the severity of HI in patients with BPH.

To provide a comprehensive account of the association of MMP-9 gene polymorphisms (rs3918242) with susceptibility to cancer. A literature search for eligible candidate gene studies published before May 27, 2022 was conducted in PubMed, Medline, Google Scholar and Web of Science. Potential sources of heterogeneity were sought out across subgroups and sensitivity analysis. Publication bias were also estimated. Overall, a total of 37 articles with 7616 cases and 8165 controls for rs3918242 gene polymorphisms were enrolled. Our meta-analysis suggests that MMP-9 rs3918242 might be associated with breast cancer and gastric cancer susceptibility, and perhaps reduce the risk of lung cancer.

OBJECTIVE:To clarify the causal relationship between obesity and male infertility through Mendelian randomization (MR) study. METHODS:We assessed the causal effect of genetically predicted body mass index (BMI) on the risk of male infertility via a two-sample MR analysis, with the BMIs of 99 998 cases and 12 746 controls as the exposure factor and genetic information on male infertility obtained from a genome-wide association study of 73 479 Europeans. In the univariable MR (UVMR) analysis of the causal relationship, we mainly used inverse variance weighting (IVW), with MR-Egger regression and weighted median filtering as the supplementary methods. Sensitivity analyses including the Cochran's Q test, Egger intercept test, MR-PRESSO, leave-one-out analysis and funnel plot were performed to verify the robustness of the MR results. To evaluate the direct causal effects of BMI on MI risk, multivariable MR (MVMR) was performed. RESULTS:UVMR indicated a causal relationship between genetically predicted BMI and an increased risk of male infertility (OR: 1.237, 95% CI: 1.090－1.404, P = 0.001). Sensitivity analysis revealed little evidence of bias in the current study (P> 0.05). With such risk factors as type 2 diabetes, alcohol consumption and smoking adjusted, MVMR confirmed a direct causal effect of genetically predicted BMI on the risk of male infertility (P<0.05). CONCLUSION:Genetically predicted BMI may be associated with an increased risk of male infertility. Further studies are expected to explore the underlying mechanisms of this association and provide some new strategies for the prevention and treatment of BMI-related male infertility.

Some studies have suggested that MNS16A polymorphism in telomerase reverse transcriptase (TERT) gene is associated with cancer risk in various populations and types of cancer. However, the results of previous studies exploring this link have been inconclusive. To be able to accurately assess the association between TERT MNS16A polymorphism and cancer risk, we performed a meta-analysis based on 17 studies described in 12 articles, including 13,764 controls and 7,132 cases. Combined odds ratios (ORs) and their corresponding 95% confidence intervals (CIs) were estimated to assess the strength of the association in either a fixed-effects model or, if applicable, a random-effects model. Heterogeneity between articles and their publication bias were also tested. Overall, pooled results showed that no significant association between this polymorphism and cancer was found in the five gene models tested.Considering that there may be too many negative studies in the included studies, diluting the results of the total sample size, we stratified these studies according to ethnicity, source of controls and cancer type. In the stratified analysis, a statistically significant association was observed between Asians and population-based studies. We also analyzed by cancer type and found a significantly increased risk of brain cancer in five genetic models. Our results suggest that TERT MNS16A polymorphism is likely to contribute to increased cancer risk.

Background: This meta-analysis was performed to examine the association of 3 endothelial nitric oxide synthase (eNOS) gene polymorphisms with male infertility. Methods: The literature on the relation between the mutant of eNOS and male infertility before July 1, 2022, was conducted in Pubmed, Medline, and Web of Science. The search strategy is as follows: (eNOS OR ECNOS OR nitric oxide synthase 3 OR NOS3) AND (polymorphism OR mutation OR variation OR SNP OR genotype) AND (male infertility). Statistical analysis was performed with the web of MetaGenyo, Stata 12, trial sequential analysis 0.9Beta, and the web of GTEx. Results: Overall, 13 studies (26 case-controls) were included involving 6518 cases and 5461 controls for 3 polymorphisms (rs2070744, rs1799983, rs61722009) of eNOS. We found that eNOS rs2070744 was correlated with an increased risk of male infertility (C vs. T: odds ratio [OR], 1.48; 95% confidence interval [CI], [1.19–1.85]; CC vs. TT: OR, 2.59; 95% CI, [1.40–4.80]; CT vs. TT: OR, 1.17; 95% CI, [1.00–1.38]; CC vs. CT + TT: OR, 2.50; 95% CI, [1.35–4.62]; CC + CT vs. TT: OR, 1.41; 95% CI, [1.21–1.64]). And eNOS rs1799983 was correlated with an increased risk of male infertility (allele contrast T vs. G: OR, 1.41; 95% CI, [1.01–1.96]; P = .043; recessive model TT vs. TG + GG: OR, 2.00; 95% CI, [1.03–3.90]; P = .042). In the stratified analysis of rs61722009, we found Asians might be correlated with an increased risk of male infertility (4a vs. 4b: OR, 1.50; 95% CI, [0.94–2.38]; 4a4a vs. 4b4b: OR, 2.56; 95% CI, [0.70–9.38]; 4a4b vs. 4b4b: OR, 1.36; 95% CI, [0.87–2.13]; 4a4a vs. 4a4b + 4b4b: OR, 2.57; 95% CI, [0.91–7.30]; 4a4a + 4a4b vs. 4b4b: OR, 1.44; 95% CI, [0.87–2.40]). Conclusion: The eNOS rs2070744 polymorphism and rs1799983 are associated with the risk of male infertility, and rs61722009 might be a risk factor for Asians.

Background Cuproptosis is a newly discovered programmed cell death dependent on mitochondrial respiratory disorder induced by copper overload. Pyruvate dehydrogenase E1 subunit beta (PDHB) is one of the cuproptosis genesand is a nuclear-encoded pyruvate dehydrogenase, which catalyzes the conversion of pyruvate to acetyl coenzyme A. However, the mechanism of PDHB in clear cell renal cell carcinoma (ccRCC) remains unclear.Methods We used data from TCGA and GEO to assess the expression of PDHB in normal and tumor tissues. We further analyzed the relationship between PDHB and somatic mutations and immune infiltration. Finally, we preliminarily explored the impact of PDHB on ccRCC.Results The expression level of PDHB was lower in tumor tissue compared with normal tissue. Meanwhile, the expression level of PDHB was also lower in high-grade tumors than low-grade tumors. PDHB is positively correlated with prognosis in ccRCC. Furthermore, PDHB may be associated with decreased risk of VHL, PBRM1 and KDM5C mutations. In 786-O cells, copper chloride could promote the expression of cuproptosis genes (DLAT, PDHB and FDX1) and inhibit cell growth. Last but not least, we found that PDHB could inhibit the proliferation and migration of ccRCC cells.Conclusion Our results demonstrated that PDHB could inhibit the proliferation, migration and invasion in ccRCC cells, which might be a prognostic predictor of ccRCC. Targeting this molecular might provide a new therapeutic strategy for patients with advanced ccRCC.

Downregulated RNA-binding motif protein 5 (RBM5) promotes the development and progression of various tumors, including bladder cancer (BC). Alternative splicing (AS) plays a crucial role in the progression of cancer by producing protein isomers with different functions or by promoting nonsense-mediated mRNA decay (NMD). However, whether RBM5 modulates the progression of BC through AS-NMD remains unexplored. In this study, we revealed that the downregulation of RBM5 expression promoted the expression of coactivator-associated arginine methyltransferase 1 (CARM1) in BC cells and tissues. Increased expression of CARM1 facilitated the activation of the Wnt/β-catenin axis and cell proliferation, which then contributed to the poor prognosis of patients with BC. Interestingly, RBM5 bound directly to CARM1 mRNA and participated in AS-NMD, downregulating the expression of CARM1. In addition, we revealed that protein kinase catalytic subunit alpha (PRKACA) functioned as a phosphorylated kinase of GSK3β, was regulated by CARM1 at the transcription level, and promoted the growth and progression of BC cells. Furthermore, in this study, we demonstrated a regulatory mechanism of Wnt/β-catenin activation through the RBM5/CARM1/PRKACA axis and identified a novel potential target for treating BC.

Sertoli cell -only syndrome (SCOS) is a type of testicular pathological failure that causes male infertility and no effective treatment strategy, is available for this condition. Moreover, the molecular mechanism underlying its development remains unknown. We identified DExD/H-Box helicase 58 (DDX58) as a key gene in SCOS based on four datasets of testicular tissue samples obtained from the Gene Expression Synthesis database. DDX58 was significantly upregulated in SCOS testicular Sertoli cells. Moreover, high expression of DDX58 was positively correlated with the expression of several testicular inflammatory factors, such as IL -1β, IL-18, and IL-6. Interestingly, DDX58 could be induced in the D-galactose (D-gal)-stimulated TM4 cell injury model. Whereas silencing of DDX58 inhibited D-gal -mediated p65 expression, inflammatory cytokine release, and growth arrest. Mechanistically, we found that DDX58 acts as an RNA-binding protein, which enhances p65 expression by promoting mRNA stability. Furthermore, p65 gene silencing decreased the expression of inflammatory cytokines and inhibition of cell growth in D-gal-induced cells. In conclusion, our findings demonstrate that DDX58 promotes inflammatory responses and growth arrest in SCOS Sertoli cells by stabilizing p65 mRNA. Accordingly, the DDX58/p65 regulatory axis might be a therapeutic target for SCOS.

Abstract Background Cuproptosis is a newly discovered programmed cell death dependent on mitochondrial respiratory disorder induced by copper overload. PDHB is one of the genes responsible for cuproptosis and is a nuclear encoded pyruvate dehydrogenase, an enzyme that catalyzes the conversion of pyruvate to acetyl coenzyme A. However, the mechanism of PDHB in renal clear cell carcinoma remains unclear. Methods We used data from TCGA and GEO to assess the expression of PDHB in normal and tumor tissues. We analysed the relationship between PDHB and somatic mutations and immune infiltration. Finally, we explored the impact of overexpressed PDHB on renal clear cell carcinoma. Results PDHB is lowly expressed in tumor tissue and reduced in high-grade tumors. Highly expressed PDHB has a better prognosis in ccRCC. In ccRCC, low PDHB expression may be associated with higher VHL, PBRM1 and KDM5C mutations. Addition of copper chloride to the 786-O cell line resulted in inhibition of cell growth and increased expression of the cuproptosis genes DLAT, PDHB and FDX1. Finally, the experiments verified that overexpression of PDHB inhibited the proliferation and migration of ccRCC cells. Conclusion Our results demonstrate that elevated PDHB expression inhibits the proliferation, migration and invasion of renal clear cell carcinoma cells, improves the prognosis of renal cancer patients and may provide a new therapeutic strategy for patients with advanced renal cancer.

BackgroundNeutrophil extracellular traps (NETs) are web-like structures formed by neutrophils, and their main function is antimicrobial defense. Moreover, NETs have numerous roles in the pathogenesis and progression of cancers. However, the potential roles of NET-related genes in renal cell carcinoma remain unclear. In this study, we comprehensively investigated the NETs patterns and their relationships with tumor environment (TME), clinicopathological features, prognosis, and prediction of therapeutic benefits in the clear cell renal cell carcinoma (ccRCC) cohort. MethodsWe obtained the gene expression profiles, clinical characteristics, and somatic mutations of patients with ccRCC from The Cancer Genome Atlas database (TCGA), Gene Expression Omnibus (GEO), and ArrayExpress datasets, respectively. ConsensusCluster was performed to identify the NET clusters. The tumor environment scores were evaluated by the "ESTIMATE," "CIBERSORT," and ssGSEA methods. The differential analysis was performed by the "limma" R package. The NET-scores were constructed based on the differentially expressed genes (DEGs) among the three cluster patterns using the ssGSEA method. The roles of NET scores in the prediction of immunotherapy were investigated by Immunophenoscores (TCIA database) and validated in two independent cohorts (GSE135222 and IMvigor210). The prediction of targeted drug benefits was implemented using the "pRRophetic" and Gene Set Cancer Analysis (GSCA) datasets. Real-time quantitative reverse transcription polymerase chain reaction (RT-PCR) was performed to identify the reliability of the core genes' expression in kidney cancer cells. ResultsThree NET-related clusters were identified in the ccRCC cohort. The patients in Cluster A had more metabolism-associated pathways and better overall survival outcomes, whereas the patients in Cluster C had more immune-related pathways, a higher immune score, and a poorer prognosis than those in Cluster B. Based on the DEGs among different subtypes, patients with ccRCC were divided into two gene clusters. These gene clusters demonstrated significantly different immune statuses and clinical features. The NET scores were calculated based on the ten core genes by the Gene Set Variation Analysis (GSVA) package and then divided ccRCC patients into two risk groups. We observed that high NET scores were associated with favorable survival outcomes, which were validated in the E-MTAB-1980 dataset. Moreover, the NET scores were significantly associated with immune cell infiltration, targeted drug response, and immunotherapy benefits. Subsequently, we explored the expression profiles, methylation, mutation, and survival prediction of the 10 core genes in TCGA-KIRC. Though all of them were associated with survival information, only four out of the 10 core genes were differentially expressed genes in tumor samples compared to normal tissues. Finally, RT-PCR showed that MAP7, SLC16A12, and SLC27A2 decreased, while SLC3A1 increased, in cancer cells. ConclusionNETs play significant roles in the tumor immune microenvironment of ccRCC. Identifying NET clusters and scores could enhance our understanding of the heterogeneity of ccRCC, thus providing novel insights for precise individual treatment.

To provide a comprehensive account of the association of ACYP2 gene polymorphisms with susceptibility to cancer. A literature search for eligible candidate gene studies published before April 20, 2022 was conducted in the PubMed, Medline and Web of Science. The following combinations of main keywords were used: (ACYP2 OR acylphosphatase 2) AND (polymorphism OR mutation OR variation OR SNP OR genotype) AND (cancer OR tumor OR neoplasm OR malignancy OR carcinoma OR adenocarcinoma). Potential sources of heterogeneity were sought out via subgroup and sensitivity analysis. Publication bias were also estimated. Overall, a total of 10 articles with 5,230 cases and 5,086 controls for thirteen polymorphisms of ACYP2 gene were enrolled. We found that ACYP2 rs11125529, rs11896604, rs12615793, rs17045754, rs6713088, rs843645, rs843706, rs843711 and rs843752 were correlated with an increased risk of cancer. However, we found that ACYP2 rs12621038 might have less susceptibility to cancer. While for other polymorphisms, the results showed no significant association with cancer risk. ACYP2 rs11125529, rs11896604, rs12615793, rs17045754, rs6713088, rs843645, rs843706, rs843711 and rs843752 are associated with cancer risk. ACYP2 rs12621038 polymorphism is inversely associated with cancer risk.

Early clinical studies indicated that estrogen receptor beta (ER beta) might play key roles to impact the progression of clear cell renal cell carcinoma (ccRCC). The detailed molecular mechanisms, however, remain unclear. Here, we found ER beta could increase the cancer stem cell (CSC) population via altering the circPHACTR4/miR-34b-5p/c-Myc signaling. Mechanism dissection revealed that ER beta could suppress circular RNA PHACTR4 (circPHACTR4) expression via direct binding to the estrogen response elements (EREs) on the 5 ' promoter region of its host gene, phosphatase and actin regulator 4 (PHACTR4) to decrease miR-34b-5p expression. The decreased miRNA-34b-5p could then increase c-Myc mRNA translation via targeting its 3 ' untranslated region (3 ' UTR). The in vivo mouse model with subcutaneous xenografts of ccRCC cells also validated the in vitro data. Importantly, analysis results from ccRCC TCGA database and our clinical data further confirmed the above in vitro/in vivo data. Together, these results suggest that ER beta may increase CSC population in ccRCC via altering ER beta/circPHACTR4/miR-34b-5p/c-Myc signaling and that targeting this newly identified signal pathway may help physicians to better suppress ccRCC progression.

BackgroundUrinary stones are a common and frequently-occurring disease of the urinary system, among which upper urinary tract stones are the most common, imposing a heavy burden on patients. The causes of upper urinary tract stones are complex, which are closely associated with gender, age, geographic condition, climate, diet, and so on. However, it is still unclear whether upper urinary stone constituents vary by geographical conditions.ObjectiveTo analyze the constituents of upper urinary tract stones among adults in different geographic regions of Hebei, providing evidence for clinical treatment and prevention of upper urinary tract stones.MethodsOutpatients and inpatients (n=1 192, ≥18 years old) with upper urinary calculis who were from three geographical regions (mountainous, plain and coastal) of Hebei were selected from the Second Hospital of Hebei Medical University in 2019. Upper urinary tract stones of the outpatients removed by extracorporeal shock wave lithotripsy, and those of the inpatients removed by surgery were collected for quantitative and qualitative constituent analyses by geographical region using infrared spectrometry.ResultsUpper urinary tract stones were more often found in those 30 to 70 years old, with a male to female ratio about 1.75∶1. Kidney stones and ureteral stones accounted for similar proportions (about 1.1∶1) , and the mixed stones were more common (61.5%) . Calcium-containing stones were the major type of upper urinary tract stones in participants from each geographic regions, with calcium oxalate monohydrate being the most. The prevalence of infectious stones showed no significant differences across participants from three regions (P>0.05) . The prevalence of uric acid-containing stones in participants from plain was significantly different from that of participants from mountainous or coastal region (P<0.05) .ConclusionCalcium-containing stones were the most common prevalent in upper urinary tract stones patients across three geographic regions of Hebei, and the prevalence of uric acid-containing stones in those from mountainous or coastal region was higher, which require the attention of urologists.

Introduction: Laparoendoscopic single-site adrenalectomy (LESSA) has the advantages of early recovery and better cosmetic appearance. However, there are still debates on the efficacy and safety of LESSA and conventional laparoscopic adrenalectomy (CLA). Aim: To reevaluate the efficacy and safety of LESSA vs CLA for adrenal lesions. Material and methods: A systematic literature research of PubMed, Ovid, Scopus (up to February 2021), and citation lists was performed to identify eligible studies. All studies comparing LESSA versus CLA were included. Data were analyzed using the RevMan 5.4 software. Results: Overall, eighteen studies including 1307 patients (LESSA 520; CLA 787) were included. LESSA was associated with smaller mean tumor size (weighted mean difference (WMD) = 0.53 cm, 95% CI: -0.81 to -0.24; p < 0.001). The operative time for LESSA was longer than CLA (WMD = 13.86 min, 95% CI: 4.43 to 23.30; p = 0.004). LESSA had a better visual analog scale (VAS) score (WMD = -0.56, 95% CI: -1.01 to -0.11; p = 0.02), shorter return to diet time (WMD = -0.27 days, 95% CI: -0.52 to -0.03; p = 0.03), shorter length of hospital stay (WMD = -0.56 days, 95% CI: -1.01 to -0.11; p = 0.01), and comparable postoperative complications (OR = 0.98, 95% CI: 0.56 to 1.70; p = 0.93). The wound size of LESSA was definitely smaller (WMD = -2.72 cm, 95% CI: -3.50 to -1.94; p < 0.001). The subgroup analysis of studies via the transperitoneal approach showed reasonable results. Conclusions: LESSA is significantly better in terms of postoperative pain, time to diet, length of hospital stay and wound size, but the operative time is significantly longer.

RNA‐binding motif protein 5 (RBM5) acts as a tumor suppressor in various human cancers and presents with several important characteristics, such as the potentiation of apoptosis, inhibition of the cell cycle, and alternative splicing of Fas and caspase‐2 precursor mRNA. However, its role in bladder urothelial carcinoma (BUC) remains unknown. In this study, we found that RBM5 expression was significantly down‐regulated in BUC tissues when compared with the adjacent nontumor tissues. The down‐regulation of RBM5 activates ²‐catenin, which binds to the T‐cell factor/lymphocyte enhancer factor element of the miR‐432‐5p promoter and elevates the expression of miR‐432‐5p in bladder cancer cells. The up‐regulated miR‐432‐5p directly targets 3′‐UTR and depresses RBM5 expression. Thus, RBM5–miR‐432‐5p–²‐catenin forms a feedback loop in regulating bladder cancer cell apoptosis. Our findings provide evidence that the regulatory feedback loop among RBM5, miR‐432‐5p, and Wnt–²‐catenin is responsible for the progress of bladder cancer cells.—Zhang, Y.‐P., Liu, K.‐L., Wang, Y.‐X., Yang, Z., Han, Z.‐W., Lu, B.‐S., Qi, J.‐C, Yin, Y.‐W., Teng, Z.‐H., Chang, X.‐L., Li, J.‐D., Xin, H., Li, W. Down‐regulated RBM5 inhibits bladder cancer cell apoptosis by initiating an miR‐432‐5p/²‐catenin feedback loop. FASEB J. 33, 10973–10985 (2019). www.fasebj.org

INTRODUCTION: This manuscript is a review of current studies and conducts a meta-analysis on the topic of partial nephrectomy (PN) and radical nephrectomy (RN) in larger renal tumors (cT2 and greater). EVIDENCE ACQUISITION: A systematic research of PubMed, Ovid, Scopus (up to January 2019), and reference lists was performed to identify eligible comparative studies. All studies comparing PN with RN for cT2 or greater renal tumors were included. The quality of the included trials was assessed and the data were extracted independently by two reviewers. Statistical analyses were performed using the Cochrane Collaboration's Review Manager (RevMan) 5.3 software. EVIDENCE SYNTHESIS: Overall, 11 retrospective cohort studies including 19,281 patients (PN 1,146; RN 18,135) were included in the analysis. The tumor size was likely smaller in PN compared with RN (WMD -0.85 cm; P=0.05). Lower estimated blood loss (EBL) was found for RN (WMD 100.44 mL; P<0.001). The length of hospital stay was longer for PN (WMD 1.07 days; P=0.002). There was a higher likelihood of postoperative complications for PN (RR 1.96; P<0.001). PN was associated with better postoperative renal function (eGFR; WMD 7.31 mL/min/1.73 m2; P<0.001), and lower decline in eGFR (WMD -9.00 mL/min/1.73 m2; P<0.001). The positive margins were more common in PN (RR 4.19; P=0.003). The PN group might be non-inferior to RN for tumor recurrence (RR 0.57; P<0.001), tumor-specific mortality (RR 0.58; P=0.007), and all-cause mortality (RR 0.78; P=0.004). CONCLUSIONS: PN shows a feasible, safe and viable treatment option for larger renal tumors because it provides better preservation of kidney function and non-inferior survival. However, PN in patients with stage T2 or greater renal masses should be more selective, because of higher complications.