Background Non-alcoholic fatty liver disease (NAFLD) is the most common chronic liver disease globally, with the potential to progress to non-alcoholic steatohepatitis (NASH), cirrhosis, and even hepatocellular carcinoma. Given the absence of effective treatments to halt its progression, novel molecular approaches to the NAFLD diagnosis and treatment are of paramount importance. Methods Firstly, we downloaded oxidative stress-related genes from the GeneCards database and retrieved NAFLD-related datasets from the GEO database. Using the Limma R package and WGCNA, we identified differentially expressed genes closely associated with NAFLD. In our study, we identified 31 intersection genes by analyzing the intersection among oxidative stress-related genes, NAFLD-related genes, and genes closely associated with NAFLD as identified through Weighted Gene Co-expression Network Analysis (WGCNA). In a study of 31 intersection genes between NAFLD and Oxidative Stress (OS), we identified three hub genes using three machine learning algorithms: Least Absolute Shrinkage and Selection Operator (LASSO) regression, Support Vector Machine - Recursive Feature Elimination (SVM-RFE), and RandomForest. Subsequently, a nomogram was utilized to predict the incidence of NAFLD. The CIBERSORT algorithm was employed for immune infiltration analysis, single sample Gene Set Enrichment Analysis (ssGSEA) for functional enrichment analysis, and Protein-Protein Interaction (PPI) networks to explore the relationships between the three hub genes and other intersecting genes of NAFLD and OS. The distribution of these three hub genes across six cell clusters was determined using single-cell RNA sequencing. Finally, utilizing relevant data from the Attie Lab Diabetes Database, and liver tissues from NASH mouse model, Western Blot (WB) and Reverse Transcription Quantitative Polymerase Chain Reaction (RT-qPCR) assays were conducted, this further validated the significant roles of CDKN1B and TFAM in NAFLD. Results In the course of this research, we identified 31 genes with a strong association with oxidative stress in NAFLD. Subsequent machine learning analysis and external validation pinpointed two genes: CDKN1B and TFAM, as demonstrating the closest correlation to oxidative stress in NAFLD. Conclusion This investigation found two hub genes that hold potential as novel targets for the diagnosis and treatment of NAFLD, thereby offering innovative perspectives for its clinical management.

Integrative analysis identifies oxidative stress biomarkers in non-alcoholic fatty liver disease via machine learning and weighted gene co-expression network analysis

Abstract Introduction Although previous studies have linked obesity and erectile dysfunction, the novel surrogate indicators of adipose accumulation are more essential and dependable factors to consider. Therefore, the primary objective of the current investigation was to examine and clarify the association between metabolic score for visceral fat (METS-VF) and erectile dysfunction. Methods Firstly, multivariate logistic regression analysis, smoothed curve fitting, and threshold effect analysis were employed to investigate the association between METS-VF and erectile dysfunction. Mediation analysis was also performed to evaluate the mediating role of homocysteine and inflammation. After that, subgroup analysis was carried out to examine the stability of the correlation of METS-VF with erectile dysfunction in various population settings. Furthermore, the area under the receiver operating characteristic (ROC) curve and eXtreme Gradient Boosting (XGBoost) algorithm were utilized to assess the capability of identifying METS-VF in comparison to the other four obesity-related indicators in identifying erectile dysfunction. Results After adjusting for all confounding factors, METS-VF was strongly and favourablely correlated with erectile dysfunction. With each additional unit rise in METS-VF, the prevalence of erectile dysfunction increased by 141%. A J-shaped relationship between METS-VF and erectile dysfunction was discovered through smoothed curve fitting. Marital status, physical activity, and smoking status can potentially modify this association. This finding of the ROC curve suggests that METS-VF had a powerful identifying capacity for erectile dysfunction (AUC = 0.7351). Homocysteine and inflammation mediated 4.24% and 2.81%, respectively. Conclusion The findings of the current investigation suggest that METS-VF can be considered a dependable identifying indicator of erectile dysfunction. 

Investigating a novel surrogate indicator of adipose accumulation in relation to erectile dysfunction

Rheumatoid arthritis (RA) is a long-term, systemic, and progressive autoimmune disorder. It has been established that ferroptosis, a type of iron-dependent lipid peroxidation cell death, is closely associated with RA. Fibroblast-like synoviocytes (FLS) are the main drivers of RA joint destruction, and they possess a high concentration of endoplasmic reticulum structure. Therefore, targeting ferroptosis and RA-FLS may be a potential treatment for RA.Four machine learning algorithms were utilized to detect the essential genes linked to RA, and an XGBoost model was created based on the identified genes. SHAP values were then used to visualize the factors that affect the development and progression of RA, and to analyze the importance of individual features in predicting the outcomes. Moreover, WGCNA and PPI were employed to identify the key genes related to RA, and CIBERSORT was used to analyze the correlation between the chosen genes and immune cells. Finally, the findings were validated through in vitro cell experiments, such as CCK-8 assay, lipid peroxidation assay, iron assay, GSH assay, and Western blot.Bioinformatics and machine learning were employed to identify cathepsin B (CTSB) as a potential biomarker for RA. CTSB is highly expressed in RA patients and has been found to have a positive correlation with macrophages M2, neutrophils, and T cell follicular helper cells, and a negative correlation with CD8 T cells, monocytes, Tregs, and CD4 memory T cells. To investigate the effect of CTSB on RA-FLS from RA patients, the CTSB inhibitor CA-074Me was used and it was observed to reduce the proliferation and migration of RA-FLS, as indicated by the accumulation of lipid ROS and ferrous ions, and induce ferroptosis in RA-FLS.This study identified CTSB, a gene associated with ferroptosis, as a potential biomarker for diagnosing and managing RA. Moreover, CA-074Me, a CTSB inhibitor, was observed to cause ferroptosis and reduce the migratory capacity of RA-FLS. 

Cathepsin B serves as a potential prognostic biomarker and correlates with ferroptosis in rheumatoid arthritis.

(1) Background: Arteriovenous fistulas (AVFs) are the preferred site for hemodialysis. Unfortunately, approximately 60% of patients suffer from AVF failure within one year. Oxidative stress plays an important role in the occurrence and development of AVF. However, the underlying mechanisms remain unclear. Therefore, specific oxidative stress-related biomarkers are urgently needed for the diagnosis and treatment of AVF failure. (2) Methods: Bioinformatics analysis was carried out on dataset GSE119296 to screen for PTGS2 as a candidate gene related to oxidative stress and to verify the expression level and diagnostic efficacy of PTGS2 in clinical patients. The effects of NS398, a PTGS2 inhibitor, on hemodynamics, smooth muscle cell proliferation, migration, and oxidative stress were evaluated in a mouse AVF model. (3) Results: Based on 83 oxidative stress-related differentially expressed genes, we identified the important pathways related to oxidative stress. PTGS2 may have diagnostic and therapeutic efficacy for AVF failure. We further confirmed this finding using clinical specimens and validation datasets. The animal experiments illustrated that NS398 administration could reduce neointimal area (average decrease: 49%) and improve peak velocity (average increase: 53%). (4) Conclusions: Our study identified PTGS2 as an important oxidative stress-related biomarker for AVF failure. Targeting PTGS2 reduced oxidative stress and improved hemodynamics in an AVF mouse model.

Identification and Validation of PTGS2 Gene as an Oxidative Stress-Related Biomarker for Arteriovenous Fistula Failure

: Diabetic kidney disease (DKD), is a common microvascular complication and a major cause of death in patients with diabetes. Disorders of immune cells and immune cytokines can accelerate DKD development of in a number of ways. As the kidney is composed of complex and highly differentiated cells, the interactions among different cell types and immune cells play important regulatory roles in disease development. Here, we summarize the latest research into the molecular mechanisms underlying the interactions among various immune and renal cells in DKD. In addition, we discuss the most recent studies related to single cell technology and bioinformatics analysis in the field of DKD. The aims of our review were to explore immune cells as potential therapeutic targets in DKD and provide some guidance for future clinical treatments.

The Role of Immune Cells in DKD: Mechanisms and Targeted Therapies

Background Diabetic nephropathy (DN) is the primary cause of end-stage renal disease, but existing therapeutics are limited. Therefore, novel molecular pathways that contribute to DN therapy and diagnostics are urgently needed. Methods Based on the Gene Expression Omnibus (GEO) database and Limma R package, we identified differentially expressed genes of DN and downloaded oxidative stress-related genes based on the Genecard database. Then, immune and oxidative stress-related hub genes were screened by combined WGCNA, machine learning, and protein-protein interaction (PPI) networks and validated by external validation sets. We conducted ROC analysis to assess the diagnostic efficacy of hub genes. The correlation of hub genes with clinical characteristics was analyzed by the Nephroseq v5 database. To understand the cellular clustering of hub genes in DN, we performed single nucleus RNA sequencing through the KIT database. Results Ultimately, we screened three hub genes, namely CD36, ITGB2, and SLC1A3, which were all up-regulated. According to ROC analysis, all three demonstrated excellent diagnostic efficacy. Correlation analysis revealed that the expression of hub genes was significantly correlated with the deterioration of renal function, and the results of single nucleus RNA sequencing showed that hub genes were mainly clustered in endothelial cells and leukocyte clusters. Conclusion By combining three machine learning algorithms with WGCNA analysis, this research identified three hub genes that could serve as novel targets for the diagnosis and therapy of DN.

/pdf/identification-and-validation-of-immune-and-oxidative-stress-rlldntra.pdf

Identification and validation of immune and oxidative stress-related diagnostic markers for diabetic nephropathy by WGCNA and machine learning

The risk of visceral obesity on erectile function has recently attracted much attention. The visceral adiposity index (VAI) is a brief and reliable indicator of visceral obesity measurement. Nevertheless, the association between VAI and erectile dysfunction (ED) is not completely clarified.Data from NHANES 2001–2004 were enrolled in this study. Erectile function was assessed by a database-self-administered questionnaire. VAI was calculated with body mass index (BMI), waist circumference (WC), triglyceride (TG), and high-density lipoprotein (HDL) cholesterol. The weighted logistic regression model was performed to evaluate the association between VAI and ED.Ultimately, 3380 participants were enrolled in the study, including 900 with ED and 2480 without ED. Compared to participants without ED, those with ED generally had higher levels of VAI (1.76 vs. 1.53). The weighted logistic regression analyses demonstrated increased odds of developing ED in participants within the 4th quartile (Q4) of VAI compared to the 1st quartile (Q1) of VAI (OR = 2.023; 95% CI, 1.534–2.669; P < 0.001). Similar results were still obtained after adjusting for the relevant covariates (OR = 1.404; 95% CI, 1.008–1.954; P = 0.044). In subgroup analyses grouped by smoking status, higher VAI was associated with increased odds of developing ED only in the current smoking group (OR = 1.092; 95% CI, 1.021–1.167; P = 0.010).This study indicated that higher VAI is independently related to ED risk and that early intervention is necessary to reduce the progression of ED with high VAI levels.

Correlation between visceral adiposity index and erectile dysfunction in American adult males: a cross-sectional study based on NHANES

Background Prostate cancer (PCa) is the second most common type of cancer and the fifth leading cause of cancer-related death in men. Androgen deprivation therapy (ADT) has become the first-line therapy for inhibiting PCa progression; however, nearly all patients receiving ADT eventually progress to castrate-resistant prostate cancer. Therefore, this study aimed to identify hub genes related to bicalutamide resistance in PCa and provide new insights into endocrine therapy resistance. Methods The data were obtained from public databases. Weighted correlation network analysis was used to identify the gene modules related to bicalutamide resistance, and the relationship between the samples and disease-free survival was analyzed. Gene Ontology and Kyoto Encyclopedia of Genes and Genomes analyses were performed, and hub genes were identified. The LASSO algorithm was used to develop a bicalutamide resistance prognostic model in patients with PCa, which was then verified. Finally, we analyzed the tumor mutational heterogeneity and immune microenvironment in both groups. Results Two drug resistance gene modules were identified. Gene Ontology and Kyoto Encyclopedia of Genes and Genomes analyses revealed that both modules are involved in RNA splicing. The protein–protein interaction network identified 10 hub genes in the brown module LUC7L3, SNRNP70, PRPF3, LUC7L, CLASRP, CLK1, CLK2, U2AF1L4, NXF1, and THOC1) and 13 in the yellow module (PNN, PPWD1, SRRM2, DHX35, DMTF1, SALL4, MTA1, HDAC7, PHC1, ACIN1, HNRNPH1, DDX17, and HDAC6). The prognostic model composed of RNF207, REC8, DFNB59, HOXA2, EPOR, PILRB, LSMEM1, TCIRG1, ABTB1, ZNF276, ZNF540, and DPY19L2 could effectively predict patient prognosis. Genomic analysis revealed that the high- and low-risk groups had different mutation maps. Immune infiltration analysis showed a statistically significant difference in immune infiltration between the high- and low-risk groups, and that the high-risk group may benefit from immunotherapy. Conclusion In this study, bicalutamide resistance genes and hub genes were identified in PCa, a risk model for predicting the prognosis of patients with PCa was constructed, and the tumor mutation heterogeneity and immune infiltration in high- and low-risk groups were analyzed. These findings offer new insights into ADT resistance targets and prognostic prediction in patients with PCa.

/pdf/identification-of-bicalutamide-resistance-related-genes-and-3m2lne5h.pdf

Identification of bicalutamide resistance-related genes and prognosis prediction in patients with prostate cancer

PURPOSE
Aspirin (ASA) is often stopped prior to percutaneous nephrolithotomy (PCNL) due to the surgical bleeding risk. However, this practice is based on expert opinion only, and mounting evidence suggests holding aspirin perioperatively can be more harmful than once thought. In our review we aimed to discuss the safety of low dose aspirin continued or discontinued in the whole perioperative period of PCNL.


PATIENTS AND METHOD
We performed a computerized PubMed, EMBASE and Cochrane Library search of relevant studies. Study identification satisfied the PRISMA guidelines. Newcastle-Ottawa scale (NOS) was used to evaluate the quality of including studies. Favored outcomes such as operative time, complications and change in hemoglobin were extracted. Statistical analysis was performed with Rev-Man software 5.3 and forest plots were used to illustrate our findings.


RESULTS
After screening, four studies were included in the present systematic review. There was no difference in the number of total complications (OR:1.25; 95 % CI 0.82-1.90; p=0.30), major complications (OR: 1.24; 95 % CI 0.53-2.93; p=0.62) and blood transfusion rate (OR:0.99; 95 % CI 0.46-2.12; p=0.98) between the continuing low dose aspirin group and discontinuing group. Moreover, the overall stone-free rate was also not statistically significant (OR:3.17; 95 % CI 0.89-11.25; p=0.07). It was similar about the change in hemoglobin, hematocrit and creatinine levels between two groups.


CONCLUSION
Based on our findings, transient cessation of aspirin perioperatively seems not to be necessary for patients who need PCNL complicated with the necessity of aspirin therapy. However, further well-designed prospective studies with large sample size are needed to confirm and validate our findings.

The Safety of Continuing Low-dose Aspirin Therapy Perioperatively in the Patients had Undergone Percutaneous Nephrolithotomy: A Systematic Review and Meta-analysis.

BACKGROUND
Benign prostatic hyperplasia (BPH) is a common condition that affects the quality of life of older men. Specific micronutrients, including retinol, retinyl esters, carotenoids, vitamin E, and vitamin C, have antioxidant and anti-inflammatory properties. However, the correlation between serum concentrations of these micronutrients and BPH is unclear.


METHODS
We used data from the National Health and Nutrition Examination Survey (NHANES), which included 2067 representative US men. BPH was assessed using the self-reported questionnaire. This association was explored by adjusting for confounders using multivariate logistic regression.


RESULTS
After fully adjusting for confounders, for every 0.01 μmol/L increase in serum retinyl esters, the risk of BPH increased by 2% (OR = 1.02; 95% CI: 1.01-1.03; p = 0.006). Based on the Bonferroni-corrected p-value, we found this correlation to be significant. One μmol/L increase in total carotenoids was associated with a 22% increase in BPH risk (OR = 1.22; 95% CI: 1.03-1.46; p = 0.025). By analyzing the correlation between different types of carotenoids and BPH, we also found that β-carotenoids (OR = 1.43; 95% CI: 1.03-1.99; p = 0.036) was also positively correlated with BPH. The subgroup analysis revealed a positive correlation between serum vitamin E (OR = 1.02; 95% CI: 1.00-1.04; p = 0.018) and BPH in men under 60 years of age. Serum retinyl ester (OR = 1.02; 95% CI: 1.01-1.04; p = 0.008) and carotenoid (OR = 1.52; 95% CI: 1.22-1.87; p < 0.001) concentrations were positively correlated with BPH in men over 60 years of age.


CONCLUSION
Our study suggests that excessive serum retinyl esters, total carotenoids, and especially β-carotenoids are potential risk factors for BPH, and this association should be further investigated.

The association between several serum micronutrients and benign prostatic hyperplasia: Results from NHANES 2003-2006.

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