Association between DCP levels and kidney stone prevalence in US female adults based on NHANES data.

Our study aimed to evaluate the correlation between levels of 2,4-DCP(2,4-Dichlorophenol) and 2,5-DCP(2,5-Dichlorophenol) and the prevalence of kidney stones in US female adults. Participants were chosen from the National Health and Nutrition Examination Survey database, spanning the years 2007-2016. Dose-response curves were analyzed using logistic regression, subgroup analyses, and other statistical methods to evaluate the relationship between 2,4-DCP and 2,5-DCP levels and the prevalence of kidney stones. The final study included 3220 participants aged over 20 years, with 252 females reporting a history of kidney stones. After accounting for all interfering variables, we found that every 0.1 ug/ml increase in 2.4-DCP correlated with a 1% rise in kidney stone prevalence (OR = 1.01, 95% CI 1.00, 1.01), whereas the same increase in 2.5-DCP was linked to a 27% growth in prevalence (OR = 1.27, 95% CI 1.01, 1.61). Sensitivity analysis was performed by triangulating 2,4-DCP and 2,5-DCP levels. The dose-response curves demonstrated a linear positive relationship between 2,4-DCP and 2,5-DCP levels and the risk of stone development. Our findings indicate a positive correlation between 2,4-DCP and 2,5-DCP levels and the prevalence of kidney stones in US female adults. This association is of clinical significance; however, a direct causal relationship cannot be definitively established.

Epigenetic dysregulated long non-coding RNAs in renal cell carcinoma based on multi-omics data and their influence on target drugs sensibility.

Purpose: Epigenetic modifications play a crucial role in cancer development, and our study utilized public data to analyze which leads to the discovery of significant epigenetic abnormalities in lncRNAs, offering valuable insights into prognosis and treatment strategies for renal carcinoma. Methods: Public data were obtained from the Cancer Genome Atlas (TCGA), International Cancer Genome Consortium (ICGC) and Gene Expression Omnibus (GEO) database. The analysis of the online public data was all completed in R software. Results: We discovered a great number of epigenetic abnormalities of lncRNA in renal cancer, which is achieved by comparing the following modification and methylation of histone region changes on the promoter and enhancer of lncRNA: H3K27ac, H3K4me1, H3K4me3. As a result, 12 specific epigenetic disorders of lncRNA genes in renal cancer were identified. Finally, based on this lncRNA, we investigated the prognosis of renal cancer samples, among which 8 lncRNA can be seen as markers of prognosis in renal cancer, which had great prediction ability for ccRCC prognosis. Meanwhile, high risk score may pose response better to axitinib and nilotinib, but not sorafenib or sunitinib. Beyond, we observed an elevated level of risk score in immunotherapy non-responders. Further, biological enrichment and immuno-infiltration analysis was conducted to investigate the fundamental differences between patients categorized as high or low risk. Conclusion: Our research improves the understanding in the function of epigenetic dysregulated long non-coding RNAs in renal carcinoma.

Integrated single-cell and bulk characterization of branched chain amino acid metabolism-related key gene BCAT1 and association with prognosis and immunogenicity of clear cell renal cell carcinoma.

BACKGROUND: The relationship between clear cell renal cell carcinoma (ccRCC) and branched-chain amino acids (BCAA) metabolism has yet to be thoroughly explored. METHODS: The BCAA metabolism-related clusters were constructed using non-negative matrix factorization (NMF). The features of BCAA metabolism in ccRCC were evaluated by building a prognostic model using least absolute shrinkage and selection operator (LASSO) regression algorithm. Real-time quantitative PCR (RT-qPCR) was employed to analyze differential expression of branched-chain amino acid transaminase 1 (BCAT1) between cancer and paracancer tissues and between different cell lines. Cell counting kit-8, wound healing and Transwell chamber assays were conducted to determine changes in proliferative and metastatic abilities of A498 and 786-O cells. RESULTS: Two BCAA metabolism-related clusters with distinct prognostic and immune infiltration characteristics were identified in ccRCC. The BCAA metabolic signature (BMS) was capable of distinguishing immune features, tumor mutation burden, responses to immunotherapy, and drug sensitivity among ccRCC patients. RT-qPCR revealed overexpression of BCAT1 in ccRCC tissues and cell lines. Additionally, single-gene RNA sequencing analysis demonstrated significant enrichment of BCAT1 in macrophages and tumor cells. BCAT1 played tumor-promoting role in ccRCC and was closely associated with immunosuppressive cells and checkpoints. BCAT1 promoted ccRCC cell proliferation and metastasis. CONCLUSIONS: The BMS played a crucial role in determining the prognosis, tumor mutation burden, responses to immunotherapy and drug sensitivity of ccRCC patients, as well as the immune cell infiltration features. BCAT1 was linked to immunosuppressive microenvironments and may offer new sights into ccRCC immunotherapeutic targets.