Background. Clear cell renal cell carcinoma (ccRCC) is the most common subtype of kidney cancers. As cuproptosis, a new cell death mechanism proposed recently, differs from all other known mechanisms regulating cell death, we aimed to create prognostic markers using cuproptosis-related long non-coding ribonucleic acids (RNAs; lncRNAs) and elucidate the molecular mechanism. Methods. Data from transcriptome RNA sequencing of ccRCC samples and the relevant clinical data were downloaded from The Cancer Genome Atlas, and Pearson’s correlation analysis was implemented to obtain the cuproptosis-related lncRNAs. Then, univariate Cox, multivariate Cox, and Least Absolute Shrinkage and Selection Operator Cox analyses were performed to construct the risk signatures. The cuproptosis-related lncRNAs predictive signature was evaluated with receiver operating characteristic curves and subgroup analysis. Finally, Gene Set Enrichment Analysis (GSEA), single-sample GSEA (ssGSEA), tumor immune microenvironment (TIME), and immune checkpoints were performed to explore the relationship between immunity and patient prognosis. Results. Five cuproptosis-related lncRNAs, including FOXD2-AS1, LINC00460, AC091212.1, AC007365.1, and AC026401.3, were used to construct the signature. In the training and test sets, low-risk groups (as identified by a risk score lower than the median) demonstrated a better prognosis with an area under the curve for 1-, 3-, and 5-year survival being 0.793, 0.716, and 0.719, respectively. GSEA analysis suggested significant enrichment of the tricarboxylic acid cycle and metabolism-related pathways in the low-risk group. Besides, both ssGSEA and TIME suggested that the high-risk group exhibited more active immune infiltration. Conclusion. We proposed a cuproptosis-related lncRNAs signature, which had the potential for prognoses and prediction. Our findings might contribute to elucidating potential genomic biomarkers and targets for future therapies in the cuproptosis-related signaling pathways.

The purpose of this study was to investigate the effects of ejaculatory duct obstruction (EDO) on contractile efficacy, smooth muscle ultrastructure, and α1A and M3 receptors of rat seminal vesicles (SVs). A total of 48 male rats, aged 14-15 weeks, were randomly divided into three groups, namely, the control, complete EDO, and partial EDO. SV tissues were collected at 4 and 8 weeks postoperatively for further experiments. Results revealed a marked reduction in SV contractile efficacy over time following obstruction in the complete EDO group. The contractile force and frequency decreased and increased in the partial EDO group at week 4, respectively, whereas contractile efficacy significantly reduced at week 8. Moreover, obstruction resulted in significant downregulation in expression of α1A and M3 proteins and mRNAs in rats from the complete EDO group over time. Rats in the partial EDO group initially exhibited an increase followed by a decrease. Analysis of the ultrastructure of SV smooth muscles confirmed the above changes. In conclusion, complete EDO can lead to a progressive decrease in contractile efficiency of SVs. On the other hand, partial EDO can first compensate for the contraction of SVs and gradually decompensate afterwards.