The purpose of this study was to investigate the regulatory mechanism of miR-450a-2-3p in myocardial fibrosis in patients with atrial fibrillation. For this purpose, the expression profile of GSE55296 was extracted from the GEO database, and differentially expressed lncRNAs were identified. Gene ontology analysis of the target genes of mir-450a-2-3p indicated that there was a regulatory relationship between LINC00636 and miR-450a-2-3p. Further, the expression levels of the analyzed RNAs were confirmed by RT-qPCR. TGF-β1-induced cardiac fibroblasts (CFs) and human umbilical vein endothelial cells (HUVECs) were used to establish a myocardial fibrosis model and endothelium-mesenchymal transformation (EMT) model in vivo. We hypothesized that exosomes containing LINC00636 regulate the expression of miR-450a-2-3p. LINC00636 was positively correlated with the expression of miR-450a-2-3p. The overexpression of miR-450a-2-3p suppressed the MAPK1 expression in CFs, thereby inhibiting the expression of α-SMA, COL1, and COL3 and preventing CF proliferation. In HUVECs, the miR-450a-2-3p overexpression upregulated the expression of VE-Cadherin (VE-Cad) and platelet endothelial cell adhesion molecule-1 (PECAM-1/CD31) by inhibiting the mitogen-activated protein kinase 1 (MAPK1) expression, whereas the expression levels of vimentin, COL1, and COL3 decreased. These results indicate that LINC00636, which is present in human pericardial fluid, is an antifibrotic molecule that inhibits MAPK1 through the miR-450a-2-3p overexpression and improves cardiac fibrosis in patients with atrial fibrillation.

BackgroundTumor cell dissemination after needle biopsy has been reported in a variety of malignancies, including non-small-cell lung cancer (NSCLC). However, there is little clinical evidence in regard to whether preoperative biopsy increases the risk of recurrence in completely resected NSCLC.Patients and methodsA total of 322 patients diagnosed as pathological stage I NSCLC using intraoperative biopsy (IOB) (control group), preoperative percutaneous needle biopsy (PNB) or bronchoscopic biopsy were included in this study. Baseline characteristics were collected and compared. The disease-free survival (DFS) of patients was analyzed using Kaplan–Meier method. Subgroup analysis and Cox regression were performed to evaluate the effect of preoperative biopsy on recurrence risk with adjustment for potential confounders.ResultsAmong these patients, 202 (63%) underwent IOB, 66 (20%) underwent PNB, and 54 (17%) underwent bronchoscopic biopsy. DFS of patients who had preoperative PNB or bronchoscopic biopsy was similar to those who had IOB (P=0.514 and 0.869). Neither preoperative PNB nor transbronchial biopsy significantly affected recurrence incidence across all the relevant subgroups. Furthermore, multivariate analysis showed that preoperative biopsy was not associated with increased recurrence risk in NSCLC patients with adjustment for confounders, while squamous cell carcinoma and adjuvant chemotherapy were associated with prolonged DFS.ConclusionNeither preoperative PNB nor bronchoscopic biopsy increased the recurrence risk in patients with resected stage I NSCLC, indicating that these procedures could be safely used for diagnosis of early-stage NSCLC.

Background Coronary artery disease (CAD) is a multifactorial cardiovascular disease that causes high mortality worldwide. Cuproptosis is a newly discovered method of programmed cell death, but it is unclear whether it is involved in the development of CAD. Methods GSE180081 was downloaded from the GEO database and genes that were differentially expressed in controls and patients with CAD were identified. These were clustered according to the cuproptosis gene set, to identify differentially expressed cuproptosis related genes. The intersection of the two sets of differentially expressed genes was used to identify genes relevant to the diagnosis of CAD using LASSO regression. A diagnostic model was created using the selected genes and logistic regression. Enriched immune genes were identified, the associated ceRNA network was characterized, and drugs that may target the identified genes were searched for. Results We identified 818 differentially expressed genes that were common to the CAD and cuproptosis gene sets, which principally represented the cell-substrate junction and the positive regulation of leukemia. Furthermore, HIST1H4E, IL6ST, RN7SKP45, LST1, and SNORD50B were found be potentially useful for the diagnosis of CAD using the diagnostic model. These genes were found to be closely associated with immune modification. Conclusion We have constructed a diagnostic prediction model based on a cuproptosis gene set using whole-blood transcriptome data. Using this, we have identified HIST1H4E, IL6ST, and LST1 as potential biomarkers of the risk of CAD. These findings provide a novel approach to the prediction, prevention, and individualized treatment of CAD.