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Objective Stroke is a severe complication of atrial fibrillation (AF). We aimed to discover key genes and microRNAs related to stroke risk in patients with AF using bioinformatics analysis. Methods GSE66724 microarray data, including peripheral blood samples from eight patients with AF and stroke and eight patients with AF without stroke, were downloaded from the Gene Expression Omnibus (GEO) database. Differentially expressed genes (DEGs) between AF patients with and without stroke were identified using the GEO2R online tool. Functional enrichment analysis was performed using the DAVID database. A protein–protein interaction (PPI) network was obtained using the STRING database. MicroRNAs (miRs) targeting these DEGs were obtained from the miRNet database. A miR–DEG network was constructed using Cytoscape software. Results We identified 165 DEGs (141 upregulated and 24 downregulated). Enrichment analysis showed enrichment of certain inflammatory processes. The miR–DEG network revealed key genes, including MEF2A, CAND1, PELI1, and PDCD4, and microRNAs, including miR-1, miR-1-3p, miR-21, miR-21-5p, miR-192, miR-192-5p, miR-155, and miR-155-5p. Conclusion Dysregulation of certain genes and microRNAs involved in inflammation may be associated with a higher risk of stroke in patients with AF. Evaluating these biomarkers could improve prediction, prevention, and treatment of stroke in patients with AF.

Curcumin was reported to exhibit a wide range of pharmacological effects including antioxidant, anti-inflammatory, and antiproliferative activities and significantly prevent smooth muscle cells migration. In the present study, a novel kind of curcumin loaded nanoparticles (Cur-NP) has been prepared and characterized with the aim of inhibiting inflammation formation and accelerating the healing process of the stented arteries. Cur-NP was administrated intravenously after stent implantation twice a week and detailed tissue responses were evaluated. The results demonstrated that intravenous administration of Cur-NP after stent implantation accelerated endothelial cells restoration and endothelium function recovery and may potentially be an effective therapeutic alternative to reduce adverse events for currently available drug eluting stents.

Objective We aimed to explore potential microRNAs (miRNAs) and target genes related to atrial fibrillation (AF). Methods Data for microarrays GSE70887 and GSE68475, both of which include AF and control groups, were downloaded from the Gene Expression Omnibus database. Differentially expressed miRNAs between AF and control groups were identified within each microarray, and the intersection of these two sets was obtained. These miRNAs were mapped to target genes in the miRNet database. Functional annotation and enrichment analysis of these target genes was performed in the DAVID database. The protein-protein interaction (PPI) network from the STRING database and the miRNA-target-gene network were merged into a PPI-miRNA network using Cytoscape software. Modules of this network containing miRNAs were detected and further analyzed. Results Ten differentially expressed miRNAs and 1520 target genes were identified. Three PPI-miRNA modules were constructed, which contained miR-424, miR-15a, miR-542-3p, and miR-421 as well as their target genes, CDK1, CDK6, and CCND3. Conclusion The identified miRNAs and genes may be related to the pathogenesis of AF. Thus, they may be potential biomarkers for diagnosis and targets for treatment of AF.

Liangxue Tongyu Formula ameliorates brain edema in rats after intracerebral hemorrhage by inhibiting MMP-9 expression and activity and up-regulating TIMP-1.

The mechanisms of chronic pain are complex, and genetic factors play an essential role in the development of chronic pain. Neuropathic pain (NP) and inflammatory pain (IP) are two primary components of chronic pain. Previous studies have uncovered some common biological processes in NP and IP. However, the shared genetic mechanisms remained poorly studied. We utilized multi-omics systematic analyses to investigate the shared genetic mechanisms of NP and IP. First, by integrating several genome-wide association studies (GWASs) with multi-omics data, we revealed the significant overlap of the gene co-expression modules in NP and IP. Further, we uncovered the shared biological pathways, including the previously reported mitochondrial electron transport and ATP metabolism, and stressed the role of genetic factors in chronic pain with neurodegenerative diseases. Second, we identified 24 conservative key drivers (KDs) contributing to NP and IP, containing two well-established pain genes, IL1B and OPRM1, and some novel potential pain genes, such as C5AR1 and SERPINE1. The subnetwork of those KDs highlighted the processes involving the immune system. Finally, gene expression analysis of the KDs in mouse models underlined two of the KDs, SLC6A15 and KCNQ5, with unidirectional regulatory functions in NP and IP. Our study provides strong evidence to support the current understanding of the shared genetic regulatory networks underlying NP and IP and potentially benefit the future common therapeutic avenues for chronic pain.

Our current understanding of how T lymphocytes enter the airways in response to respiratory tract infections is limited. Here we show a role for type I interferon (IFN) signaling in regulating T lymphocyte transmigration into the airway mucosa. IFNα receptor (IFNAR) deficiency led to a reduction in the number of T lymphocytes that entered the airways but not the lung parenchyma. This effect was mediated both at the T lymphocyte and epithelial cell level. IFNAR-deficient airway epithelial cells failed to express the chemoattractants CCL3-5, CCL8 and CXCL9-11, and did not up-regulate the adhesion molecules ICAM1 and VCAM1. Lack of IFNAR signaling on T lymphocytes impaired Ly-6C expression and lymphocyte function-associated antigen-1 (LFA-1) clustering, which resulted in reduced cell adhesion. Finally, we show that IFNAR-deficiency inhibited T lymphocyte recruitment to the airways during respiratory syncytial virus (RSV) infection.