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Background. Acute type A aortic dissection (AAD) is a catastrophic disease with high mortality, but the pathogenesis has not been fully elucidated. This study is aimed at identifying hub genes and immune cells associated with the pathogenesis of AAD. Methods. The datasets were downloaded from Gene Expression Omnibus (GEO). Gene Set Enrichment Analysis (GSEA), gene set variation analysis (GSVA), and differential analysis were performed. The differentially expressed genes (DEGs) were intersected with specific genes collected from MSigDB. The gene function and pathway enrichment analysis were also performed on intersecting genes. The key modules were selected by weighted gene coexpression network analysis (WGCNA). Hub genes were identified by least absolute shrinkage and selection operator (LASSO) analysis and were verified in the metadataset. The immune cell infiltration was analyzed by CIBERSORT, and the relationship between hub genes and immune cells was performed by Pearson’s correlation analysis. The single-cell RNA sequencing (scRNA-seq) dataset was used to verify the differences in DNA damage and repair signaling pathways and hub genes in different cell types. Results. The results of GSEA and GSVA indicated that DNA damage and repair processes were activated in the occurrence of AAD. The gene function and pathway enrichment analysis on differentially expressed DNA damage- and repair-related genes showed that these genes were mainly involved in the regulation of the cell cycle process, cellular response to DNA damage stimulus, response to wounding, p53 signaling pathway, and cellular senescence. Three key modules were identified by WGCNA. Five genes were screened as hub genes, including CDK2, EIF4A1, GLRX, NNMT, and SLCO2A1. Naive B cells and Gamma delta T cells (γδ T cells) were decreased in AAD, but monocytes and M0 macrophages were increased. scRNA-seq analysis included that DNA damage and repair processes were activated in smooth muscle cells (SMCs), tissue stem cells, and monocytes in the aortic wall of patients with AAD. Conclusions. Our results suggested that DNA damage- and repair-related genes may be involved in the occurrence of AAD by regulating many biological processes. The hub genes and immune cells reported in this study also increase the understanding of AAD.

Objectives: To provide a reference for CT imaging changes for patients discharged from a Fangcang shelter hospital, a large-scale, temporary hospital for the centralized treatment of patients with mild to moderate Coronavirus disease 2019 (COVID-19) to provide essential functions (isolation, triage, basic medical care, frequent monitoring and rapid referral, essential living and social engagement) to them..Methods: Patients with mild to moderate COVID-19 admitted to the Wuchang Fangcang Shelter Hospital who had undergone pre-discharge and previous CT scans were included. Changes in the CT imaging features were defined as progression, no change, improvement or recovery. Basic patient information was obtained, and imaging signs were compared between the two CT scans.Results: A total of 83 patients were included. The median age was 53 years old. The course of disease was 28.3±10.7 days. CT imaging changes indicated progression, no change, improvement, and recovery in 3, 12, 66, and 2 patients, respectively. Between the two CT scans, the imaging signs showed a significant reduction in consolidation, a significant increase in fibrosis, and a reduction or / and thinning of ground-glass opacities. None of the patients showed signs of deterioration on follow-up and thus did not need to return to the hospital for treatment.Conclusion: In the COVID-19 Fangcang shelter hospital, given the shortage of medical staff and lack of medical resources, CT imaging diagnostic methods can be used to accurately discharge patients who had met the discharge criteria for isolation and observation from the Fangcang Shelter Hospital.

The proliferation of vascular smooth muscle cells (VSMCs) serves an important role in cigarette smoking-associated vascular diseases; however, the underlying mechanisms responsible for this remain unclear. The aim of the present study was to elucidate the role of P16 in cigarette smoke extract (CSE)-induced VSMC proliferation and the underlying mechanism responsible. Human aortic smooth muscle cells (HAOSMCs) were exposed to CSE, and an MTT assay and flow cytometry were performed to evaluate cell proliferation and cell cycle distribution. Western blotting was conducted to examine protein expression and bisulfite genomic sequencing polymerase chain reaction was used to determine the methylation status of the P16 promoter CpG island. It was demonstrated that treatment with CSE significantly promoted the proliferation of HAOSMCs in a concentration- and time-dependent manner and induced a downregulation in P16 expression (all P