The commonness in immune infiltration of rheumatoid arthritis and atherosclerosis: Screening for central targets via microarray data analysis.

Background: Although increasing evidence has reported an increased risk of atherosclerosis (AS) in rheumatoid arthritis (RA), the communal molecular mechanism of this phenomenon is still far from being fully elucidated. Hence, this article aimed to explore the pathogenesis of RA complicated with AS. Methods: Based on the strict inclusion/exclusion criteria, four gene datasets were downloaded from the Gene Expression Omnibus (GEO) database. After identifying the communal differentially expressed genes (DEGs) and hub genes, comprehensive bioinformatics analysis, including functional annotation, co-expression analysis, expression validation, drug-gene prediction, and TF-mRNA-miRNA regulatory network construction, was conducted. Moreover, the immune infiltration of RA and AS was analyzed and compared based on the CIBERSORT algorithm, and the correlation between hub genes and infiltrating immune cells was evaluated in RA and AS respectively. Results: A total of 54 upregulated and 12 downregulated communal DEGs were screened between GSE100927 and GSE55457, and functional analysis of these genes indicated that the potential pathogenesis lies in immune terms. After the protein-protein interaction (PPI) network construction, a total of six hub genes (CCR5, CCR7, IL7R, PTPRC, CD2, and CD3D) were determined as hub genes, and the subsequent comprehensive bioinformatics analysis of the hub genes re-emphasized the importance of the immune system in RA and AS. Additionally, three overlapping infiltrating immune cells were found between RA and AS based on the CIBERSORT algorithm, including upregulated memory B cells, follicular helper T cells and γδT cells. Conclusions: Our study uncover the communal central genes and commonness in immune infiltration between RA and AS, and the analysis of six hub genes and three immune cells profile might provide new insights into potential pathogenesis therapeutic direction of RA complicated with AS.

Analysis of Communal Molecular Mechanism and Potential Therapeutic Targets in Heart Failure and Type 2 Diabetes Mellitus.

BACKGROUND: Although increasing evidence has suggested an interaction between heart failure (HF) and Type 2 diabetes mellitus (T2DM), the common mechanisms of the two diseases remain unclear. Therefore, this study aimed to obtain the differentially expressed genes (DEGs) and potential biomarkers or therapeutic targets in HF and T2DM. METHODS: The communal DEGs of HF and T2DM were identified by analyzing the two microarray datasets (GSE84796 and GSE95849), and functional annotation was performed for the communal DEGs to uncover the potential molecular mechanisms of HF and T2DM. Subsequently, STRING database and Cytoscape software were used to construct the protein-protein interaction (PPI) network and screen the hub genes. Finally, co-expression and drug-gene interaction prediction analysis and mRNA-miRNA regulatory network analysis were performed for hub genes. RESULTS: A total of 233 up-regulated genes and 3 down-regulated genes were found between HF and T2DM. The functional enrichment of DEGs and genes in each four modules were mainly involved in immunity. In addition, five hub genes were identified from PPI network, including SYK, SELL, RAC2, TLR8 and ITGAX. CONCLUSION: The communal DEGs and hub genes identified in this research contribute to discover the underlying biological mechanisms and presents potential biomarkers or therapeutic targets in HF and T2DM.

Identification of Independent and Communal Differentially Expressed Genes as Well as Potential Therapeutic Targets in Ischemic Heart Failure and Non-Ischemic Heart Failure.

BACKGROUND: Heart failure (HF) is a rapidly growing public health problem, and its two main etiological types are non-ischemic heart failure (NIHF) and ischemic heart failure (IHF). However, the independent and common mechanisms of NIHF and IHF have not been fully elucidated. Here, bioinformatic analysis was used to characterize the difference and independent pathways for IHF and NIHF, and more importantly, to unearth the common potential markers and therapeutic targets in IHF and NIHF. METHODS: Two data sets with accession numbers GSE26887 and GSE84796 were downloaded from the Gene Expression Omnibus (GEO) database. After identifying the independent and communal DEGs of NIHF and IHF, a functional annotation, protein-protein interaction (PPI) network analysis, co-expression and drug-gene interaction prediction analysis, and mRNA-miRNA regulatory network analysis were performed for DEGs. RESULTS: We found 1146 independent DEGs (DEGs2) of NIHF mainly enriched in transcription-related and 2595 independent DEGs (DEGs3) of IHF mainly enriched in immune-related. Moreover, 185 communal DEGs (DEGs1) were found between NIHF and IHF, including 93 upregulated genes and 92 downregulated genes. Pathway enrichment analysis results showed that GPCR pathways and biological processes are closely related to the occurrence of HF. In addition, three hub genes were identified from PPI network, including CCL5, C5 and TLR3. CONCLUSION: The identification of DEGs and hub genes in this study contributes to a novel perception for potential functional mechanisms and biomarkers or therapeutic targets in NIHF and IHF.

Predictive Value of the Age, Creatinine, and Ejection Fraction (ACEF) Score in Patients With Acute Fulminant Myocarditis.

OBJECTIVE: Patients with acute fulminant myocarditis often have more adverse cardiovascular events and higher mortality. The purpose of this study was to evaluate the usefulness of age, creatinine, and left ventricular ejection fraction (ACEF score), in determining the risk that acute fulminant myocarditis will lead to serious cardiovascular events, death, and cardiac dysfunction. METHODS: We retrospectively reviewed the demographics, laboratory tests, medications, echocardiographic examinations, in-hospital clinical outcomes, major adverse cardiovascular events (MACE), and survival rate at 1 year in the medical records of 220 consecutive subjects suffering from acute fulminant myocarditis from January 2013 to June 2019. RESULTS: Two hundred twenty patients were divided into a survivor group and a non-survivor group. This study found that patients in the non-survivor group were older, had higher heart rates, and had more serious injuries to multiple organ functions. A high ACEF score at admission was independently associated with an unfavorable prognosis, and it was a predictor of in-hospital mortality. The current analysis extends the predictive performance of the ACEF scores at 30 days by evaluating echocardiographic data as applied to survivors of fulminant myocarditis and cumulative rates of MACE at 1 year. The results indicated that patients with high ACEF scores had poor recovery of cardiac function, and higher rates of MACE, all-cause death, and heart failure at 1 year than the low-ACEF group. CONCLUSION: The ACEF score was identified as an effective predictor of poor in-hospital outcomes, worse cardiac recovery after 30 days, and higher rates of MACE, all-cause death, and heart failure at 1 year in patients who had acute fulminant myocarditis. These data suggest that its predictive accuracy means the ACEF score could be used to assess the prognosis of patients with acute fulminant myocarditis.