Background. Atrial fibrillation (AF) is the most common arrhythmia in the world. Long noncoding RNA (lncRNA) has been found to play an important role in cardiovascular diseases including heart failure, myocardial infarction, and atherosclerosis. However, the role of lncRNA in AF has rarely been studied. The purpose of this study is to identify the expression profile of lncRNA in AF patients, explore the function of lncRNA in AF, and provide a potential scientific basis for the treatment of AF in the future. Methods. The lncRNA and mRNA expression profiles were obtained from the atrial appendage samples of GSE31821, GSE411774, GSE79768, and GSE115574 in the Gene Expression Omnibus (GEO) database. Functional analysis was performed via Gene Ontology (GO), Kyoto Encyclopedia of Genes and Genomes (KEGG), and Gene Set Variation Analysis (GSVA). The “CIBERSORT” R kit was used to analyze 22 immune cell infiltrates in AF and sinus rhythm (SR) patients. The “CORRPLOT” R package was used to analyze the immune correlation between lncRNA and immune cells. Results. A total of 6 differentially expressed lncRNAs and 45 differentially expressed mRNAs were identified in the AF and SR groups. GO, KEGG, and GSVA results showed that abnormally expressed lncRNAs were involved in signaling pathways related to the atrium, including the Toll-like receptor signaling pathway and calcium signaling pathway. Immune cell infiltration analysis revealed that native B cells, follicular helper T cells, and resting dendritic cells may be involved in the AF process. In addition, LINC00844 was negatively correlated with resting dendritic cells. Conclusion. The expression profile of lncRNA in AF patients was different from that in normal controls. The physiological functions of these differentially expressed lncRNAs may be related to the pathogenesis of AF, which provide a scientific basis for the prognosis and treatment of patients with AF.

The general aggression model (GAM) has suggested that the interaction between person factors (e.g., personality variables) and situation factors (e.g., playing violent video games [VVGs]) can increase individuals' aggressive behaviors through their cognition (e.g., hostile attributions), affect (e.g., negative affect), and/or arousal. The present study employed a modified competitive reaction time task to test the effects of shyness, violent (vs. nonviolent) gameplay, and shyness on individuals' positive -negative affect, hostile attributions, and aggressive behaviors. In addition, the present study also employed structural equation modeling (SEM) to test the mediation (by cognition and affect) and moderation (by shyness). Results showed that playing a VVG increased aggressive behaviors, negative affect, and hostile attributions primarily among shy participants. In addition, the results of SEM also revealed that this moderating role was mediated by negative affect and hostile attributions. The present study supported GAM and showed that individuals' aggressive behaviors are differentially susceptible to VVGs, depending on their level of shyness in a "for bad and for worse" manner. K E Y W O R D S aggressive behaviors, hostile attributions, positive-negative affect, shyness, VVGs

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