BACKGROUND: Senescence is a series of degenerative changes in the structure and physiological function of an organism. Whether JPX (just proximal to XIST)—a newly identified age-related noncoding RNA by us—is associated with atherosclerosis is still unknown. Our study was to investigate the role of JPX and provide insights into potential therapies targeting atherosclerosis. METHODS: We analyzed clinical data from multiple tissues including meniscus tissue, leukemia cells, and peripheral blood monocytes to identify age-related noncoding RNAs in senescent vascular smooth muscle cells (VSMCs). The molecular mechanism of JPX was investigated by capture hybridization analysis of RNA targets and chromatin immunoprecipitation. IGVTools and real-time quantitative polymerase chain reaction were used to evaluate the JPX expression during phenotype regulation in age-related disease models. The therapeutic potential of JPX was evaluated after establishing an atherosclerosis model in smooth muscle–specific Jpx knockout mice. RESULTS: JPX expression was upregulated in activated ras allele (H- ras V12)-induced senescent VSMCs and atherosclerotic arteries. JPX knockdown substantially reduced the elevation of senescence-associated secretory phenotype (SASP) genes in senescent VSMCs. Cytoplasmic DNA leaked from mitochondria via mitochondrial permeability transition pore formed by VDAC1 (voltage-dependent anion channel 1) oligomer activates the STING (stimulator of interferon gene) pathway. JPX could act as an enhancer for the SASP genes and functions as a scaffold molecule through interacting with phosphorylated p65/RelA and BRD4 (bromodomain-containing protein 4) in chromatin remodeling complex, promoting the transcription of SASP genes via epigenetic regulation. Smooth muscle knockout of Jpx in Apoe ^KO mice resulted in a decrease in plaque area, a reduction in SASP gene expression, and a decrease in senescence compared with controls. CONCLUSIONS: As an enhancer RNA, JPX can integrate p65 and BRD4 to form a chromatin remodeling complex, activating SASP gene transcription and promoting cellular senescence. These findings suggest that JPX is a potential therapeutic target for the treatment of age-related atherosclerosis.

Numerous studies have demonstrated the significance of trimethylamine-N-oxide (TMAO) in the progression of atrial fibrillation (AF). However, the association between TMAO and AF recurrence (RAF) post-catheter ablation is not yet fully understood. This study aims to elucidate the predictive capability of pre-procedural TMAO levels in determining RAF following catheter ablation (CA). This study was conducted as a prospective, single-center observational study. Between June 2021 and June 2022, 152 patients from the Department of Cardiology at The Affiliated Huaian No. 1 People’s Hospital of Nanjing Medical University were enrolled. Baseline characteristics and serum TMAO levels were assessed for all participants. Patients with AF who underwent CA were monitored for recurrences of AF using electrocardiography (ECG) or 24-hour Holter monitoring during the follow-up period. The study found that serum TMAO levels were significantly higher in persistent AF (PeAF) patients compared to those in sinus rhythm (SR) and paroxysmal AF (PaAF) patients (3.96 ± 1.69 vs. 1.81 ± 0.59, 3.02 ± 1.50 µM, P < 0.001 and P < 0.01, respectively). After a one-year follow-up, 29 (21.2%) AF patients experienced recurrence after CA. Multivariate Cox proportional hazards regression analysis revealed that pre-procedural serum TMAO was an independent predictor of recurrent AF (HR = 1.78, 95% CI = 1.43–2.21, P < 0.001). The receiver operating characteristic (ROC) curve analysis identified a cut-off value of 4.3µM for serum TMAO levels in predicting recurrent AF (area under the curve: 0.835, P < 0.001). The Kaplan-Meier plot demonstrated that patients with TMAO levels greater than 4.3µM had a significantly higher rate of recurrent AF (HR = 13.53, 95% CI = 6.19–29.56, P < 0.001). Patients with AF exhibited elevated levels of circulating TMAO compared to patients with SR. The findings suggest a potential role of TMAO in the development of AF, with pre-procedural serum TMAO levels serving as a reliable predictor of recurrence of AF CA.

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A new image registration method for infrared images and visible images is proposed in this paper. This method is a modified version of SIFT algorithm. Salient points of infrared images and visible images are extracted along edges of images. Each salient point is assigned a dominant direction which is the peak of orientation histogram of local image around it and a feature vector which is formed from the orientation histograms of sub-region around it. After salient points matching, RANSAC algorithm is used to eliminate wrong corresponding pairs. Experimental results show that this method has a good registration result for infrared images and visible images.

Iterative back-projection (IBP) technique is commonly used to minimize the super resolution (SR) reconstruction error and acquire a high spatial resolution image with appealing visual effect. However, the IBP based SR method suffers from the chessboard and ringing effect around edges. In this paper, we employ total variation (TV) as a part of penalty function to minimize the reconstruction error, which helps to avoid across-edge smoothing and suppress the above-mentioned artifacts simultaneously. The experimental results validate that the proposed algorithm can promote the SR reconstruction precision considerably.

Exposure to benzene poses significant health risks, with cardiovascular toxicity emerging as a primary adverse effect. However, the exact influence of benzene on the development of atrial fibrillation (AF) remains unclear. The occurrence of AF is influenced by environmental factors and genetic factors that should not be overlooked. Previous studies have found an association between accelerated biological aging and benzene and AF. This study explored the effects of benzene exposure on the risk of incident AF later in life, examining the interaction with genetic susceptibility and the mediating role of accelerated biological aging. From 2006 to 2010, 432,522 participants in the UK Biobank who were free of cardiovascular disease at baseline were included. The annual average benzene concentrations during the follow-up period were assessed using air dispersion models. AF patients were identified using the International Classification of Diseases 10th Revision (ICD-10) code. Cox proportional hazard models were employed to explore the association between benzene exposure and incident AF. Restricted cubic spline models were utilized to estimate the exposureresponse relationships. The polygenic risk score (PRS) for AF was used to examine the gene-environment interactions related to AF risk. Exposure to benzene significantly increased the risk of AF, with the hazard ratio (95 % confidence interval) for a standard deviation increase in benzene concentration reaching 1.02 (1.00, 1.04). Participants with high benzene exposure and high genetic risk had a greater risk of AF than those with low benzene exposure and low genetic risk (HR, 3.12; 95 % CI, 2.82, 3.46). Accelerated biological aging significantly mediated the association between benzene exposure and AF. Exposure to benzene is associated with an increased risk of AF, particularly in populations at high genetic risk. Accelerated biological aging partially mediated these associations.