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Introduction: Atrial fibrillation (AF) is a common arrhythmia associated with aging. Many known risk factors are associated with AF, but many senior individuals do not develop AF despite having multiple risk factors. This finding suggests that other factors may be involved in AF onset. This study aimed to identify upregulated genes in the peripheral blood and left atrium of patients with AF. These genes may serve as potential biomarkers to predict AF onset risk and its complications. Methods: Gene expression data were analyzed from blood (n = 3) and left atrial samples (n = 15) of patients with AF and sinus rhythm. We evaluated the significant genes identified using p value analysis of weighted average difference to confirm their rankings. We created figures for the genes using GeneMANIA and performed a functional analysis using Cytoscape3.10.1. Hub and bottleneck genes were identified based on degree and betweenness centrality. We used reference expression (RefEx) to confirm the organs in which the extracted genes were expressed. Heatmaps and Gene ontology term evaluation were performed to further elucidate the biological functions of the genes. Results: We identified 12 upregulated genes (CAST, ASAH1, MAFB, VCAN, DDIT4, FTL, HEXB, PROS1, BNIP3L, PABPC1, YBX3, and S100A6) in both the blood and left atrium of patients with AF. We analyzed the gene functions using GeneMANIA and Cytoscape. The identified genes were involved in a variety of pathways, including lysosomal function and lipid and sphingolipid catabolism. Next, we investigated whether the 12 identified genes identified were systemically expressed or had high organ specificity. Finally, RefEx was used to analyze the gene expression levels in various tissues. Four genes, FTL, ASAH1, S100A6, and PABPC1, were highly expressed in the normal heart tissue. Finally, we evaluated the expression levels of the 12 genes in the blood of patients with AF using a heatmap. Our findings suggest that the 12 genes identified in this study, especially the lysosome-related genes (FTL and ASAH1), may be involved in AF pathogenesis. Conclusion: Lysosome-related genes may be important to understand the AF pathophysiology and to develop AF-related future studies. Plain Language Summary: Atrial fibrillation (AF) is an aging disorder and risk factor for patients with cardiovascular disease, which is the leading cause of mortality among senior individuals. Despite intensive research, the prevalence of AF is rising in the senior population, and identifying new therapeutic targets and prognostic markers is therefore critically important. Our research focuses on the lysosomal pathway. Lysosome mediates protein degradation, which is activated in the heart and blood. We conducted bioinformatics analyses of publicly available databases to identify the upregulated genes and pathways in patients with AF. We analyzed gene expression data from blood and left atrium samples of patients with AF and sinus rhythm. We identified 12 upregulated genes in the blood and left atrium in patients with AF. These genes are mainly involved in lysosome-related functions. These findings suggest that the 12 genes identified in this study, especially lysosome-related genes, may be involved in the AF pathogenesis. Lysosome-related genes are important for cellular homeostasis and waste degradation. Therefore, their upregulation in patients with AF may play a role in disease development and progression. Our study proposes new insights into the underlying molecular mechanisms of AF and identifies potential biomarkers for predicting the AF onset risk or complications. [ABSTRACT FROM AUTHOR]

Vital signs are crucial for assessing the condition of a patient and detecting early symptom deterioration. Noncontact sensor technology has been developed to take vital measurements with minimal burden. This study evaluated the accuracy of a mat-type noncontact sensor in measuring respiratory and pulse rates in patients with cardiovascular diseases compared to conventional methods. Forty-eight hospitalized patients were included; a mat-type sensor was used to measure their respiratory and pulse rates during bed rest. Differences between mat-type sensors and conventional methods were assessed using the Bland–Altman analysis. The mean difference in respiratory rate was 1.9 breaths/min (limits of agreement (LOA): −4.5 to 8.3 breaths/min), and proportional bias existed with significance (r = 0.63, p < 0.05). For pulse rate, the mean difference was −2.0 beats/min (LOA: −23.0 to 19.0 beats/min) when compared to blood pressure devices and 0.01 beats/min (LOA: −11.4 to 11.4 beats/min) when compared to 24-h Holter electrocardiography. The proportional bias was significant for both comparisons (r = 0.49, p < 0.05; r = 0.52, p < 0.05). These were considered clinically acceptable because there was no tendency to misjudge abnormal values as normal. The mat-type noncontact sensor demonstrated sufficient accuracy to serve as an alternative to conventional assessments, providing long-term monitoring of vital signs in clinical settings. [ABSTRACT FROM AUTHOR]

Objectives: We conducted a text mining analysis of 40 years of literature on cardiac aging from PubMed to investigate the current understanding on cardiac aging and its mechanisms. This study aimed to embody what most researchers consider cardiac aging to be. Methods: We used multiple text mining and machine learning tools to extract important information from a large amount of text. Results: Analysis revealed that the terms most frequently associated with cardiac aging include "diastolic," "hypertrophy," "fibrosis," "apoptosis," "mitochondrial," "oxidative," and "autophagy." These terms suggest that cardiac aging is characterized by mitochondrial dysfunction, oxidative stress, and impairment of autophagy, especially mitophagy. We also revealed an increase in the frequency of occurrence of "autophagy" in recent years, suggesting that research on autophagy has made a breakthrough in the field of cardiac aging. Additionally, the frequency of occurrence of "mitophagy" has increased significantly since 2019, suggesting that mitophagy is an important factor in cardiac aging. Conclusions: Cardiac aging is a complex process that involves mitochondrial dysfunction, oxidative stress, and impairment of autophagy, especially mitophagy. Further research is warranted to elucidate the mechanisms of cardiac aging and develop strategies to mitigate its detrimental effects. [ABSTRACT FROM AUTHOR]

[Ca.sub.v]3.2 subunit underlies the functional T-type [Ca.sup.2+] channel in murine hearts during the embryonic period. Am J Physiol Heart Circ Physiol 286: H2257-H2263, 2004. First published February 26, 2004; 10.1152/ajpheart.01043.2003.--T-type [Ca.sup.2+] channels are implicated in cardiac automaticity, cell growth, and cardiovascular remodeling. Two voltagegated [Ca.sup.2+] subtypes [Ca.sub.v]3.1 and [Ca.sub.v]3.2 have been cloned for the pore-forming [alpha.sub.1]-subunit of the T-type [Ca.sup.2+] channel in cardiac muscle, but their differential roles remain to be clarified. The aim of this study was to elucidate the relative contribution of the two subtypes in the normal development of mouse hearts. A whole cell patch clamp was used to record ionic currents from ventricular myocytes isolated from mice of early (E9.5) and late embryonic days (El8) and from adult 10-wk-old mice. Large T-type [Ca.sup.2+] current [I.sub.Ca,T] was observed at both E9.5 and El8, displaying similar voltage-dependence and kinetics of activation and inactivation. The current was inhibited by [Ni.sup.2+] at relatively low concentrations I[C.sub.50] 26-31 ([micro]M). [I.sub.Ca,T] was undetectable in adult myocytes. Quantitative PCR analysis revealed that [Ca.sub.v]3.2 mRNA is the predominant subtype encoding T-type [Ca.sup.2+] channels at both E9.5 and El8. [Ca.sub.v]3.1 mRNA increased from E9.5 to El 8, but remained low compared with [Ca.sub.v]3.2 mRNA during the whole embryonic period. In the adulthood, in contrast, [Ca.sub.v]3.1 mRNA is greater than [Ca.sub.v]3.2 mRNA. These results indicate that [Ca.sub.v]3.2 underlies the functional T-type [Ca.sup.2+] channels in the embryonic murine heart, and there is a subtype switching of transcripts from [Ca.sub.v]3.2 to [Ca.sub.v]3.1 in the perinatal period. ion channel; gene expression; fetal development; [alpha.sub.1]-subunit; cardiac myocyte