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Background Diabetes mellitus is an important risk factor for atrial fibrillation (AF) development. Sodium–glucose co-transporter-2 (SGLT-2) inhibitors are used for the treatment of type 2 diabetes mellitus (T2DM). Their cardioprotective effects have been reported but whether they prevent AF in T2DM patients are less well-explored. We tested the hypothesis that the SGLT-2 inhibitor, empagliflozin, can prevent atrial remodeling in a diabetic rat model. Methods High-fat diet and low-dose streptozotocin (STZ) treatment were used to induce T2DM. A total of 96 rats were randomized into the following four groups: (i) control (ii) T2DM, (iii) low-dose empagliflozin (10 mg/kg/day)/T2DM; and (iv) high-dose empagliflozin (30 mg/kg/day)/T2DM by the intragastric route for 8 weeks. Results Compared with the control group, left atrial diameter, interstitial fibrosis and the incidence of AF inducibility were significantly increased in the DM group. Moreover, atrial mitochondrial respiratory function, mitochondrial membrane potential, and mitochondrial biogenesis were impaired. Empagliflozin treatment significantly prevented the development of these abnormalities in DM rats, likely via the peroxisome proliferator-activated receptor-c coactivator 1α (PGC-1α)/nuclear respiratory factor-1 (NRF-1)/mitochondrial transcription factor A (Tfam) signaling pathway. Conclusions Empagliflozin can ameliorate atrial structural and electrical remodeling as well as improve mitochondrial function and mitochondrial biogenesis in T2DM, hence may be potentially used in the prevention of T2DM-related atrial fibrillation.

The lncRNA Chaer controls hypertrophic heart growth by binding to and interfering with the function of the epigenetic regulator PRC2. Epigenetic reprogramming is a critical process of pathological gene induction during cardiac hypertrophy and remodeling, but the underlying regulatory mechanisms remain to be elucidated. Here we identified a heart-enriched long noncoding (lnc)RNA, named cardiac-hypertrophy-associated epigenetic regulator ( Chaer ), which is necessary for the development of cardiac hypertrophy. Mechanistically, Chaer directly interacts with the catalytic subunit of polycomb repressor complex 2 (PRC2). This interaction, which is mediated by a 66-mer motif in Chaer , interferes with PRC2 targeting to genomic loci, thereby inhibiting histone H3 lysine 27 methylation at the promoter regions of genes involved in cardiac hypertrophy. The interaction between Chaer and PRC2 is transiently induced after hormone or stress stimulation in a process involving mammalian target of rapamycin complex 1, and this interaction is a prerequisite for epigenetic reprogramming and induction of genes involved in hypertrophy. Inhibition of Chaer expression in the heart before, but not after, the onset of pressure overload substantially attenuates cardiac hypertrophy and dysfunction. Our study reveals that stress-induced pathological gene activation in the heart requires a previously uncharacterized lncRNA-dependent epigenetic checkpoint.

Deep convolutional neural networks (CNNs) are of great improvement for single image super‐resolution (SISR). However, most existing SISR pre‐trained models can only perform single image restoration and the upscale factors cannot be non‐integers, which limits its application in real‐world scenarios. In this letter, an enhanced dual branches network (EDBNet) in upsampling network is proposed to generate arbitrary‐scale super‐resolution (SR) images. Specifically, the authors design a scale‐guidance upsampling module (SGU) by adding the scale factors and pixel‐level features to guide the weights of convolution. The SGU module performs discriminant learning for each instance in the same batch. Extensive experiments on four benchmark datasets show that the proposed method can achieve superior SR results. In this letter, the authors propose a enhanced dual branches network (EDBNet) to fuse pixel feature and scale information to generate arbitrary‐scale SR images in upsampling network. Specifically, a scale‐guidance upsampling module (SGU) is designed by adding the scale factors and pixel‐level features to guide the weights of convolution. The SGU module performs discriminant learning for each instance in the same batch.

With the advent of autonomous vehicle applications, the importance of LiDAR point cloud 3D object detection cannot be overstated. Recent studies have demonstrated that methods for aggregating features from voxels can accurately and efficiently detect objects in large, complex 3D detection scenes. Nevertheless, most of these methods do not filter background points well and have inferior detection performance for small objects. To ameliorate this issue, this paper proposes an Attention-based and Multiscale Feature Fusion Network (AMFF-Net), which utilizes a Dual-Attention Voxel Feature Extractor (DA-VFE) and a Multi-scale Feature Fusion (MFF) Module to improve the precision and efficiency of 3D object detection. The DA-VFE considers pointwise and channelwise attention and integrates them into the Voxel Feature Extractor (VFE) to enhance key point cloud information in voxels and refine more-representative voxel features. The MFF Module consists of self-calibrated convolutions, a residual structure, and a coordinate attention mechanism, which acts as a 2D Backbone to expand the receptive domain and capture more contextual information, thus better capturing small object locations, enhancing the feature-extraction capability of the network and reducing the computational overhead. We performed evaluations of the proposed model on the nuScenes dataset with a large number of driving scenarios. The experimental results showed that the AMFF-Net achieved 62.8% in the mAP, which significantly boosted the performance of small object detection compared to the baseline network and significantly reduced the computational overhead, while the inference speed remained essentially the same. AMFF-Net also achieved advanced performance on the KITTI dataset.

The emergence of coronavirus disease 2019 (COVID‐19), caused by the severe acute respiratory syndrome coronavirus 2 (SARS‐CoV‐2) has become a major global public health concern. Although SARS‐CoV‐2 causes primarily respiratory problems, concurrent cardiac injury cannot be ignored since it may be an independent predictor for adverse outcomes. Cardiac arrhythmias are often observed in patients with COVID‐19, especially in severe cases, and more likely contribute to the high risk of adverse outcomes. Arrhythmias should be regarded as one of the main complications of COVID‐19. Mechanistically, a number of ion channels can be adversely affected in COVID‐19, leading to alterations in cardiac conduction and/or repolarization properties, as well as calcium handling, which can predispose to cardiac arrhythmogenesis. In addition, several antimicrobials that are currently used as potential therapeutic agents for COVID‐19, such as chloroquine, hydroxychloroquine and azithromycin, have uncertain benefit, and yet may induce electrocardiographic QT prolongation with potential ventricular pro‐arrhythmic effects. Continuous electrocardiogram monitoring, accurate and prompt recognition of arrhythmias are important. The present review focuses on cardiac arrhythmias in patients with COVID‐19, its underlying mechanisms, and proposed preventive and therapeutic strategies. Diagnosis and management of coronavirus disease 2019 (COVID‐19) related arrhythmias. Arrhythmias are the main complications of COVID‐19. Tachycardia, atrioventricular/intraventricular conduction block, ST‐T changes, QT interval prolongation, and even malignant arrhythmias are observed in COVID‐19 patients. Continuous electrocardiogram monitoring, accurate and prompt recognition, and ppropriate treatments of arrhythmias are important. COVID‐19, Coronavirus disease 2019; ECG, Electrocardiogram; MCOT, Mobile continuous telemetry monitor.

The present study aimed to explore the direct toxicity of proprotein convertase subtilisin/kexin type 9 (PCSK9) to atherosclerosis (AS) and its association with apoptotic endothelial cells. Apolipoprotein E−/− mice were randomly divided into two groups, control and experimental. The control group was administered a normal diet and the experimental group was administered a high-fat diet. After 20 weeks, the aorta was isolated and dissected. Hematoxylin and eosin staining, and immunohistochemical analysis were performed. Human umbilical vein endothelial cells were incubated with varied concentrations of oxidized low-density lipoprotein (ox-LDL) for different times. The apoptotic rate was detected by flow cytometry. Western blotting and reverse transcription-quantitative polymerase chain reaction analysis were conducted to detect the expression of PCSK9, B-cell lymphoma 2 (Bcl-2), bcl-2-like protein 4 (Bax) and caspase-3. Short hairpin (sh) RNA-PCSK9 was transfected into endothelial cells using lentiviral transfection. The expression levels of PCSK9, Bax, Bcl-2, caspase-3 and the mitogen-activated protein kinase (MAPK) pathway proteins were detected. The high-fat group was successfully established as an AS model and PCSK9 was highly expressed in the AS plaque. Treatment with ox-LDL induced apoptosis and increased mRNA and protein levels of PCSK9. PCSK9 mRNA and proteins levels were downregulated by shRNA-PCSK9. The deficiency of PCSK9 markedly inhibited the expression of pro-apoptotic proteins and promoted anti-apoptotic proteins. In addition, phosphorylation of p38 and c-Jun N-terminal kinases was altered by shRNA-PCSK9. Targeting of PCSK9 by shRNA-PCSK9 may repress endothelial cell apoptosis through MAPK signaling in AS, providing a novel direction for understanding the mechanism and treatment of AS.

One of the most globally prevalent supraventricular arrhythmias is atrial fibrillation (AF). Knowledge of the structures and functions of messenger RNA (mRNA) has recently increased. It is no longer viewed as solely an intermediate molecule between DNA and proteins but has come to be seen as a dynamic and modifiable gene regulator. This new perspective on mRNA has led to rising interest in it and its presence in research into new therapeutic schemes. This paper, therefore, focuses on microRNAs (miRNAs), which are small noncoding RNAs that regulate posttranscriptional gene expression and play a vital role in the physiology and normative development of cardiovascular systems. This means they play an equally vital role in the development and progression of cardiovascular diseases. In recent years, multiple studies have pinpointed particular miRNA expression profiles as being associated with varying histological features of AF. These studies have been carried out in both animal models and AF patients. The emergence of miRNAs as biomarkers and their therapeutic potential in AF patients will be discussed in the body of this paper.

Atherosclerosis represents a significant cause of morbidity and mortality in both the developed and developing countries. Animal models of atherosclerosis have served as valuable tools for providing insights on its aetiology, pathophysiology and complications. They can be used for invasive interrogation of physiological function and provide a platform for testing the efficacy and safety of different pharmacological therapies. Compared to studies using human subjects, animal models have the advantages of being easier to manage, with controllable diet and environmental risk factors. Moreover, pathophysiological changes can be induced either genetically or pharmacologically to study the harmful effects of these interventions. There is no single ideal animal model, as different systems are suitable for different research objectives. A good understanding of the similarities and differences to humans enables effective extrapolation of data for translational application. In this article, we will examine the different mouse models for the study and elucidation of the pathophysiological mechanisms underlying atherosclerosis. We also review recent advances in the field, such as the role of oxidative stress in promoting endoplasmic reticulum stress, mitochondrial dysfunction and mitochondrial DNA damage, which can result in vascular inflammation and atherosclerosis. Finally, novel therapeutic approaches to reduce vascular damage caused by chronic inflammation using microRNA and nano-medicine technology, are discussed.

Objective. To investigate the prognostic significance of serum soluble triggering receptor expressed on myeloid cells-1 (sTREM-1), procalcitonin (PCT), N-terminal probrain natriuretic peptide (NT-pro-BNP), C-reactive protein (CRP), cytokines, and clinical severity scores in patients with sepsis. Methods. A total of 102 patients with sepsis were divided into survival group ( n = 60 ) and nonsurvival group ( n = 42 ) based on 28-day mortality. Serum levels of biomarkers and cytokines were measured on days 1, 3, and 5 after admission to an ICU, meanwhile the acute physiology and chronic health evaluation II (APACHE II) and sequential organ failure assessment (SOFA) scores were calculated. Results. Serum sTREM-1, PCT, and IL-6 levels of patients in the nonsurvival group were significantly higher than those in the survival group on day 1 ( P < 0.01 ). The area under a ROC curve for the prediction of 28 day mortality was 0.792 for PCT, 0.856 for sTREM-1, 0.953 for SOFA score, and 0.923 for APACHE II score. Multivariate logistic analysis showed that serum baseline sTREM-1 PCT levels and SOFA score were the independent predictors of 28-day mortality. Serum PCT, sTREM-1, and IL-6 levels showed a decrease trend over time in the survival group ( P < 0.05 ). Serum NT-pro-BNP levels showed the predictive utility from days 3 and 5 ( P < 0.05 ). Conclusion. In summary, elevated serum sTREM-1 and PCT levels provide superior prognostic accuracy to other biomarkers. Combination of serum sTREM-1 and PCT levels and SOFA score can offer the best powerful prognostic utility for sepsis mortality.

The existing data regarding the role of QRS duration (QRSd) change on cardiac resynchronization therapy (CRT) response show some inconsistent results. We conducted a meta-analysis of data obtained from observational studies to examine the impact of QRS change after CRT device implantation on the clinical and/or echocardiographic response. We searched the PubMed and EMBASE databases for relevant studies published before January 2016. Twenty-seven studies were retrieved for detailed evaluation of which 12 studies with a total population of 1,545 patients met our eligibility criteria. The analysis demonstrated that QRSd narrowing was a positive predictor of response to CRT (mean difference [MD] = −19.24 ms, 95% CI = −24.00 to −14.48 ms, p <0.00001). This effect was consistent in the studies using clinical criteria (MD = −19.91 ms, 95% CI = −27.20 to −12.62 ms, p <0.00001) and in those that used echocardiographic criteria (MD = −19.51 ms, 95% CI = −25.78 to −13.25 ms, p <0.00001). The heterogeneity test showed moderate differences among the individual studies (I2 = 42%). Subgroup analysis showed that QRSd change was more pronounced in studies having a follow-up ≤6 months. We did not find significant differences in studies measuring postimplantation QRSd after a certain follow-up period compared with studies measuring QRSd immediately after CRT device implantation. Further studies should clarify the exact timing of QRSd assessments during follow-up. In conclusion, QRSd shortening after CRT device implantation is associated with a favorable clinical and echocardiographic response.