Selenium deficiency is a causative factor in heart failure and microRNAs (known as miRNAs or miRs) play an important role in numerous cardiovascular diseases. However, the changes of miRNA expression during selenium deficiency and whether selenium deficiency is involved in cardiac dysfunction remain unclear. In the present study, miRNA expression profiling was carried out in normal rats, selenium-deficient rats and selenium-supplemented rats by miRNA microarray. Cardiac function was evaluated by analyzing the plasma brain natriuretic peptide level, echocardiographic parameters and hemodynamic parameters. Cardiac glutathione peroxidase activity was assessed by spectrophotometry. The histological changes were examined by hematoxylin and eosin staining. Electrocardiograph was used to test the arrhythmia. The differentially expressed miRNAs were verified by reverse transcription-polymerase chain reaction. Additionally, the underlying mechanism associated with the Wnt/β-catenin signaling pathway was further explored. The cardiac dysfunction of the rat with selenium deficiency was mainly associated with five upregulated miRNAs, which were miR-374, miR-16, miR-199a-5p, miR-195 and miR-30e*, and three downregulated miRNAs, which were miR-3571, miR-675 and miR-450a*. Among these, the expression of miR-374 was the highest, which may be of vital importance in rats with selenium deficiency. In conclusion, the possible mechanism of selenium deficiency-induced cardiac dysfunction was associated with the Wnt/β-catenin signaling pathway.

Diabetic cardiomyopathy (DCM) is a serious complication of diabetes mellitus (DM). One of the hallmarks of the DCM is enhanced oxidative stress in myocardium. The aim of this study was to research the underlying mechanisms involved in the effects of dapagliflozin (Dap) on myocardial oxidative stress both in streptozotocin-induced DCM rats and rat embryonic cardiac myoblasts H9C2 cells exposed to high glucose (33.0 mM). In in vivo studies, diabetic rats were given Dap (1 mg/ kg/ day) by gavage for eight weeks. Dap treatment obviously ameliorated cardiac dysfunction, and improved myocardial fibrosis, apoptosis and oxidase stress. In in vitro studies, Dap also attenuated the enhanced levels of reactive oxygen species and cell death in H9C2 cells incubated with high glucose. Mechanically, Dap administration remarkably reduced the expression of membrane-bound nicotinamide adenine dinucleotide phosphate (NADPH) oxidase subunits gp91phox and p22phox, suppressed the p67phox subunit translocation to membrane, and decreased the compensatory elevated copper, zinc superoxide dismutase (Cu/Zn-SOD) protein expression and total SOD activity both in vivo and in vitro. Collectively, our results indicated that Dap protects cardiac myocytes from damage caused by hyperglycemia through suppressing NADPH oxidase-mediated oxidative stress.

The present study addresses the cardiac arrhythmia (CA) classification problem using the deep learning (DL)-based method for electrocardiography (ECG) data analysis. Recently, various DL techniques have been utilized to classify arrhythmias, with one typical approach to developing a one-dimensional (1D) convolutional neural network (CNN) model to handle the ECG signals in the time domain. Although the CA classification in the time domain is very prevalent, current methods’ performances are still not robust or satisfactory. This study aims to develop a solution for CA classification in two dimensions by introducing the recurrence plot (RP) combined with an Inception-ResNet-v2 network. The proposed method for nine types of CA classification was tested on the 1st China Physiological Signal Challenge 2018 dataset. During implementation, the optimal leads (lead II and lead aVR) were selected, and then 1D ECG segments were transformed into 2D texture images by the RP approach. These RP-based images as input signals were passed into the Inception-ResNet-v2 for CA classification. In the CPSC, Georgia, and the PTB_XL ECG databases of the PhysioNet/Computing in Cardiology Challenge 2020, the RP-based method achieved an average F1-score of 0.8521, 0.8529, and 0.8862, respectively. The results suggested the excellent generalization ability of the proposed method. To further assess the performance of the proposed method, we compared the 2D RP-image-based solution with the published 1D ECG-based works on the same dataset. Also, it was compared with two traditional ECG transform into 2D image methods, including the time waveform of the ECG recordings and time-frequency images based on continuous wavelet transform (CWT). The proposed method achieved the highest average F1-score of 0.844, with only two leads of the 12-lead ECG original data, which outperformed other works. Therefore, the promising results indicate that the 2D RP-based method has a high clinical potential for CA classification using fewer lead ECG signals.

The possible mechanism of adriamycin (ADR) and/or selenium (Se) deficiency-induced cardiac dysfunction, and cardioprotective effects of Se against ADR-induced cardiac toxicity were investigated in this study. Cardiac function was evaluated by plasma brain natriuretic peptide level and echocardiographic and hemodynamic parameters. Cardiac glutathione peroxidase (GPx) activity was assessed spectrophotometrically. Expression of ATP-sensitive potassium channels (KATP) subunits-SUR2A and Kir6.2-were examined by real-time PCR and Western blotting. The results showed that cardiac function and cardiac GPx activity decreased remarkably after administration of ADR or Se deficiency; more dramatic impairment of cardiac function and cardiac GPx activity were observed after co-administration of ADR and Se deficiency. Mechanically, it is novel for us to find down-regulation of KATP subunits gene expression in cardiac tissue after administration of ADR or Se deficiency, and more significant inhibition of cardiac KATP gene expression was identified after co-administration of ADR and Se deficiency. Furthermore, cardiac toxicity of ADR was found alleviated by Se supplementation, accompanied by restoring of cardiac GPx activity and cardiac KATP gene expression. These results indicate that decreased expression of cardiac KATP is involved in adriamycin and/or Se deficiency-induced cardiac dysfunction; Se deficiency exacerbates adriamycin-induced cardiac dysfunction by future inhibition of KATP expression; Se supplementation seems to protect against adriamycin-induced cardiac dysfunction via restoring KATP expression, showing potential clinical application in cancer chemotherapy.