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It is evident that voluntary effort plays a crucial role in electrical stimulation rehabilitation, facilitating neuroplasticity enhancement in patients with neurological disorders. In this paper, we present a multichannel system designed for simultaneous functional electrical stimulation (FES) and volitional EMG (vEMG) acquisition using shared electrodes. The system employs hardware blanking with electrodes shorting to suppress stimulation artifacts and accelerate residual charge dissipation. Additionally, we adapt the Savitzky-Golay filter to extract high-quality, real-time vEMG from FES-contaminated signals, with the optimal filter parameters for different stimulation and blanking periods determined using a genetic algorithm and semi-synthesized signals. Simulation and experimental results confirm that the proposed system ensures robust and high-quality vEMG acquisition, even under varying parameters and across different individuals. In summary, this work advances the development of closed-loop rehabilitation applications and enables further investigation of neuromuscular characteristics under FES.

Background: The mechanism of cardiac reverse remodeling (CRR) mediated by the left ventricular assist device remains unclear. This study aims to identify the specific cell type responsible for CRR and develop the therapeutic target that promotes CRR., Methods: The nuclei were extracted from the left ventricular tissue of 4 normal controls, 4 CRR patients, and 4 no cardiac reverse remodeling patients and then subjected to single-nucleus RNA sequencing for identifying key cell types responsible for CRR. Gene overexpression in transverse aortic constriction and dilated cardiomyopathy heart failure mouse model (C57BL/6J background) and pathological staining were performed to validate the results of single-nucleus RNA sequencing., Results: Ten cell types were identified among 126 156 nuclei. Cardiomyocytes in CRR patients expressed higher levels of ATP5F1A than the other 2 groups. The macrophages in CRR patients expressed more anti-inflammatory genes and functioned in angiogenesis. Endothelial cells that elevated in no cardiac reverse remodeling patients were involved in the inflammatory response. Echocardiography showed that overexpressing ATP5F1A through cardiomyocyte-specific adeno-associated virus 9 demonstrated an ability to improve heart function and morphology. Pathological staining showed that overexpressing ATP5F1A could reduce fibrosis and cardiomyocyte size in the heart failure mouse model., Conclusions: The present results of single-nucleus RNA sequencing and heart failure mouse model indicated that ATP5F1A could mediate CRR and supported the development of therapeutics for overexpressing ATP5F1A in promoting CRR., Competing Interests: None.

The vascular endothelial barrier dysfunction is associated with the pathogenesis of many cardiovascular diseases, such as atherosclerosis (AS). This study aims to identify specific antigen (Ag, in short)-specific polymorphonuclear neutrophils (PMN) in AS patients and to investigate the role of "Ag-specific" PMN activation in causing vascular endothelial barrier dysfunction. In this study, PMNs were isolated from blood samples collected from patients with AS and analyzed with immunological approaches. Human umbilical vein endothelial cells (HUVEC) monolayers were used as a vascular endothelial barrier model. The results showed that "Ag-specific" PMNs were identified in the blood of 50 AS patients. This subset of PMN was featured as the FcγRI and specific IgG (sIgG) complexes on the cell surface; exposure to specific Ags triggered the "Ag-specific" PMNs to release proinflammatory cytokines. PMN-derived cytokine levels in the serum were positively correlated with the serum levels of sIgG in AS patients. Exposure of naive PMNs to sIgG formed FcγRI and sIgG complexes on the surface; this conferred PMNs the property to be recognized and activated by specific Ag. Stimulation of "Ag-specific" PMN activated the mitogen-activated protein kinase and the activities of nuclear factor activated T cells and promoted the gene transcription of tumor necrosis factor-α. Coculture of "Ag-specific" PMNs and HUVEC monolayers in the presence of specific Ag resulted in the HUVEC monolayer barrier dysfunction. In conclusion, "Ag-specific" PMNs were identified in AS patients. Activation of the PMNs compromised vascular endothelial barrier function. Therefore, to regulate the "Ag-specific" PMN's activities may have translational potential in the treatment of AS., Competing Interests: None., (AJTR Copyright © 2020.)