No abstract

To find out the feasibility of different neural networks in sEMG-based force estimation, in this paper, three types of networks, namely convolutional neural network (CNN), long short-term memory (LSTM) network and their combination (C-LSTM) were applied to predict muscle force generated in static isometric elbow flexion across three different circumstances (multi-subject, subject-dependent and subject-independent). Eight healthy men were recruited for the experiments, and the results demonstrated that all the three models were applicable for force estimation, and LSTM and C-LSTM achieved better performances. Even under subject-independent situation, they maintained mean RMSE% of as low as 9.07 ± 1.29 and 8.67 ± 1.14. CNN turned out to be a worse choice, yielding a mean RMSE% of 12.13 ± 1.98. To our knowledge, this work was the first to employ CNN, LSTM and C-LSTM in sEMG-based force estimation, and the results not only prove the strength of the proposed networks, but also pointed out a potential way of achieving high accuracy in real-time, subject-independent force estimation.

The cardiac autonomic nerve system (CANS) is a potentially potent modulator of the initiation and perpetuation of atrial fibrillation (AF). In this review, we focus on the relationship between the autonomic nervous system (ANS) and the pathophysiology of AF and the potential benefit and limitations of neuromodulation in the management of this arrhythmia from eight aspects. We conclude that Activation and Remodeling of CANS involved in the initiation and maintenance of AF. The network control mechanism, innervation regions, and sympathetic/parasympathetic balance play an important role in AF substrate. And the formation of Complex Fractional Atrial Electrograms also related to CANS activity. In addition, modulating CANS function by potential therapeutic applications include ganglionated plexus ablation, renal sympathetic denervation, and low‐level vagal nerve stimulation, may enable AF to be controlled. Although the role of the ANS has long been recognized, a better understanding of the complex interrelationships of the various components of the CANS will lead to improvement of treatments for this common arrhythmia.

Edited by Dennis R. VoelkerMineralocorticoid receptor (MR) has been considered as a potential target for treating atherosclerosis. However, the cellular and molecular mechanisms are not completely understood. We aim to explore the functions and mechanisms of macrophage MR in atherosclerosis. Atherosclerosis-susceptible LDLRKO chimeric mice with bone marrow cells from floxed control mice or from myeloid MR knock-out (MRKO) mice were generated and fed with high cholesterol diet. Oil red O staining showed that MRKO decreased atherosclerotic lesion area in LDLRKO mice. In another mouse model of atherosclerosis, MRKO/APOEKO mice and floxed control/APOEKO mice were generated and treated with angiotensin II. Similarly, MRKO inhibited the atherosclerotic lesion area in APOEKO mice. Histological analysis showed that MRKO increased collagen coverage and decreased necrosis and macrophage accumulation in the lesions. In vitro results demonstrated that MRKO suppressed macrophage foam cell formation and up-regulated the expression of genes involved in cholesterol efflux. Furthermore, MRKO decreased accumulation of apoptotic cells and increased effective efferocytosis in atherosclerotic lesions. In vitro study further revealed that MRKO increased the phagocytic index of macrophages without affecting their apoptosis. In conclusion, MRKO reduces high cholesterol-or angiotensin II-induced atherosclerosis and favorably changes plaque composition, likely improving plaque stability. Mechanistically, MR deficiency suppresses macrophage foam cell formation and up-regulates expression of genes related to cholesterol efflux, as well as increases effective efferocytosis and phagocytic capacity of macrophages.Atherosclerosis is the underlying basis of coronary heart disease and cerebrovascular disease, which together account for nearly 80% of all deaths caused by cardiovascular diseases (1). Atherosclerotic cardiovascular diseases remain to be a leading cause of mortality and morbidity worldwide, posing a great threat to public health (2). New strategies and new targets are in need to treat atherosclerosis more effectively.Macrophages are the major immune cells in atherosclerotic plaques and play essential roles during the whole process of atherosclerosis in different aspects, including inflammation, foam cell formation, necrosis, and phagocytic clearance (3, 4). In the early stages, macrophages accumulated in the subendothelial space ingest modified lipids to become foam cells that are a hallmark of atherosclerosis and the major component of early fatty streak lesions (5). These macrophage-derived foam cells secrete inflammatory cytokines and chemokines to amplify inflammatory response and to induce more accumulation of macrophages/foam cells, propelling expansion and progression of atherosclerotic plaques. In advanced lesions, apoptosis of macrophages/foam cells rapidly increases, whereas the ability of neighboring macrophages/foam cells to effectively clear the apoptotic cells (effective efferocytosis) decreases, both of which contribu...