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Compared with optical sensors, wearable inertial sensors have many advantages such as low cost, small size, more comprehensive application range, no space restrictions and occlusion, better protection of user privacy, and more suitable for sports applications. This article aims to solve irregular actions that table tennis enthusiasts do not know in actual situations. We use wearable inertial sensors to obtain human table tennis action data of professional table tennis players and non-professional table tennis players, and extract the features from them. Finally, we propose a new method based on multi-dimensional feature fusion convolutional neural network and fine-grained evaluation of human table tennis actions. Realize ping-pong action recognition and evaluation, and then achieve the purpose of auxiliary training. The experimental results prove that our proposed multi-dimensional feature fusion convolutional neural network has an average recognition rate that is 0.17 and 0.16 higher than that of CNN and Inception-CNN on the nine-axis non-professional test set, which proves that we can better distinguish different human table tennis actions and have a more robust generalization performance. Therefore, on this basis, we have better realized the enthusiast of table tennis the purpose of the action for auxiliary training.

Schistosomiasis is a serious and neglected disease with a high prevalence in tropical and subtropical countries. The primary pathology of hepatic schistosomiasis caused by Schistosoma japonicum (S. japonicum) or Schistosoma mansoni (S. mansoni) infection is egg-induced granuloma and subsequent fibrosis in the liver. Activation of hepatic stellate cells (HSCs) is the central driver of liver fibrosis. Macrophages (Mφ), making up 30% of cells in hepatic granulomas, directly or indirectly regulate HSC activation by paracrine mechanisms, via secreting cytokines or chemokines. Currently, Mφ-derived extracellular vesicles (EVs) are broadly involved in cell communication with adjacent cell populations. However, whether Mφ-derived EVs could target neighboring HSCs to regulate their activation during schistosome infection remains largely unknown. Schistosome egg antigen (SEA) is considered to be the main pathogenic complex mixture involved in liver pathology. Here, we demonstrated that SEA induced Mφ to produce abundant extracellular vesicles, which directly activated HSCs by activating their autocrine TGF-β1 signaling. Mechanistically, EVs derived from SEA-stimulated Mφ contained increased miR-33, which were transferred into HSCs and subsequently upregulated autocrine TGF-β1 in HSCs through targeting and downregulating SOCS3 expression, thereby promoting HSC activation. Finally, we validated that EVs derived from SEA-stimulated Mφ utilized enclosed miR-33 to promote HSC activation and liver fibrosis in S. japonicum-infected mice. Overall, our study indicates that Mφ-derived EVs play important roles in the paracrine regulation of HSCs during the progression of hepatic schistosomiasis, representing a potential target for the prevention of liver fibrosis in hepatic schistosomiasis. Author summary: Schistosomiasis is a neglected parasitic disease affecting over 250 million people in tropical and subtropical regions. Among the common pathogenic species, Schistosoma japonicum and Schistosoma mansoni mainly cause hepatic schistosomiasis, which is mainly attributed to liver-trapped schistosome eggs, leading to granulomatous inflammation and liver fibrosis. HSC activation is the central driver of liver fibrosis during hepatic schistosomiasis. Macrophages (Mφ) are tightly connected to HSC activity. Currently, much evidence supports the pivotal role of Mφ-derived extracellular vesicles (EVs). However, the potential involvement of Mφ-derived EVs in HSC communication and modulation in hepatic schistosomiasis remains largely unknown. In this study, the authors illustrate that S. japonicum infection utilizes Mφ-derived EVs to promote HSC activation and liver fibrosis. Briefly, schistosome egg antigen (SEA) induces Mφ to secrete abundant miR-33-enriched EVs, which are transferred to enhance autocrine TGF-β1 production by targeting SOCS3 in HSCs, thereby promoting HSC activation and liver fibrosis. These discoveries provide a previously unrecognized Mφ-EVs-based therapeutic target regarding HSC activation, which can be manipulated to prevent liver fibrosis during hepatic schistosomiasis. [ABSTRACT FROM AUTHOR]