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        Research on feature enhancement method of weak fault signal of rotating machinery based on adaptive stochastic resonance

        Kangping Gao,Xinxin Xu,Jiabo Li,Shengjie Jiao,Ning Shi 대한기계학회 2022 JOURNAL OF MECHANICAL SCIENCE AND TECHNOLOGY Vol.36 No.2

        Aiming at the problem that the traditional filtering method will filter out some useful signals when extracting weak fault features of rotating machinery, resulting in the loss of characteristic signals, a method for extracting weak fault features based on sin-cosine algorithm (SCA) is proposed. Combining the sensitivity of kurtosis to impact signals and correlation coefficients to interference noise, the paper proposes a new stochastic resonance (SR) performance evaluation index-weighted power spectrum kurtosis (WPSK), which solves the shortcoming of the traditional evaluation index that the fault frequency needs to be known in advance. The structural parameters of the SR are optimized by the SCA to improve the “resonance” effect. The SCA-based SR method is applied to the weak feature extraction of faulty bearings and compared with the SR model of particle swarm optimization, the results show that when the bearing inner-race fails, the value of WPSK increases by 33.5 %, and when the outerrace fails, the value of WPSK increases by 44.1 %.

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        In vivo therapeutic success of microRNA-155 antagomir in a mouse model of pulmonary fibrosis induced by bleomycin

        ( Xiaoyuan Sun ),( Yu Kang ),( Shan Xue ),( Jing Zou ),( Jiabo Xu ),( Daoqiang Tang ),( Hui Qin ) 대한내과학회 2021 The Korean Journal of Internal Medicine Vol.36 No.0

        Background/Aims: MicroRNAs (miRNAs) play critical regulatory roles in the pathogenesis of pulmonary fibrosis. The aim of this study was to explore whether miRNA antagomirs could serve as potential therapeutic agents in interstitial lung diseases. Methods: A mouse model of pulmonary fibrosis was established by intratracheal injection of bleomycin (BLM). Using microarray analysis, up-regulated miRNAs were identified during the development of pulmonary fibrosis. miR-155 was chosen as the candidate miRNA. Fifteen mice were then randomized into the following three groups: BLM + antagomiR-155 group, treated with BLM plus intravenously injected with antagomiR-155; BLM group, treated with intratracheal BLM plus phosphate-buffered saline (PBS); and a control group, treated with PBS only. Lung tissues were collected for histopathological analysis, hydroxyproline measurement, and Western blotting. Enzyme-linked immunosorbent assays were used for the measurement of cytokines associated with pulmonary fibrosis. Results: Histological changes and hydroxyproline levels induced by BLM were significantly inhibited by antagomiR-155. The levels of interleukin 4 (IL-4) and transforming growth factor-β (TGF-β) expression were increased after BLM treatment. However, miR-155 silencing decreased the expression of IL-4, TGF-β, and interferon-γ. TGF-β-activated kinase 1/mitogen-activated protein kinase kinase kinase 7 (MAP3K7)-binding protein 2 (TAB2) of the mitogen-activated protein kinase (MAPK) signaling pathway, was activated by BLM and inhibited by in vivo silencing of miR-155 via antagomiR-155. Conclusions: In vivo treatment with antagomiR-155 alleviated the pathological changes induced by BLM and may be a promising therapeutic strategy for pulmonary fibrosis.

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