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A Continuous Abnormal Speech Detection Method Based on Time Domain features Weighted
He Jun,Ji-chen Yang,Qing-hua Zhang,Guo-xi Sun,Jian-bing Xiong 보안공학연구지원센터 2014 International Journal of Control and Automation Vol.7 No.12
In this brief, a novel pathological continuous speech detection method based on time domain features weighted. First, different optimal threshold for time domain features, including zero crossing ratio, short-time energy and autocorrelation, are obtained from training speech data. Second, a difference evaluation technique is proposed, and with it, the difference of the same time domain feature selected from testing speech data and training speech data were obtained. Finally, to distinguish a given speech well, a novel weighting method based on difference evaluation for each kinds of time domain is employed, respectively. Experiments were conducted on the pathological speech database to prove the power and effectiveness of the proposed method. Results obtained shown that this method outperforms other early proposed time domain feature method, creating a more reliable technique for pathological continuous speech detection.
Yang Hui-Hui,Jiang Hui-Ling,Tao Jia-Hao,Zhang Chen-Yu,Xiong Jian-Bing,Yang Jin-Tong,Liu Yu-Biao,Zhong Wen-Jing,Guan Xin-Xin,Duan Jia-Xi,Zhang Yan-Feng,Liu Shao-Kun,Jiang Jian-Xin,Zhou Yong,Guan Cha-Xi 생화학분자생물학회 2022 Experimental and molecular medicine Vol.54 No.-
Necroptosis is the major cause of death in alveolar epithelial cells (AECs) during acute lung injury (ALI). Here, we report a previously unrecognized mechanism for necroptosis. We found an accumulation of mitochondrial citrate (citratemt) in lipopolysaccharide (LPS)-treated AECs because of the downregulation of Idh3α and citrate carrier (CIC, also known as Slc25a1). shRNA- or inhibitor–mediated inhibition of Idh3α and Slc25a1 induced citratemt accumulation and necroptosis in vitro. Mice with AEC-specific Idh3α and Slc25a1 deficiency exhibited exacerbated lung injury and AEC necroptosis. Interestingly, the overexpression of Idh3α and Slc25a1 decreased citratemt levels and rescued AECs from necroptosis. Mechanistically, citratemt accumulation induced mitochondrial fission and excessive mitophagy in AECs. Furthermore, citratemt directly interacted with FUN14 domain-containing protein 1 (FUNDC1) and promoted the interaction of FUNDC1 with dynamin-related protein 1 (DRP1), leading to excessive mitophagy-mediated necroptosis and thereby initiating and promoting ALI. Importantly, necroptosis induced by citratemt accumulation was inhibited in FUNDC1-knockout AECs. We show that citratemt accumulation is a novel target for protection against ALI involving necroptosis.
Jiangzhou Zhuang,Xiaoyin Jin,Xianlin Shen,Junjun Tan,Longhui Nie,Jian Xiong,Bing Hu 대한화학회 2015 Bulletin of the Korean Chemical Society Vol.36 No.7
A series of catalysts, ionic liquid-modified SBA-15 (denoted ILSBA) doped with H5PMo10V2O40 (HPMoV2) have been synthesized and characterized by XRD, FT-IR, 1H NMR, TG-DTA, and TEM. The catalyst was used for the removal of dibenzothiophene (DBT) in model oil combined with hydrogen peroxide (the oxidant) and acetonitrile (the phase-transfer agent). It was observed that the sulfur content of DBT can be reduced from 500 to 2 ppm by adjusting the amount of catalyst, the reaction temperatures and the reaction time. Besides, the catalyst activity for different sulfur compounds showed a huge difference which may be mainly affected by the electron densities of sulfur atom. Moreover, the catalyst can be recycled seven times without a significant loss in activity, which could be ascribed to the strong electrostatic interaction between ILSBA and HPMoV2. In addition, a postulated mechanism was proposed to reveal the oxidative desulfurization process.