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您的检索式：作者名="Qijing Fan"
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| 1 | Mechanisms of fluoroquinolone and macrolide resistance in Campylobacter spp.显示文摘 | Sophie Payot Jean-Michel Bolla Deborah Corcoran Séamus Fanning Francis Mégraud Qijing Zhang | 2006 | Microbes and Infection2006，，7： | 1 |
| 2 | Loss Analysis of Electromagnetic Linear Actuator Coupling Control Electromagnetic Mechanical System显示文摘As an energy converter,electromagnetic linear actuators(EMLAs)have been widely used in industries.Multidisciplinary methodology is a preferred tool for the design and optimization of EMLA.In this paper,a multidisciplinary method was proposed for revealing the influence mechanism of load on EMLA’s loss.The motion trajectory of EMLA is planned through tracking differentiator,an adaptive robust control was adopted to compensate the influence of load on motion trajectory.A control-electromagnetic-mechanical coupling model was established and verified experimentally.The influence laws of load change on EMLA’s loss,loss composition and loss distribution were analyzed quantitatively.The results show that the data error of experiment,and simulation result of input energy,mechanical work,and iron loss is less than 3%.The iron loss accounts for less than 54.9%of the total loss under no-load condition,while the iron loss increases with the increase of load.For iron loss distribution,only the percentage of inner yoke keeps increasing with the increase of load.The composition and distribution of loss are the basis of thermal analysis and design. | Jiayu Lu Qijing Qin Cao Tan Bo Li Xinyu Fan | 2021 | Energy Engineering2021，118，6： | 0 |
| 3 | The S100 calcium binding protein A11 promotes liver fibrogenesis by targeting TGF-βsignaling显示文摘Liver fibrosis is a key transformation stage and also a reversible pathological process in various types of chronic liver diseases.However,the pathogenesis of liver fibrosis still remains elusive.Here,we report that the calcium binding protein A11(S100A11)is consistently upregulated in the integrated data from GSE liver fibrosis and tree shrew liver proteomics.S100A11 is also experimentally activated in liver fibrosis in mouse,rat,tree shrew,and human with liver fibrosis.While overexpression of S100A11 in vivo and in vitro exacerbates liver fibrosis,the inhibition of S100A11 improves liver fibrosis.Mechanistically,S100A11 activates hepatic stellate cells(HSCs)and the fibrogenesis process via the regulation of the deacetylation of Smad3 in the TGF-βsignaling pathway.S100A11 physically interacts with SIRT6,a deacetylase of Smad2/3,which may competitively inhibit the interaction between SIRT6 and Smad2/3.The subsequent release and activation of Smad2/3 promote the activation of HSCs and fibrogenesis.Additionally,a significant elevation of S100A11 in serum is observed in clinical patients.Our study uncovers S100A11 as a novel profibrogenic factor in liver fibrosis,which may represent both a potential biomarker and a promising therapy target for treating liver fibrosis and fibrosis-related liver diseases. | Tingting Zhu Linqiang Zhang Chengbin Li Xiaoqiong Tan Jing Liu Huiqin Li Qijing Fan Zhiguo Zhang Mingfeng Zhan Lin Fu Jinbo Luo Jiawei Geng Yingjie Wu Xiaoju Zou Bin Liang | 2022 | Journal of Genetics and Genomics2022，49，4： | 0 |
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