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RISS 인기검색어
- 검색키워드
- 저자 : Feiyun Xiao (검색결과 2 건)
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Design and evaluation of a 7-DOF cable-driven upper limb exoskeleton
Feiyun Xiao,Yongsheng Gao,Yong Wang,Yanhe Zhu,Jie Zhao 대한기계학회 2018 JOURNAL OF MECHANICAL SCIENCE AND TECHNOLOGY Vol.32 No.2
This paper presents a seven degrees of freedom cable-driven upper limb exoskeleton (CABXLexo-7), which is compact, lightweight, and comfortable for post-stroke patients. To achieve the compactness of exoskeleton, two types of cable-driven differential mechanisms were designed. The cable-conduit mechanisms were applied to transmit the power of motors mounted on the backboard to the corresponding joints, then the whole weight of the exoskeleton could be light to ensure a comfortable motion assistance. In the course of experiments, the surface electromyography signals of major muscles related with the movements of upper limb were collected to evaluate the assistant ability of exoskeleton. The experimental results showed that the activation levels of corresponding muscles were reduced by using the seven degrees of freedom cable-driven upper limb exoskeleton in the course of rehabilitation, and it demonstrated that the exoskeleton can provide effective movements assistance to the post-stroke patients.
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The Role of Macrophage Migration Inhibitory Factor (MIF) in Asthmatic Airway Remodeling
Li Ruyi,Wang Feiyun,Wei Jianghong,Lin Yun,Tang Guofang,Rao Lizong,Ma Libing,Xu Qing,Wu Jingjie,Lv Qian,Zhou Rui,Lei Huiren,Zhao Xueqiang,Yao Dong,Xiao Bo,Huang Haiming,Zhang Jiange,Mo Biwen 대한천식알레르기학회 2021 Allergy, Asthma & Immunology Research Vol.13 No.1
Purpose: Recent studies have demonstrated that macrophage migration inhibitory factor (MIF) is of importance in asthmatic inflammation. The role of MIF in modulating airway remodeling has not yet been thoroughly elucidated to date. In the present study, we hypothesized that MIF promoted airway remodeling by intensifying airway smooth muscle cell (ASMC) autophagy and explored the specific mechanisms. Methods: MIF knockdown in the lung tissues of C57BL/6 mice was conducted by instilling intratracheally adeno-associated virus (AAV) vectors (MIF-mutant AAV9) into mouse lung tissues. Mice genetically deficient in the autophagy marker ATG5 (ATG5+/−) was used to detect the role of autophagy in ovalbumin (OVA)-asthmatic murine models. Moreover, to block the expression of MIF and CD74 in vitro models, inhibitors, antibodies and lentivirus transfection techniques were employed. Results: First, MIF knockdown in the lung tissues of mice showed markedly reduced airway remodeling in OVA murine mice models. Secondly, ASMC autophagy was increased in the OVA-challenged models. Mice genetically deficient in the autophagy marker ATG5 (ATG5+/−) that were primed and challenged with OVA showed lower airway remodeling than genetically wild-type asthmatic mice. Thirdly, MIF can induce ASMC autophagy in vitro. Moreover, the cellular source of MIF which promoted ASMC autophagy was macrophages. Finally, MIF promoted ASMC autophagy in a CD74-dependent manner. Conclusions: MIF can increase asthmatic airway remodeling by enhancing ASMC autophagy. Macrophage-derived MIF can promote ASMC autophagy by targeting CD74.
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