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Functional Roles of Exosomes in Allergic Contact Dermatitis
Song Bocui,Chen Qian,Li Yuqi,Zhan Shuang,Zhao Rui,Shen Xue,Liu Min,Tong Chunyu 한국미생물·생명공학회 2022 Journal of microbiology and biotechnology Vol.32 No.12
Allergic contact dermatitis (ACD) is an allergen-specific T-cell-mediated inflammatory response, albeit with unclear pathogenesis. Exosomes are nanoscale extracellular vesicles secreted by several cell types and widely distributed in various biological fluids. Exosomes affect the occurrence and development of ACD through immunoregulation among other ways. Nevertheless, the role of exosomes in ACD warrants further clarification. This review examines the progress of research into exosomes and their involvement in the pathogenesis, diagnosis, and treatment of ACD and provides ideas for exploring new diagnostic and treatment methods for this disease.
Enhai Song,Weiren Zhao,Guoxiong Zhou,Xihua Dou,Huachu Ming,Chunyu Yi 한국물리학회 2011 Current Applied Physics Vol.11 No.6
A single phased white light emitting phosphors K_2Ca_(1−x−y)P_2O_7: xEu^2+, yMn^2+ were synthesized by solid state reaction method. The Effective energy transfer occurs in this phosphor due to the large spectral overlap between the emission of Eu^2+ and the excitation of Mn^2+. The emission hue of K_2Ca_(1−x−y)P_2O_7: xEu^2+, yMn^2+ from blue to white light can be obtained by tuning the Eu^2+/Mn^2+ content ratio. The energy transfer mechanism from Eu^2+ to Mn^2+ in this phosphor was carefully investigated and demonstrated to be via the dipole―quadrupole interaction.
Qi Bingchao,Song Liqiang,Hu Lang,Guo Dong,Ren Gaotong,Peng Tingwei,Liu Mingchuan,Fang Yexian,Li Chunyu,Zhang Mingming,Li Yan 생화학분자생물학회 2022 Experimental and molecular medicine Vol.54 No.-
Myocardial infarction (MI) is the leading cause of premature death among adults. Cardiomyocyte death and dysfunction of the remaining viable cardiomyocytes are the main pathological factors of heart failure after MI. Mitochondrial complexes are emerging as critical mediators for the regulation of cardiomyocyte function. However, the precise roles of mitochondrial complex subunits in heart failure after MI remain unclear. Here, we show that NADH:ubiquinone oxidoreductase core subunit S1 (Ndufs1) expression is decreased in the hearts of heart failure patients and mice with myocardial infarction. Furthermore, we found that cardiac-specific Ndufs1 overexpression alleviates cardiac dysfunction and myocardial fibrosis in the healing phase of MI. Our results demonstrated that Ndufs1 overexpression alleviates MI/hypoxia-induced ROS production and ROS-related apoptosis. Moreover, upregulation of Ndufs1 expression improved the reduced activity of complex I and impaired mitochondrial respiratory function caused by MI/hypoxia. Given that mitochondrial function and cardiomyocyte apoptosis are closely related to heart failure after MI, the results of this study suggest that targeting Ndufs1 may be a potential therapeutic strategy to improve cardiac function in patients with heart failure.
Qi Wan,Geng Liu,Chunyu Song,Yong Zhou,Shangjun Ma,Ruiting Tong 대한기계학회 2020 JOURNAL OF MECHANICAL SCIENCE AND TECHNOLOGY Vol.34 No.7
To analyze the effects of clearance joint number and dynamic interaction on responses of the flap actuation system, a dynamic analysis model is proposed based on a modified contact force model. The modified contact force model can take contact properties with small clearance, heavy load, large contact area and variable contact stiffness coefficient into consideration for the flap actuation system. Numerical results show that the actuation system presents violent fluctuation due to the dynamic interaction between multiple clearance joints, and the clearance joint closest to the input part suffers more serious contact effects. Furthermore, the combination motion modes between the multiple clearance joints are helpful to judge and analyze the motion state and dynamic behaviors of actuation systems. These simulation findings can provide a theoretical foundation for the optimization design, control strategy and engineering experiments of the actuation systems with multiple clearances.
Caspase-3 inhibitor inhibits enterovirus D68 production
Wenbo Huo,Jinghua Yu,Chunyu Liu,Ting Wu,Yue Wang,Xiangling Meng,Fengmei Song,Shuxia Zhang,Ying Su,Yumeng Liu,Jinming Liu,Xiaoyan Yu,Shucheng Hua 한국미생물학회 2020 The journal of microbiology Vol.58 No.9
Enterovirus D68 (EVD68) is an emerging pathogen that recently caused a large worldwide outbreak of severe respiratory disease in children. However, the relationship between EVD68 and host cells remains unclear. Caspases are involved in cell death, immune response, and even viral production. We found that caspase-3 was activated during EVD68 replication to induce apoptosis. Caspase-3 inhibitor (Z-DEVDFMK) inhibited viral production, protected host cells from the cytopathic effects of EVD68 infection, and prevented EVD68 from regulating the host cell cycle at G0/G1. Meanwhile, caspase-3 activator (PAC-1) increased EVD68 production. EVD68 infection therefore activates caspase-3 for virus production. This knowledge provides a potential direction for the prevention and treatment of disease related to EVD68.
Fangfang Jie,Mingjia Liao,Siwei Jiang,Chunyu Song,Chengli Tang,Boshui Chen 대한기계학회 2023 JOURNAL OF MECHANICAL SCIENCE AND TECHNOLOGY Vol.37 No.12
Phosphonation and nitrogenation of methyl epoxyoleate (MEO) were done to prepare phosphonitrogenated methyl epoxyoleate (PNMEO). The structural characteristics of PNMEO were characterized. The tribological properties of PNMEO and MEO as additives in a paraffin oil and a rapeseed oil were evaluated, and the morphologies, element compositions and tribochemical species of worn surfaces were analyzed. Results showed that PNMEO was more efficient in enhancing tribological properties of oils than MEO. Results also showed that PNMEO and MEO were more powerful in paraffin oil than in rapeseed oil in improving loadcarrying, friction-reducing and anti-wear performances, but in rapeseed oil than in paraffin oil in improving extreme pressure property. The tribological mechanisms of PNMEO in reducing friction and wear were attributed to PNMEO-involved tribo-adsorptions and tribo-reactions to produce a composite boundary lubrication film which consisted of a matrix of PNMEO with inclusions of iron oxide, polyphosphates, aminic compounds, and the base oil molecules.
IL-17A Secreted by Th17 Cells Is Essential for the Host against Streptococcus agalactiae Infections
( Jing Chen ),( Siyu Yang ),( Wanyu Li ),( Wei Yu ),( Zhaowei Fan ),( Mengyao Wang ),( Zhenyue Feng ),( Chunyu Tong ),( Baifen Song ),( Jinzhu Ma ),( Yudong Cui ) 한국미생물생명공학회(구 한국산업미생물학회) 2021 Journal of microbiology and biotechnology Vol.31 No.5
Streptococcus agalactiae is an important bacterial pathogen and causative agent of diseases including neonatal sepsis and meningitis, as well as infections in healthy adults and pregnant women. Although antibiotic treatments effectively relieve symptoms, the emergence and transmission of multidrug-resistant strains indicate the need for an effective immunotherapy. Effector T helper (Th) 17 cells are a relatively newly discovered subpopulation of helper CD4<sup>+</sup> T lymphocytes, and which, by expressing interleukin (IL)-17A, play crucial roles in host defenses against a variety of pathogens, including bacteria and viruses. However, whether S. agalactiae infection can induce the differentiation of CD4<sup>+</sup> T cells into Th17 cells, and whether IL-17A can play an effective role against S. agalactiae infections, are still unclear. In this study, we analyzed the responses of CD4<sup>+</sup> T cells and their defensive effects after S. agalactiae infection. The results showed that S. agalactiae infection induces not only the formation of Th1 cells expressing interferon (IFN)-γ, but also the differentiation of mouse splenic CD4<sup>+</sup> T cells into Th17 cells, which highly express IL-17A. In addition, the bacterial load of S. agalactiae was significantly increased and decreased in organs as determined by antibody neutralization and IL-17A addition experiments, respectively. The results confirmed that IL-17A is required by the host to defend against S. agalactiae and that it plays an important role in effectively eliminating S. agalactiae. Our findings therefore prompt us to adopt effective methods to regulate the expression of IL-17A as a potent strategy for the prevention and treatment of S. agalactiae infection.