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RISS 인기검색어
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- 저자 : Rui Rao (검색결과 3 건)
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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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Fang Wang,Jian-fang Lou,Yan Cao,Xin-hui Shi,Peng Wang,Jian Xu,Er-fu Xie,Ting Xu,Rui-hong Sun,Jianyu Rao,Pu-wen Huang,Shi-yang Pan,Hong Wang 생화학분자생물학회 2015 Experimental and molecular medicine Vol.47 No.-
MicroRNAs (miRNAs), a class of small non-coding RNAs, mediate gene expression by either cleaving target mRNAs or inhibiting their translation. They have key roles in the tumorigenesis of several cancers, including non-small cell lung cancer (NSCLC). The aim of this study was to investigate the clinical significance of miR-638 in the evaluation of NSCLC patient prognosis in response to chemotherapy. First, we detected miR-638 expression levels in vitro in the culture supernatants of the NSCLC cell line SPC-A1 treated with cisplatin, as well as the apoptosis rates of SPC-A1. Second, serum miR-638 expression levels were detected in vivo by using nude mice xenograft models bearing SPC-A1 with and without cisplatin treatment. In the clinic, the serum miR-638 levels of 200 cases of NSCLC patients before and after chemotherapy were determined by quantitative real-time PCR, and the associations of clinicopathological features with miR-638 expression patterns after chemotherapy were analyzed. Our data helped in demonstrating that cisplatin induced apoptosis of the SPC-A1 cells in a dose- and time-dependent manner accompanied by increased miR-638 expression levels in the culture supernatants. In vivo data further revealed that cisplatin induced miR-638 upregulation in the serum derived from mice xenograft models, and in NSCLC patient sera, miR-638 expression patterns after chemotherapy significantly correlated with lymph node metastasis. Moreover, survival analyses revealed that patients who had increased miR-638 levels after chemotherapy showed significantly longer survival time than those who had decreased miR-638 levels. Our findings suggest that serum miR-638 levels are associated with the survival of NSCLC patients and may be considered a potential independent predictor for NSCLC prognosis.
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Optimization of long span portal frames using spatially distributed surrogates
Zhifang Zhang,Jingwen Pan,Jiyang Fu,Hemant Kumar Singh,Yong-Lin Pi,Jiurong Wu,Rui Rao 국제구조공학회 2017 Steel and Composite Structures, An International J Vol.24 No.2
This paper presents optimization of a long-span portal steel frame under dynamic wind loads using a surrogate-assisted evolutionary algorithm. Long-span portal steel frames are often used in low-rise industrial and commercial buildings. The structure needs be able to resist the wind loads, and at the same time it should be as light as possible in order to be cost-effective. In this work, numerical model of a portal steel frame is constructed using structural analysis program (SAP2000), with the web-heights at five locations of I-sections of the columns and rafters as the decision variables. In order to evaluate the performance of a given design under dynamic wind loading, the equivalent static wind load (ESWL) is obtained from a database of wind pressures measured in wind tunnel tests. A modified formulation of the problem compared to the one available in the literature is also presented, considering additional design constraints for practicality. Evolutionary algorithms (EA) are often used to solve such non-linear, black-box problems, but when each design evaluation is computationally expensive (e.g., in this case a SAP2000 simulation), the time taken for optimization using EAs becomes untenable. To overcome this challenge, we employ a surrogate-assisted evolutionary algorithm (SAEA) to expedite the convergence towards the optimum design. The presented SAEA uses multiple spatially distributed surrogate models to approximate the simulations more accurately in lieu of commonly used single global surrogate models. Through rigorous numerical experiments, improvements in results and time savings obtained using SAEA over EA are demonstrated.
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