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RISS 인기검색어
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- 저자 : Rongchang Li (검색결과 3 건)
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Qi Liu,Rongchang Li,Qingling Zhang,Jianxun Li 제어·로봇·시스템학회 2019 International Journal of Control, Automation, and Vol.17 No.12
This paper considers the problem of sliding mode control (SMC) design for a class of nonlinear singular systems with time-varying delay and uncertainties, especially with uncertainties in the derivative matrix. By taking uncertainties of the derivative matrix into account, the state augmentation transformation is constructed such that uncertainties of the derivative matrix are eliminated. Then an appropriate integral-type sliding surface function is designed. And the resulting sliding mode dynamics is an uncertain singular time-varying delay system. A delaydependent sufficient condition which guarantees the sliding mode dynamics to be admissible with H∞ performance is established. A new version of stabilization solvability condition is then proposed in terms of linear matrix inequality (LMI), which determines the undetermined parameter K in both the sliding surface function and the SMC laws. Moreover, two distinctive controllers (i.e., an SMC law and an adaptive SMC law) are synthesized such that the finite-time reachability of the predesigned sliding surface can be ensured. Finally, simulation examples are given to demonstrate the effectiveness and the merits of the proposed theory.
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Chen Shuyu,Yu Li,Deng Yao,Liu Yuanyuan,Wang Lingwei,Li Difei,Yang Kai,Liu Shengming,Tao Ailin,Chen Rongchang 대한천식알레르기학회 2022 Allergy, Asthma & Immunology Research Vol.14 No.5
Purpose: Interleukin (IL)-17A plays a critical role in the pathogenesis of allergic airway inflammation. Yet, the exact roles of IL-17A in asthma are still controversial. Thus, the aim of this study was to dissect the roles of IL-17A in toluene diisocyanate (TDI)-induced mixed granulocytic asthma and to assess the effects of neutralizing antibody in different effector phases on TDI-induced asthma. Methods: IL-17A functions in allergic airway inflammation were evaluated using mice deficient in IL-17A (Il17a−/−) or IL-17A monoclonal antibody (IL-17A mab, intraperitoneally, 50 μg per mouse, 100 μg per mouse). Moreover, the effects of exogenous recombinant IL (rIL)-17A in vivo (murine rIL-17A, intranasally, 1 μg per mouse) and in vitro (human rIL-17A, 100 ng/mL) were investigated. Results: TDI-induced mixed granulocytic airway inflammation was IL-17A-dependent because airway hyperreactivity, neutrophil and eosinophil infiltration, airway smooth muscle thickness, epithelium injury, dysfunctional T helper (Th) 2 and Th17 responses, granulocytic chemokine production and mucus overproduction were more markedly reduced in the Il17a−/− mice or by IL-17A neutralization during the sensitization phase of wild-type (WT) mice. By contrast, IL-17A neutralization during the antigen-challenge phase aggravated TDI-induced eosinophils recruitment, with markedly elevated Th2 response. In line with this, instillation of rIL-17 during antigen sensitization exacerbated airway inflammation by promoting neutrophils aggregation, while rIL-17A during the antigen-challenge phase protected the mice from TDI-induced airway eosinophilia. Moreover, rIL-17A exerted distinct effects on eosinophil- or neutrophil-related signatures in vitro. Conclusions: Our data demonstrated that IL-17A was required for the initiation of TDI-induced asthma, but functioned as a negative regulator of established allergic inflammation, suggesting that early abrogation of IL-17A signaling, but not late IL-17A neutralization, may prevent the progression of TDI-induced asthma and could be used as a therapeutic strategy for severe asthmatics in clinical settings.
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Tissue-specific expression of the NOD-like receptor protein 3 in BALB/c mice
Zhiqiang Huang,Meng Yu,Shuang Tong,Kun Jia,Rongchang Liu,Heng Wang,Shou-Jun Li,Zhang-Yong Ning 대한수의학회 2014 Journal of Veterinary Science Vol.15 No.2
Activation of the innate immune system requires recognitionof pathogen-associated molecular patterns, such as NOD-likereceptors. The NOD-like receptor protein 3 (NLRP3)inflammasome is involved in induction of the proinflammatorycytokine, IL-1β, and subsequent inflammatoryresponses. NLRP3 inflammasome plays important roles in theinflammatory and innate immune responses associated withautoimmune/inflammatory syndrome. However, analysis of thetissue distribution and expression profiles in BALB/c mice is stillincomplete. In this study, we investigated the tissue distributionand expression pattern of NLRP3 in BALB/c mice to furtherelucidate its function in innate immunity in this commonly usedlaboratory animal model. NLRP3 mRNA expression levels andtissue distribution of the protein were investigated by real-timequantitative PCR and immunohistochemical analyses,respectively. NLRP3 mRNA expression was higher in thekidney and inguinal lymph nodes than in other tissues. Cytoplasmic expression of NLRP3 was detected in the epithelialreticular cells of the spleen and thymus, lymphocytes in theinguinal lymph nodes, cardiac muscle cells, cerebral cortexneurons, alveolar macrophages, renal tubule cells and liversinusoidal endothelial cells. The results of this study will assistinvestigators in interpreting site-specific functions and roles ofNLRP3 in inflammatory responses.
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