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Generation Method of Autonomous Evasive Maneuver Strategy in Air Combat
Lin Li,Zhen Yang,Zhixiao Sun,Guang Zhan,Haiyin Piao,Deyun Zhou 제어로봇시스템학회 2022 제어로봇시스템학회 국제학술대회 논문집 Vol.2022 No.11
Air combat is usually a continuous process involving multiple rounds of missile attacks, UCAV(Unmanned Combat Aerial Vehicle) should consider the impact of maneuver on the entire air combat countermeasure mission rather than solely focusing on safety factors when evading incoming air to air missiles. In this paper, a method of generating autonomous evasive maneuver strategy in UCAV air combat is proposed under the condition of miss distance and energy dissipation. Firstly, the UCAV-missile three-dimensional space pursuit model and the UCAV autonomous evading state space, action space and reward function model are established. Dueling DDQN (Double Deep Q Network) algorithm is used to solve the model, which integrates Double DQN and Dueling DQN Network model. Simulation experiments and analysis show that the method proposed in this paper has significant effectiveness in solving the problem of autonomous evasive maneuvers in air combat under the conditions of miss distance and energy dissipation tactical requirements. The evasive maneuvers strategy obtained can reflect the two tactical requirements of air combat while ensuring the safety of UCAV itself.
Zhengxia Wang,Ningfei Ji,Zhongqi Chen,Zhixiao Sun,Chaojie Wu,Wenqing Yu,Fan Hu,Mao Huang,Mingshun Zhang 대한천식알레르기학회 2020 Allergy, Asthma & Immunology Research Vol.12 No.5
Purpose: CD4+T cells are essential in the pathogenesis of allergic asthma. We have previously demonstrated that microRNA-1165-3p (miR-1165-3p) was significantly reduced in T-helper type (Th) 2 cells and that miR-1165-3p was a surrogate marker for atopic asthma. Little is known about the mechanisms of miR-1165-3p in the regulation of Th2-dominated allergic inflammation. We aimed to investigate the associations between Th2 differentiation and miR-1165b-3p in asthma as well as the possible mechanisms. Methods: CD4+ naïve T cells were differentiated into Th1 or Th2 cells in vitro. MiR-1165-3p was up-regulated or down-regulated using lentiviral systems during Th1/Th2 differentiation. In vivo, the lentiviral particles with the miR-1165-3p enhancer were administered by tail vein injection on the first day of a house dust mite -induced allergic airway inflammation model. Allergic inflammation and Th1/Th2 differentiation were routinely monitored. To investigate the potential targets of miR-1165-3p, biotin-microRNA pull-down products were sequenced, and the candidates were further verified with a dual-luciferase reporter assay. The roles of a target protein phosphatase, Mg2+/Mn2+-dependent 1A (PPM1A), in Th2 cell differentiation and allergic asthma were further explored. Plasma PPM1A was determined by ELISA in 18 subjects with asthma and 20 controls. Results: The lentivirus encoding miR-1165-3p suppressed Th2-cell differentiation in vitro. In contrast, miR-1165-3p silencing promoted Th2-cell development. In the HDM-induced model of allergic airway inflammation, miR-1165-3p up-regulation was accompanied by reduced airway hyper-responsiveness, serum immunoglobulin E, airway inflammation and Th2-cell polarization. IL-13 and PPM1A were the direct targets of miR-1165-3p. The expression of IL-13 or PPM1A was inversely correlated with that of miR-1165-3p. PPM1A regulated the signal transducer and activator of transcription and AKT signaling pathways during Th2 differentiation. Moreover, plasma PPM1A was significantly increased in asthmatic patients. Conclusions: MiR-1165-3p negatively may regulate Th2-cell differentiation by targeting IL-13 and PPM1A in allergic airway inflammation.
Ji Ningfei,Chen Zhongqi,Wang Zhengxia,Sun Wei,Yuan Qi,Zhang Xijie,Jia Xinyu,Wu Jingjing,Jiang Jingxian,Song Meijuan,Xu Tingting,Liu Yanan,Ma Qiyun,Sun Zhixiao,Bao Yanmin,Zhang Mingshun,Huang Mao 대한천식알레르기학회 2024 Allergy, Asthma & Immunology Research Vol.16 No.1
Purpose: The roles and mechanisms of long noncoding RNAs (lncRNAs) in T helper 2 (Th2) differentiation from allergic asthma are poorly understood. We aimed to explore a novel lncRNA, LincR-protein phosphatase 2 regulatory subunit B' gamma (PPP2R5C), in Th2 differentiation in a mouse model of asthma. Methods: LincR-PPP2R5C from RNA-seq data of CD4+ T cells of asthma-like mice were validated and confirmed by quantitative reverse transcription polymerase chain reaction, northern blotting, nuclear and cytoplasmic separation, and fluorescence in situ hybridization (FISH). Lentiviruses encoding LincR-PPP2R5C or shRNA were used to overexpress or silence LincR-PPP2R5C in CD4+ T cells. The interactions between LincR-PPP2R5C and PPP2R5C were explored with western blotting, chromatin isolation by RNA purification assay, and fluorescence resonance energy transfer. An ovalbumin-induced acute asthma model in knockout (KO) mice (LincR-PPP2R5C KO, CD4 conditional LincR-PPP2R5C KO) was established to explore the roles of LincR-PPP2R5C in Th2 differentiation. Results: LncR-PPP2R5C was significantly higher in CD4+ T cells from asthmatic mice ex vivo and Th2 cells in vitro. The lentivirus encoding LincR-PPP2R5C suppressed Th1 differentiation; in contrast, the short hairpin RNA (shRNA) lentivirus decreased LincR-PPP2R5C and Th2 differentiation. Mechanistically, LincR-PPP2R5C deficiency suppressed the phosphatase activity of the protein phosphatase 2A (PP2A) holocomplex, resulting in a decline in Th2 differentiation. The formation of an RNA-DNA triplex between LincR-PPP2R5C and the PPP2R5C promoter enhanced PPP2R5C expression and activated PP2A. LincR-PPP2R5C KO and CD4 conditional KO decreased Th2 differentiation, airway hyperresponsiveness and inflammatory responses. Conclusions: LincR-PPP2R5C regulated PPP2R5C expression and PP2A activity by forming an RNA-DNA triplex with the PPP2R5C promoter, leading to Th2 polarization in a mouse model of acute asthma. Our data presented the first definitive evidence of lncRNAs in the regulation of Th2 cells in asthma.