Dear Editor,This letter investigates the fuzzy prescribed-time control(PTC)problem for a class of uncertain pure feedback nonlinear systems.Firstly,a novel prescribed-time stability lemma is introduced,which plays a c...Dear Editor,This letter investigates the fuzzy prescribed-time control(PTC)problem for a class of uncertain pure feedback nonlinear systems.Firstly,a novel prescribed-time stability lemma is introduced,which plays a critical role in stability analysis.Unlike existing PTC algorithms,where the nonlinear functions are typically known or satisfy a linear growth condition,our approach does not require such assumptions.To address these unknown factors,fuzzy logic systems(FLSs)are employed.Based on the new prescribed-time stability lemma,it is proven that the controller and all system states converge to the origin within the prescribed time and remain there.Finally,the effectiveness of the proposed algorithm is validated through a simulation example.展开更多
This research paper tackles the complexities of achieving global fuzzy consensus in leader-follower systems in robotic systems,focusing on robust control systems against an advanced signal attack that integrates senso...This research paper tackles the complexities of achieving global fuzzy consensus in leader-follower systems in robotic systems,focusing on robust control systems against an advanced signal attack that integrates sensor and actuator disturbances within the dynamics of follower robots.Each follower robot has unknown dynamics and control inputs,which expose it to the risks of both sensor and actuator attacks.The leader robot,described by a secondorder,time-varying nonlinear model,transmits its position,velocity,and acceleration information to follower robots through a wireless connection.To handle the complex setup and communication among robots in the network,we design a robust hybrid distributed adaptive control strategy combining the effect of sensor and actuator attack,which ensures asymptotic consensus,extending beyond conventional bounded consensus results.The proposed framework employs fuzzy logic systems(FLSs)as proactive controllers to estimate unknown nonlinear behaviors,while also effectively managing sensor and actuator attacks,ensuring stable consensus among all agents.To counter the impact of the combined signal attack on follower dynamics,a specialized robust control mechanism is designed,sustaining system stability and performance under adversarial conditions.The efficiency of this control strategy is demonstrated through simulations conducted across two different directed communication topologies,underscoring the protocol’s adaptability,resilience,and effectiveness in maintaining global consensus under complex attack scenarios.展开更多
Flares of joint inflammation and resistance to currently available biologic therapeutics in rheumatoid arthritis(RA)patients could reflect activation of innate immune mechanisms.Herein,we show that a TLR7 GU-rich endo...Flares of joint inflammation and resistance to currently available biologic therapeutics in rheumatoid arthritis(RA)patients could reflect activation of innate immune mechanisms.Herein,we show that a TLR7 GU-rich endogenous ligand,miR-Let7b,potentiates synovitis by amplifying RA monocyte and fibroblast(FLS)trafficking.miR-Let7b ligation to TLR7 in macrophages(MΦs)and FLSs expanded the synovial inflammatory response.Moreover,secretion of M1 monokines triggered by miR-Let7b enhanced Th1/Th17 cell differentiation.We showed that IRAK4 inhibitor(i)therapy attenuated RA disease activity by blocking TLR7-induced M1 MΦor FLS activation,as well as monokine-modulated Th1/Th17 cell polarization.IRAK4i therapy also disrupted RA osteoclastogenesis,which was amplified by miR-Let7b ligation to joint myeloid TLR7.Hence,the effectiveness of IRAK4i was compared with that of a TNF inhibitor(i)or anti-IL-6R treatment in collagen-induced arthritis(CIA)and miR-Let7b-mediated arthritis.We found that TNF or IL-6R blocking therapies mitigated CIA by reducing the infiltration of joint F480+iNOS+MΦs,the expression of certain monokines,and Th1 cell differentiation.Unexpectedly,these biologic therapies were unable to alleviate miR-Let7b-induced arthritis.The superior efficacy of IRAK4i over anti-TNF or anti-IL-6R therapy in miR-Let7b-induced arthritis or CIA was due to the ability of IRAK4i therapy to restrain the migration of joint F480+iNOS+MΦs,vimentin+fibroblasts,and CD3+T cells,in addition to negating the expression of a wide range of monokines,including IL-12,MIP2,and IRF5 and Th1/Th17 lymphokines.In conclusion,IRAK4i therapy may provide a promising strategy for RA therapy by disconnecting critical links between inflammatory joint cells.展开更多
基金supported by the National Natural Science Foundation of China(U20A20187,U22A2050)the Science Fund of Hebei Province(F2024203134,F2023203100)+3 种基金the Science and Technology Development Grant of Hebei Province(20311803D)Hebei Innovation Capability Improvement Plan project(22567619H)Basic Research Project of Shijiazhuang(241791007A)the China Scholarship Council(CSC 202308130190).
文摘Dear Editor,This letter investigates the fuzzy prescribed-time control(PTC)problem for a class of uncertain pure feedback nonlinear systems.Firstly,a novel prescribed-time stability lemma is introduced,which plays a critical role in stability analysis.Unlike existing PTC algorithms,where the nonlinear functions are typically known or satisfy a linear growth condition,our approach does not require such assumptions.To address these unknown factors,fuzzy logic systems(FLSs)are employed.Based on the new prescribed-time stability lemma,it is proven that the controller and all system states converge to the origin within the prescribed time and remain there.Finally,the effectiveness of the proposed algorithm is validated through a simulation example.
文摘This research paper tackles the complexities of achieving global fuzzy consensus in leader-follower systems in robotic systems,focusing on robust control systems against an advanced signal attack that integrates sensor and actuator disturbances within the dynamics of follower robots.Each follower robot has unknown dynamics and control inputs,which expose it to the risks of both sensor and actuator attacks.The leader robot,described by a secondorder,time-varying nonlinear model,transmits its position,velocity,and acceleration information to follower robots through a wireless connection.To handle the complex setup and communication among robots in the network,we design a robust hybrid distributed adaptive control strategy combining the effect of sensor and actuator attack,which ensures asymptotic consensus,extending beyond conventional bounded consensus results.The proposed framework employs fuzzy logic systems(FLSs)as proactive controllers to estimate unknown nonlinear behaviors,while also effectively managing sensor and actuator attacks,ensuring stable consensus among all agents.To counter the impact of the combined signal attack on follower dynamics,a specialized robust control mechanism is designed,sustaining system stability and performance under adversarial conditions.The efficiency of this control strategy is demonstrated through simulations conducted across two different directed communication topologies,underscoring the protocol’s adaptability,resilience,and effectiveness in maintaining global consensus under complex attack scenarios.
基金This work was supported in part by awards from the Department of Veteran’s Affairs MERIT Award(1I01BX002286)the National Institutes of Health(AR056099 and AR065778)+2 种基金the National Psoriasis Foundation(NPF)the Pfizer Investigator Initiated Research(IIR)Programthe Chicago Biomedical Consortium(CBC)Accelerator Award.
文摘Flares of joint inflammation and resistance to currently available biologic therapeutics in rheumatoid arthritis(RA)patients could reflect activation of innate immune mechanisms.Herein,we show that a TLR7 GU-rich endogenous ligand,miR-Let7b,potentiates synovitis by amplifying RA monocyte and fibroblast(FLS)trafficking.miR-Let7b ligation to TLR7 in macrophages(MΦs)and FLSs expanded the synovial inflammatory response.Moreover,secretion of M1 monokines triggered by miR-Let7b enhanced Th1/Th17 cell differentiation.We showed that IRAK4 inhibitor(i)therapy attenuated RA disease activity by blocking TLR7-induced M1 MΦor FLS activation,as well as monokine-modulated Th1/Th17 cell polarization.IRAK4i therapy also disrupted RA osteoclastogenesis,which was amplified by miR-Let7b ligation to joint myeloid TLR7.Hence,the effectiveness of IRAK4i was compared with that of a TNF inhibitor(i)or anti-IL-6R treatment in collagen-induced arthritis(CIA)and miR-Let7b-mediated arthritis.We found that TNF or IL-6R blocking therapies mitigated CIA by reducing the infiltration of joint F480+iNOS+MΦs,the expression of certain monokines,and Th1 cell differentiation.Unexpectedly,these biologic therapies were unable to alleviate miR-Let7b-induced arthritis.The superior efficacy of IRAK4i over anti-TNF or anti-IL-6R therapy in miR-Let7b-induced arthritis or CIA was due to the ability of IRAK4i therapy to restrain the migration of joint F480+iNOS+MΦs,vimentin+fibroblasts,and CD3+T cells,in addition to negating the expression of a wide range of monokines,including IL-12,MIP2,and IRF5 and Th1/Th17 lymphokines.In conclusion,IRAK4i therapy may provide a promising strategy for RA therapy by disconnecting critical links between inflammatory joint cells.
