A New Event-Triggered Adaptive Fixed-Time Control Design for Uncertain Nonlinear Systems.

This article investigates the problem of dynamic memory event-triggered (DMET) fixed-time tracking control within time-varying asymmetric constraints for nonaffine nonstrict-feedback uncertain nonlinear systems with unmodeled dynamics and unknown disturbances. The existing dynamic event-triggered control methods cannot handle the nonlinear systems with unmodeled dynamics and nonaffine inputs, which greatly limits the applicability of the strategy. To this end, a novel DMET adaptive fuzzy fixed-time control protocol is constructed based on the idea of command filtered backstepping, in which a new dynamic signal function is established to deal with the unmodeled dynamics and an improved DMET mechanism (DMETM) is designed to solve the problem of nonaffine inputs. It is proved that the newly DMET control strategy ensures the tracking error converges to an arbitrarily small compact set in a fixed time and all the signals of the closed-loop systems are bounded. The effectiveness of the proposed approach is demonstrated by two simulation examples.

Event-Based Remote State Estimation for Nonlinear Systems: A Box Particle Filtering Method.

This article is concerned with the problem of event-based remote state estimation for nonlinear/non-Gaussian systems on a wireless network with limited bandwidth. To reduce unnecessary data transmissions, a novel event-triggering mechanism is developed by using the least-square technique. Based on this, an event-triggered box particle filtering scheme is designed to realize the minimum mean-squared error estimation at the remote estimator end, in which the posterior probability density functions are calculated separately according to the information of the event-triggered indicator to avoid the problem of excessive estimation error. Different from the existing approaches, the proposed algorithm does not depend on any Gaussian assumptions and reduces the computational complexity under the premise of ensuring the estimation performance. Finally, two simulation examples are performed to demonstrate the validity of the proposed algorithm.

Event-Triggered Adaptive Output Feedback Control for a Class of Uncertain Nonlinear Systems With Actuator Failures.

This paper investigates the event-triggered adaptive output feedback control problem for a class of uncertain nonlinear systems in the presence of actuator failures and unknown control direction. By utilizing the adaptive backstepping technique, an event-based output feedback controller is developed together with a time-variant event-triggered rule. In this design, the radial basis function neural network algorithms are first introduced to identify the unknown terms of the systems. Then, a new state observer with adaptive compensation is designed to estimate the state vector. The overall control strategy guarantees that the output signal tracks the reference signal and all the signals of the closed-loop systems are bounded. Unlike the existing methods, the proposed control scheme can handle the coupling term incurred by the loss of effectiveness fault of the actuator, the event-triggered rule, and unknown control direction. Finally, an example is performed to demonstrate the validity of the proposed strategy.

Structural diversity directed by switchable coordination of substitute groups in a ternary Cu(II)-triazole-sulfoisophthalate self-assembly system: synthesis, crystal structures and magnetic behavior.

Four magnetic samples with different building blocks and dimensionalities, {[Cu(4)(atr)(2)(µ(3)-OH)(2)(sip)(2)]·4H(2)O}(n) (1), {[Cu(4)(atr)(2)(H(2)O)(8)(µ-OH)(2)(sip)(2)]·1.3CH(3)OH·0.7H(2)O}(n) (2), {[Cu(3)(atr)(4)(H(2)O)(2)(sip)(2)]·4H(2)O}(n) (3) and {[Cu(3)(atr)(4)(H(2)O)(2)(µ(3)-OH)(sip)(Hsip)]·2CH(3)OH·2.75H(2)O}(n) (4) (atr = 4-amino-1,2,4-triazole and sip(3-) = 5-sulfoisophthalate), were obtained and characterized structurally and magnetically. Complex 1 exhibits a three-dimensional (3D) robust framework with butterfly-like Cu(II)(4) clusters periodically extended by tetratopic sip(3-) connectors. Complex 2 possesses a 2D layer with alternating Cu(II)(3) + Cu(II)(1) chains crosslinked by pairs of ditopic sip(3-) linkers. By contrast, the latter two entities feature 1D broad ribbons with linear (for 3) and triangular Cu(II)(3) cores (for 4) propagated by bidirectional sip(3-) connectors. Structural analysis reveals that the diverse building blocks and dimensionalities of 1-4 are significantly dominated by the tunable coordination of exocyclic amino- and/or sulfonate-group of the mixed ligands. Magnetically, antiferromagnetic interactions with variable strength transmitted by -NN- moiety of atr and hydroxyl mediators result in overall S = 0 (for 1) and 1/2 (for 3 and 4) spin ground states. These interesting results indicate that coordinative side group in the ternary metal ion-azolate-carboxylate system can be utilized to generate aesthetically pleasing building units and variably polytopic connectors, leading to differently extended superstructures and magnetic behavior.

[Inhibition of HLA-DRB1*0405 gene expression by siRNA].

OBJECTIVE: To investigate the effects of small interfering RNA (siRNA) of HLA DRB1(*)0405 HLA-DRB1(*)0405 gene expression with plasmid-based siRNAs. METHOD: Plasmid expressing HLA-DRB1(*)0405-renilla fusion protein-siCHECK-2/HLA-DRB1(*)0405, 6 different short hairpin RNAs (shRNAs) targeting 6 19 bp nucleotide sequences of HLA-DRB1(*)0405 (siRNA1 approximately 6), and one shRNA targeting the control non-specific sequence (siRNAC) were designed and constructed. Human embryonic kidney cells of the line 293 were cultured and co-transfected by lipids some with the plasmid siCHECK-2/HLA-DRB1(*)0405 and one specific shRNA expressing vector transiently, and cells without shRNA-transfection were used as negative controls. The impact of RNAi on HLA-DRB1(*)0405 expression was analyzed by real time fluorescence quantification RT-PCR and luciferase test. RESULTS: The expression of HLA-DRB1(*)0405 gene RNA of the 293 cells transfected with siRNA1, siRNA2, siRNA3, siRNA, and siRNA6 were down-regulated to 10.75%, 83.22%, 30.63%, 48.54%, and 89.92% that of the control group with the inhibition rates of 89.25%, 16.78%, 69.37%, 51.46%, and 10.08% respectively. However, no significant downregulation was showed in the cells transfected with siRNA4 and siRNAC. The 293 cells transfected with siRNA1 and siRNA 3 showed a significant downregulation of the protein expression of HLA-DRB1(*)0405 gene with the inhibitory rates of 6.70% and 36.85% respectively; however, the cells transfected with siRNA2, siRNA4, siRNA5, and siRNA6 did not show a significant downregulation. CONCLUSION: The significant inhibition of HLA-DRB1(*)0405 gene expression by siRNA suggests a therapeutic approach in rheumatoid arthritis: to use RNA interference (RNAi) to inhibit the abnormal immune reaction mediated by HLA-DRB1 in rheumatoid arthritis.

[The study of inhibitory peptides on T cell activation in rheumatoid arthritis].

OBJECTIVE: To study the inhibitory role of altered HA308 - 317 peptides in T cell responses in patients with rheumatoid arthritis (RA). METHODS: Peripheral blood mononuclear cells (PBMC) were obtained from 27 HLA-DRB1 positive RA patients. T cell responses to altered HA308-317 peptides were examined by using (3)H incorporation assay. The level of IL-2 and IFNgamma in the supernatants was identified by an enzyme-linked immunosorbent assay. The CD69 expression on T cell surface was studied by using flow cytometry. RESULTS: Compared to wild type CII263 - 272 or HA308 - 317, altered HA308 - 317 peptides failed to stimulate T cell proliferation (P < 0.05) and production of IL-2 as well as IFNgamma and resulted in lower expression of CD69 in RA patients (P < 0.05). SI values for T cell coincubated with altered HA308 - 317 peptides and CII263 - 272 or wild type HA308 - 317 were significantly lower than coincubated with CII263 - 272 and wild type HA308 - 317 alone (P < 0.05). CONCLUSION: Substitution of TCR-binding residue of HA308 - 317 yielded weak or non-T-cell stimulating peptides, which might be potentially effective in blocking abnormal T cell responses in RA.