
Since the emergence of SARS-COV-2, many updates and assumptions are being discussed based on the emerging understanding of the pathophysiology and outcomes of the infection. The host immune response is the critical factor in disease severity and the unique immune response of each individual has resulted in a broad spectrum of disease severity and clinical presentations. In this article, combining the emerging knowledge on the immunopathogenesis of COVID-19 infection with insights into the underlying mechanisms of certain autoimmune and chronic Immune-mediated inflammatory diseases we propound our hypothesis that SARS-CoV-2 infection produces chronic viral inflammatory syndrome.
Citation: DharmaSaranya Gurusamy, Vasuki Selvamurugesan, Swaminathan Kalyanasundaram, Shantaraman Kalyanaraman. Is COVID 19, a beginning of new entity called chronic viral systemic inflammatory syndrome?[J]. AIMS Allergy and Immunology, 2021, 5(2): 127-134. doi: 10.3934/Allergy.2021010
[1] | Federica Di Michele, Bruno Rubino, Rosella Sampalmieri, Kateryna Stiepanova . Stationary solutions to a hybrid viscous hydrodynamic model with classical boundaries. Mathematics in Engineering, 2024, 6(5): 705-725. doi: 10.3934/mine.2024027 |
[2] | Hao Zheng . The Pauli problem and wave function lifting: reconstruction of quantum states from physical observables. Mathematics in Engineering, 2024, 6(4): 648-675. doi: 10.3934/mine.2024025 |
[3] | Roberto Feola, Felice Iandoli, Federico Murgante . Long-time stability of the quantum hydrodynamic system on irrational tori. Mathematics in Engineering, 2022, 4(3): 1-24. doi: 10.3934/mine.2022023 |
[4] | Riccardo Adami, Raffaele Carlone, Michele Correggi, Lorenzo Tentarelli . Stability of the standing waves of the concentrated NLSE in dimension two. Mathematics in Engineering, 2021, 3(2): 1-15. doi: 10.3934/mine.2021011 |
[5] | Dheeraj Varma, Manikandan Mathur, Thierry Dauxois . Instabilities in internal gravity waves. Mathematics in Engineering, 2023, 5(1): 1-34. doi: 10.3934/mine.2023016 |
[6] | Lars Eric Hientzsch . On the low Mach number limit for 2D Navier–Stokes–Korteweg systems. Mathematics in Engineering, 2023, 5(2): 1-26. doi: 10.3934/mine.2023023 |
[7] | Biagio Cassano, Lucrezia Cossetti, Luca Fanelli . Spectral enclosures for the damped elastic wave equation. Mathematics in Engineering, 2022, 4(6): 1-10. doi: 10.3934/mine.2022052 |
[8] | George Contopoulos . A Review of the “Third” integral. Mathematics in Engineering, 2020, 2(3): 472-511. doi: 10.3934/mine.2020022 |
[9] | Paola F. Antonietti, Ilario Mazzieri, Laura Melas, Roberto Paolucci, Alfio Quarteroni, Chiara Smerzini, Marco Stupazzini . Three-dimensional physics-based earthquake ground motion simulations for seismic risk assessment in densely populated urban areas. Mathematics in Engineering, 2021, 3(2): 1-31. doi: 10.3934/mine.2021012 |
[10] | Emilia Blåsten, Fedi Zouari, Moez Louati, Mohamed S. Ghidaoui . Blockage detection in networks: The area reconstruction method. Mathematics in Engineering, 2019, 1(4): 849-880. doi: 10.3934/mine.2019.4.849 |
Since the emergence of SARS-COV-2, many updates and assumptions are being discussed based on the emerging understanding of the pathophysiology and outcomes of the infection. The host immune response is the critical factor in disease severity and the unique immune response of each individual has resulted in a broad spectrum of disease severity and clinical presentations. In this article, combining the emerging knowledge on the immunopathogenesis of COVID-19 infection with insights into the underlying mechanisms of certain autoimmune and chronic Immune-mediated inflammatory diseases we propound our hypothesis that SARS-CoV-2 infection produces chronic viral inflammatory syndrome.
disabled homolog 1;
surfeit locus protein 1;
apoptosis-inducing factor mitochondrial;
T cell immunoglobulin and mucin domain 3;
cytotoxic T lymphocyte associated protein 4;
programmed cell death protein 1;
T cell immunoglobulin and ITIM domain receptor;
mitochondrial antiviral signaling proteins;
voltage dependent anion channel;
angiotensin converting enzyme II;
angiotensin I receptor;
nuclear NOD, LRR, pyrin domain containing protein 3;
interleukin;
granulocyte monocyte colony stimulating factor;
tumor necrosis factor;
platelet derived growth factor;
fibroblast growth factor;
Interferon gamma;
tumor necrosis factor alpha;
nuclear factor κB
Chaotic systems exhibit intricate nonlinear dynamics, characterized by features such as pseudo-random behavior and a heightened sensitivity to initial conditions. Lur'e systems (LSs), which encompass a wide range of chaotic systems such as Chua's circuits [1] neural networks [2], and n-scroll attractors [3], have attracted significant research attention in the past decades. Chaos synchronization of LSs has found applications in diverse areas including image encryption [4,5,6], cryptography [7,8] and confidential communication [9,10,11]. The existence of time delay and stochastic perturbations are often unavoidable in a real-world control system and can cause the system to be unstable. Correspondingly, substantial efforts have been devoted to chaos synchronization of stochastic time-delay LSs, and a few results have been reported [12,13,14,15].
When implementing chaos synchronization in a networked environment, network-induced phenomena, such as packet losses [16], link failures [17] and cyber attacks [18,19,20], can introduce inconsistencies between the system and the controller/filter modes [21]. Therefore, researchers have shown interest in studying chaos synchronization using asynchronous/mode-unmatched controllers. The hidden Markov model (HMM), proposed by Rabiner [22], serves as a suitable tool for describing the asynchronous phenomena. Building upon the HMM framework, Li et al. [23] investigated the synchronization control in Markov-switching neural networks, while Ma et al. [24] explored the drive-response synchronization in fuzzy complex dynamic networks. Despite these advancements, to our knowledge, there is a scarcity of research addressing chaos synchronization in stochastic time-delay LSs under asynchronous controllers.
Moreover, in networked control systems, the bandwidth of the communication network is usually limited, which can impact the control performance significantly. To eliminate unnecessary resource waste and achieve efficient resource allocation, recent studies on chaos synchronization of LSs have utilized event-triggered mechanism (ETM)-based control methods. For instance, Wu et al. [25] conducted research on exponential synchronization and joint performance issues of chaotic LSs by designing a switching ETM based on perturbation terms. He et al. [26] proposed a secure communication scheme through synchronized chaotic neural networks based on quantized output feedback ETM. Besides, several studies on memory-based ETM for chaos synchronization in LSs have been reported in [27,28,29]. Notably, the above literature employed fixed thresholds in the designed ETM, limiting their ability to conserve communication resources.
Motivated by the above discussion, we explore the master-slave chaos synchronization of stochastic time-delay LSs within an asynchronous and adaptive event-triggered (AAET) control framework. Unlike previous works [25,26,27,28,29], the thresholds of the ETM used can be adjusted adaptively with real-time system states. The objective is to determine the required AAET controller gains to ensure that the synchronization-error system (SES) has both stochastic stability (SS) and L2−L∞ disturbance-suppression performance (LDSP) [30]. The contributions of this paper are:
1) The AAET controller is first applied to tackle the chaos synchronization issue of stochastic time-delay LSs;
2) A criterion on the SS and LDSP is proposed using a Lyapunov-Krasovskii functional (LKF), a Wirtinger-type inequality, the Itô formula, as well as a convex combination inequality (CCI);
3) A method for determining the desired AAET controller is proposed by decoupling the nonlinearities that arise from the Lyapunov matrices and controller gains.
Throughout, we employ Rn1, Rn1×n2 and N to stand for the n1-dimensional Euclidean space, the set of all n1×n2 real matrices, and the set of natural numbers, respectively. The symbol ‖⋅‖ is the Euclidean vector norm, (⋅)T represents the matrix transposition, He(G) means the sum of matrix G and its transpose GT, ∗ indicates the symmetric term in a matrix and E{⋅} and Prob{⋅} indicate, respectively, the expectation and probability operator. Furthermore, we utilize col{⋅} to denote a column vector, diag{⋅} to stand for a block-diagonal matrix and sup{⋅} and inf{⋅} to indicate the supremum and infimum of a set of real numbers, respectively.
Consider the following master-slave stochastic time-delay LSs:
{dxm(t)=[Aα(t)xm(t)+Bα(t)xm(t−τ(t))+Wα(t)ψ(Fxm(t))]dt+Dα(t)xm(t)dϖ(t),ym(t)=Cα(t)xm(t),xm(t)=ξm0,t∈[−τ2,0], | (2.1) |
{dxs(t)=[Aα(t)xs(t)+Bα(t)xs(t−τ(t))+Wα(t)ψ(Fxs(t))+u(t)+Eα(t)v(t)]dt+Dα(t)xs(t)dϖ(t),ys(t)=Cα(t)xs(t),xs(t)=ξs0,t∈[−τ2,0] | (2.2) |
with xm(t)∈Rnx and xs(t)∈Rnx being the state vectors, ξm0 and ξs0 being the initial values, ym(t)∈Rny and ys(t)∈Rny being the output vectors, ψ(⋅)∈Rq being the nonlinear term with all components within [ˊgr,ˊgr] for r=1,2,⋯,q, u(t)∈Rq being the control signal to be designed, v(t) being the disturbance in L2[0,∞) [31], one-dimension Brownian motion ϖ(t) satisfying E{dϖ(t)}=0 and E{dϖ2(t)}=dt, and time-varying delay τ(t) satisfying 0<τ1⩽τ(t)⩽τ2 and μ1⩽˙τ(t)⩽μ2, where τ1, τ2, μ1, and μ2 are constants. {α(t),t⩾0} is the Markovian process and belongs to the state space N={1,2,⋯,N}. The transition rate (TR) matrix and transition probability is given by Π=[πij]N×N and
Prob{α(t+ς)=j|α(t)=i}={πijς+o(ς),i≠j.1+πiiς+o(ς),i=j, |
with ς>0, limς→0o(ς)/ς=0, πij⩾0, i≠j and πii=−∑Ni=1,i≠jπij [32,33,34]. Aα(t), Bα(t), Cα(t), Dα(t), Eα(t) and Wα(t), which can be abbreviated as Ai, Bi, Ci, Di, Ei, and Wi for α(t)=i∈N, are matrices with appropriate dimensions.
In order to minimize information transmission, the adaptive ETM is employed to determine whether the current sampled data should be transmitted to the controller, as illustrated in Figure 1. Let tkh denote the latest transmission time of the output signal, where h>0 is the sampling period. y(tkh) and y(t) denote the latest output signal and the current one, respectively. Defining e(t)=y(tkh)−y(t), the event-triggered condition is designed as follows:
t0h=0,tk+1h=tkh+infp∈N{ph|eT(t)Ψie(t)<ρ(t)yT(tkh)Ψiy(tkh)},t∈[tkh,tk+1h), | (2.3) |
where Ψi>0 is the trigger matrix and ρ(t) is a threshold parameter adjusted by an adaptive law as
ρ(t)=ρ1+(ρ2−ρ1)2πarccot(κ‖e(t)‖2), | (2.4) |
where ρ1 and ρ2 are predetermined parameters with 0<ρ1⩽ρ2<1, κ is a positive scalar used to adjust the sensitivity of the function ‖e(k)‖2.
Remark 1. The value of ρ(t) has a certain influence on the trigger condition (2.3). The trigger condition will be stricter with the value of ρ(t) being higher, resulting in less data being transmitted to the controller. Conversely, the trigger condition will be relaxed with the value of ρ(t) being lower, allowing more data to be transmitted. Furthermore, it is worth to mention that, when ρ(t) takes a constant on (0,1], the adaptive ETM will be transformed into the periodic ETM (PETM); when ρ(t) is set as 0, it will be transformed into the sampled-data mechanism (SDM).
Remark 2. The arccot function, incorporated in the adaptive law (2.4), enables the threshold parameter of ETM to be dynamically adjusted as the output error changes within the range of (ρ1,ρ2]. The presence of the arccot function results in an inverse relationship between the threshold parameter ρ(t) and the output error e(t). It can be observed that ρ(t) tends to ρ2 as ‖e(t)‖2 approaches 0, and ρ(t) tends to ρ1 as ‖e(t)‖2 approaches ∞.
Consider the following controller:
u(t)=Kβ(t)(ym(tkh)−ys(tkh)),t∈[tkh,tk+1h). | (2.5) |
Unlike [35,36,37], the controller is based on output feedback, which is known to be more easily implemented. In the controller, we introduce another stochastic variable with state space M={1,2,⋯,M} to describe this stochastic process {β(t),t⩾0}. The conditional transition probability (CTP) matrix is signed as Φ=[φiι]N×M with
φiι=Prob{β(t)=ι|α(t)=i} |
and ∑Mι=1φiι=1. Kβ(t), which will be abbreviated as Kι, is the controller gain to be designed. Note that {{α(t),t⩾0}{β(t),t⩾0}} constitutes a HMM [38,39].
Define x(t)=xm(t)−xs(t). Then, from (2.1), (2.2) and (2.5), one can establish the following SES:
dx(t)=F(t)dt+G(t)dϖ(t),t∈[tkh,tk+1h), | (2.6) |
where F(t)=(Ai−KιCi)x(t)+Bix(t−τ(t))+Wi˜ψ(Fx(t))−Kιe(t)−Eiv(t), G(t)=Dix(t), ˜ψ(Fx(t))=ψ(F(x(t)+xs(t)))−ψ(Fxs(t)) that satisfies
ˊgr⩽ψr(fTr(x+xs))−ψr(fTrxs)fTrx=˜ψr(fTrx)fTrx⩽ˊgr,∀x,xs,r=1,2,⋯,q, | (2.7) |
where fTr indicates the r-th row of F. From (2.7), one can get
[˜ψr(fTrx)−ˊgrfTrx][˜ψr(fTrx)−ˊgrfTrx]⩽0. | (2.8) |
Remark 3. The constants ˊgr and ˊgr can be taken as positive, negative, or zero. By allowing ˊgr and ˊgr to have a wide range of values, the sector bounded nonlinearity can flexibly adapt to the needs of different systems and provide a more flexible regulation and control mechanism.
To streamline the subsequent analysis, we define
ζ(t)=col{x(t),x(t−τ1),x(t−τ(t)),x(t−τ2),ϕ1,ϕ2,ϕ3},ϱd=[0n×(d−1)nIn×n0n×(9−d)n](d=1,2,⋯,9),ϕ1=1τ1∫tt−τ1x(s)ds,ϕ2=1τ(t)−τ1∫t−τ1t−τ(t)x(s)ds,ϕ3=1τ2−τ(t)∫t−τ(t)t−τ2x(s)ds,τ12=τ2−τ1, |
and provide two definitions and four lemmas.
Definition 1. The SES (2.6) is said to be with SS if there exists a scalar M(α0,ξ(⋅)) satisfying
E{∫∞0‖x(t)‖2dt|α0,x(t)=ξ0,t∈[−τ2,0]}<M(α0,ξ(⋅)) |
when v(t)≡0.
Definition 2. Under the zero initial condition, for a given scalar γ>0, the SES (2.6) is said to have a LDSP if
E{supt⩾0{‖y(t)‖2}}⩽γ2E{∫t0‖v(s)‖2ds} |
holds for v(t)≠0.
Lemma 1. Given stochastic differential equation
dx(t)=F(t)dt+G(t)dϖ(t), | (2.9) |
where ϖ(t) is one-dimension Brownian motion, for scalars a, b (b>a), and a matrix R, one has
∫baFT(s)RF(s)ds⩾1b−aΩT(a,b)˜RΩ(a,b)+2b−aΩT(a,b)˜Rμ(a,b), |
where ˜R=diag{R,3R} and
Ω(a,b)=[x(b)−x(a)x(b)+x(a)−2b−a∫bax(s)ds],μ(a,b)=[−∫baG(s)dϖ(s)1b−a∫ba(b+a−2s)G(s)dϖ(s)]. |
Remark 4. Following the approaches used in [40,41], the Wirtinger-type inequality of Lemma 1 can be readily established. It should be noted that the integral term in μ(a,b) should be 1b−a∫ba(b+a−2s)G(s)dϖ(s) instead of 1b−a∫ba(b−a+2s)G(s)dϖ(s).
Lemma 2. [40] Consider the stochastic differential equation (2.9). For n×n real matrix R>0 and the piecewise function τ(t) satisfying 0<τ1⩽τ(t)⩽τ2, where τ1 and τ2 are two constants, and for S∈R2n×2n satisfying [˜RST∗˜R]⩾0 with ˜R=diag{R,3R}, the following CCI holds:
−τ12∫t−τ1t−τ2FT(s)RF(s)ds⩽−2℧T2S℧1−℧T1˜R℧1−℧T2˜R℧2−2℘(dϖ(t)), |
where
℧1=Ω(t−τ(t),t−τ1),℧2=Ω(t−τ2,t−τ(t)),℘(dϖ(t))=τ12τ(t)−τ1℧T1˜Rμ(t−τ(t),t−τ1)+τ12τ2−τ(t)℧T2˜Rμ(t−τ2,t−τ(t)). |
Lemma 3. [42] For any two matrices G and R>0 with appropriate dimensions,
−GTR−1G⩽R−GT−G |
holds true.
Lemma 4. [43] For a given scalar ε>0, suppose there are matrices Λ, U, V and W ensuring
[ΛU+εV∗−εX−εXT]<0. |
Then, one gets
Λ+He(UX−1VT)<0. |
In contrast to the common H∞ performance, LDSP imposes a limitation on the energy-to-peak gain from disturbance to the output signal, ensuring it does not exceed a specified disturbance-suppression index [44]. In this paper, we intend to develop an asynchronous controller in (2.5) with the adaptive ETM in (2.3) to guarantee the SS and LDSP of SES (2.6). First, we give a condition to ensure the SS and LDSP of SES (2.6).
Theorem 1. Given scalars γ>0 and ρ2, suppose that there exist matrices Pi>0, Q1>0, Q2>0, Q3>0, R1>0, R2>0, Ψi>0, diagonal matrix L>0, and matrices S, Kι, for any i∈N, ι∈M satisfying
[˜R2ST∗˜R2]⩾0, | (3.1) |
CTiCi−Pi<0, | (3.2) |
Λi=M∑c=1φiι([Λ1,1iιΛ1,2i∗−γ2I]+[˜ATiι−ETi](τ21R1+τ212R2)[˜ATiι−ETi]T)<0. | (3.3) |
Then the SES (2.6) has the SS and LDSP, where
Λ1,1iι=[Υ1,1iιΥ1,2iΥ1,3iι∗−He(L)0∗∗(ρ2−1)Ψi],Λ1,2i=[−ϱT1PiEi00],Υ1,1iι=He(ϱT1PiAiι−ϱT1FTˊGTLˊGFϱ1)+ϱT1(DTiPiDi+˜Pi)ϱ1+˜Q−2GT2SG1−GT0˜R1G0−GT1˜R2G1−GT2˜R2G2+ϱT1ρ2CTiΨiCiϱ1,Υ1,2i=ϱT1PiWi+ϱT1FT(ˊGT+FT)L,Υ1,3iι=ϱT1ρ2CTiΨi−ϱT1PiKι,˜Rd=diag{Rd,3Rd}(d=1,2),˜Aiι=[AiιWi−Kι],˜Q=diag{Q1,−Q1+Q2,(1−μ1)Q3−(1−μ2)Q2,−Q3,03n×3n},Aiι=[Ai−KιCi0Bi0000],˜Pi=N∑i=1πijPj,G0=[ϱ1−ϱ2ϱ1+ϱ2−2ϱ5],G1=[ϱ2−ϱ3ϱ2+ϱ3−2ϱ6],G2=[ϱ3−ϱ4ϱ3+ϱ4−2ϱ7]. |
Proof. Select a LKF candidate as:
V(t,x(t),α(t),β(t))=4∑k=1Vk(t,x(t),α(t),β(t)), | (3.4) |
where
V1(t,x(t),α(t),β(t))=xT(t)Pα(t)x(t),V2(t,x(t),α(t),β(t))=∫tt−τ1xT(s)Q1x(s)ds+∫t−τ1t−τ(t)xT(s)Q2x(s)ds+∫t−τ(t)t−τ2xT(s)Q3x(s)ds,V3(t,x(t),α(t),β(t))=τ1∫tt−τ1∫tvFT(s)R1F(s)dsdv+τ12∫t−τ1t−τ2∫tvFT(s)R2F(s)dsdv. |
Assume that α(t)=i, α(t+ς)=j, β(t)=ι and define L as the weak infinitesimal operator of the stochastic process {x(t),α(t)}. Then, along SES (2.6), we get
LV1(t,x(t),i,ι)=2xT(t)PiF(t)+GT(t)PiG(t)+xT(t)N∑i=1πijPjx(t)=ζT(t)[He(ϱT1PiAiι)+ϱT1(DTiPiDi+˜Pi)ϱ1]ζ(t)+2ζT(t)ϱT1PiWi˜ψ(Fx(t))−2ζT(t)ϱT1PiKιe(t)−2ζT(t)ϱT1PiEiv(t), | (3.5) |
LV2(t,x(t),i,ι)=xT(t)Q1x(t)+xT(t−τ1)(−Q1+Q2)x(t−τ1)+(1−˙τ(t))xT(t−τ(t))(−Q2+Q3)x(t−τ(t))−xT(t−τ2)Q3x(t−τ2)⩽ζT(t)˜Qζ(t), | (3.6) |
LV3(t,x(t),i,ι)=FT(t)(τ21R1+τ212R2)F(t)−τ1∫tt−τ1FT(s)R1F(s)ds−τ12∫t−τ1t−τ2FT(s)R2F(s)ds. | (3.7) |
Define an augmented vector as ˜ζ(t)=col{ζ(t),˜ψ(Fx(t)),e(t)}. We can derive that
FT(t)(τ21R1+τ212R2)F(t)=[˜ζ(t)v(t)]T[˜ATiι−ETi](τ21R1+τ212R2)[˜ATiι−ETi]T[˜ζ(t)v(t)]. | (3.8) |
Based on (3.1), applying Lemmas 1 and 2 to the integral terms in (3.7) yields
−τ1∫tt−τ1FT(s)R1F(s)ds⩽−ζT(t)GT0˜R1G0ζ(t)−2ζT(t)GT0˜R1μ(t−τ1,t), | (3.9) |
−τ12∫t−τ1t−τ2FT(s)R2F(s)ds⩽ζT(t)[−2GT2SG1−GT1˜R2G1−GT2˜R2G2]ζ(t)−2℘(dϖ(t)), | (3.10) |
where ℘(dϖ(t))=τ12τ(t)−τ1ζT(t)GT1˜R2μ(t−τ(t),t−τ1)+τ12τ2−τ(t)ζT(t)GT2˜R2μ(t−τ2,t−τ(t)). Recalling (3.7)–(3.10), we have
LV3(t,x(t),i,ι)⩽[˜ζ(t)v(t)]T[˜ATiι−ETi](τ21R1+τ212R2)[˜ATiι−ETi]T[˜ζ(t)v(t)]+˜℘(dϖ(t))+ζT(t)[−GT0˜R1G0−2GT2SG1−GT1˜R2G1−GT2˜R2G2]ζ(t), | (3.11) |
where ˜℘(dϖ(t))=−2ζT(t)GT0˜R1μ(t−τ1,t)−2℘(dϖ(t)). It follows from (2.8) that
−2(˜ψ(Fx(t))−ˊGFx(t))TL(˜ψ(Fx(t))−ˊGFx(t))⩾0, |
which means
0⩽−2(˜ψ(Fx(t))−ˊGFϱ1ζ(t))TL(˜ψ(Fx(t))−ˊGFϱ1ζ(t))=−˜ψT(Fx(t))He(L)˜ψ(Fx(t))+2ζT(t)ϱT1FT(ˊGT+ˊGT)L˜ψ(Fx(t))−ζT(t)He(ϱT1FTˊGTLˊGFϱ1)ζ(t). | (3.12) |
In addition, recalling the adaptive ETM (2.3), we obtain
0⩽ρ(t)yT(tkh)Ψiy(tkh)−eT(t)Ψie(t)⩽ρ2[y(t)+e(t)]TΨi[y(t)+e(t)]−eT(t)Ψie(t)=ρ2[xT(t)CTiΨiCix(t)+2xT(t)CTiΨie(t)+eTΨie(t)]−eT(t)Ψie(t)=ζT(t)ϱT1ρ2CTiΨiCiϱ1ζ(t)+2ζT(t)ϱT1ρ2CTiΨie(t)+eT(t)(ρ2−1)Ψie(t). | (3.13) |
Combining (3.5), (3.6), (3.11), (3.12) and (3.13), we find that
LV(t,x(t),i,ι)⩽ζT(t)Υ1,1iιζ(t)+2ζT(t)Υ1,2i˜ψ(Fx(t))+2ζT(t)Υ1,3iιe(t)−2ζT(t)ϱT1PiEiv(t)+eT(t)(ρ2−1)Ψie(t)−˜ψT(Fx(t))He(L)˜ψ(Fx(t))+˜℘(dϖ(t)+[˜ζ(t)v(t)]T[˜ATiι−ETi](τ21R1+τ212R2)[˜ATiι−ETi]T[˜ζ(t)v(t)]. | (3.14) |
Noting E{˜℘(dϖ(t))}=0, we can calculate E{LV(t,x(t),i,ι)} by (3.14) that
E{LV(t,x(t),i,ι)}⩽[˜ζ(t)v(t)]TD∑c=1φiι([Λ1,1iιΛ2,2i∗0]+[˜ATiι−ETi](τ21R1+τ212R2)[˜ATiι−ETi]T)[˜ζ(t)v(t)]T. | (3.15) |
Next, we discuss the SS of (2.6) under the condition of v(t)≡0 and the LDSP of (2.6) under the condition of v(t)≠0, respectively.
i) v(t)≡0, we can get the following inequality from (3.15):
E{LV(t,x(t),i,ι)}⩽˜ζT(t)Λ0i˜ζ(t), |
where Λ0i=∑Mc=1φiι(Λ1,1iι+˜ATiι(τ21R1+τ212R2)˜Aiι). From (3.3), we can find that there exists a>0 such that for any
E{LV(t,x(t),i,ι)}⩽−a‖x(t)‖2,i∈N. |
Utilizing the Itô formula, we obtain
E{V(t,x(t),α(t))}−E{V(0,x0,α0)}=E{∫t0V(s,x(s),α(s))ds}⩽−aE{∫t0‖x(s)‖2ds}, |
which means
E{∫t0‖x(s)‖2ds}⩽1aV(0,x0,α0). |
Thus, the SS of (2.6) is proved.
ii) v(t)≠0, under the zero initial condition, defining J(t)=yT(t)y(t)−γ2∫t0vT(s)v(s)ds leads to
J(t)=yT(t)y(t)−γ2∫t0vT(s)v(s)ds+E{∫t0LV(s,x(s),i,ι)ds}−(V(t,x(t),i,ι)−V(0,x0,α0,β0))⩽xT(t)(CTiCi−Pi)x(t)+∫t0[˜ζ(s)v(s)]TΛi[˜ζ(s)v(s)]ds. |
From conditions (3.2) and (3.3), we know that J(t)⩽0. According to Definition 2, the SES (2.6) has a LDSP γ.
On the basis of Theorem 1, a design method of the AAET controller can be proposed.
Theorem 2. Given scalars ε, ρ2 and γ>0, suppose that there exist matrices Pi>0, Q1>0, Q2>0, Q3>0, R1>0, R2>0, Ψi>0, diagonal matrix L>0, matrices S, Xι, Yι, and Tiι for any i∈N, ι∈M satisfying (3.1), (3.2), and
[−He(Tiι+Yι)Pi−Xι−εYTι∗−εXι−εXTι]<0, | (3.16) |
Θi=M∑c=1φiι[Θ1,1iιΛ1,2iΘ1,3iΘ1,4i∗−γ2IΘ2,3iΘ2,4i∗∗Θ3,3i0∗∗∗Θ4,4i]<0, | (3.17) |
where
Θ1,1iι=[˜Υ1,1iιΥ1,2i˜Υ1,3iι∗−He(L)0∗∗(ρ2−1)Ψi],Λ1,2i=[−ϱT1PiEi00],Θ1,3i=[τ1√φi1˜ℵTi1⋯τ1√φiM˜ℵTiM],Θ1,4i=[τ12√φi1˜ℵTi1⋯τ12˜ℵTiM],Θ2,3i=[−τ1√φi1ETiPi⋯−τ1√φiMETiPi],Θ2,4i=[−τ12√φi1ETiPi⋯−τ12√φiMETiPi],Θ3,3i=diag{R1−2Pi,⋯,R1−2Pi},Θ4,4i=diag{R2−2Pi,⋯,R2−2Pi},˜Υ1,1iι=He(ϱT1ℵiι−ϱT1FTˊGTLˊGFϱ1)+ϱT1(DTiPiDi+˜Pi)ϱ1+˜Q−2GT2SG1−GT0˜R1G0−GT1˜R2G1−GT2˜R2G2+ϱT1ρ2CTiΨiCiϱ1,Υ1,2i=ϱT1PiWi+ϱT1FT(ˊGT+ˊGT)L,˜Υ1,3iι=ϱT1ρ2CTiΨi+ϱT1Tiι,˜ℵiι=[ℵiιPiWiTiι],ℵiι=[PiAi+TiιCi0PiBi0000],˜Pi=N∑i=1πijPj,˜Rd=diag{Rd,3Rd}(d=1,2),˜Q=diag{Q1,−Q1+Q2,(1−μ1)Q3−(1−μ2)Q2,−Q3,03n×3n},G0=[ϱ1−ϱ2ϱ1+ϱ2−2ϱ5],G1=[ϱ2−ϱ3ϱ2+ϱ3−2ϱ6],G2=[ϱ3−ϱ4ϱ3+ϱ4−2ϱ7]. |
Then, AAET controller (2.5) with gains
Kι=X−1ιYι,ι∈M | (3.18) |
enables the SES (2.6) to have both SS and LDSP.
Proof. According to (3.18), we have −PiKι<Tiι by applying Lemma 4 to (3.16). Then, we can conclude that PiAiι<ℵiι and Pi˜Aiι<˜ℵiι lead to
Λ1,1iι⩽Θ1,1iι, | (3.19) |
Λ1,3i⩽Θ1,3i, | (3.20) |
Λ1,4i⩽Θ1,4i, | (3.21) |
where
Λ1,3i=[τ1√φi1˜ATi1Pi⋯τ1√φiD˜ATiDPi],Λ1,4i=[τ12√φi1˜ATi1Pi⋯τ12√φiD˜ATiDPi]. |
Based on Lemma 3, we can get that −PiR−11Pi⩽R1−2Pi and −PiR−12Pi⩽R2−2Pi, which means
Λ3,3i⩽Θ3,3i, | (3.22) |
Λ4,4i⩽Θ4,4i, | (3.23) |
where Λ3,3i=diag{−PiR−11Pi,⋯,−PiR−11Pi}, Λ4,4i=diag{−PiR−12Pi,⋯,−PiR−12Pi}. Due to φiι>0, combining (3.19)–(3.23) yields
Λ0i⩽Θi<0, | (3.24) |
where
Λ0i=D∑c=1φiι[Λ1,1iιΛ1,2iΛ1,3iΛ1,4i∗−γ2IΘ2,3iΘ2,4i∗∗Λ3,3i0∗∗∗Λ4,4i]. |
By applying Schur's complement to (3.24), we find that (3.3) can be guaranteed by (3.17). The proof is completed.
Remark 5. The coupling between parameter Pi and the controller gain Kι in Theorem 1 is addressed by introducing a slack matrix Tiι. It is worth mentioning that directly setting the coupling term KιP−1i equal to the matrix Tiι (i.e. Kι=TiιPi) would result in non-uniqueness of controller gains Kι. In this paper, we introduce Tiι such that −PiKι<Tiι. By designing the controller gains, as given in equation (3.18), and combining it with Lemma 4, the aforementioned issue is avoided.
Remark 6. Theorem 1 provides a analysis result of the SS and LDSP for SES (2.6) based on HMM, while Theorem 2 presents a design scheme for the needed AAET controller. The proofs of these theorems involve the use of the LKF in (3.4), Itô formula, as well as the inequalities in Lemmas 1-4. To further reduce the conservatism of the obtained results, one may refer to the augmented LKFs in [45,46], the free-matrix-based approaches in [47,48,49], the refined CCIs in [50,51] and the decoupling methods in [52].
Example 1. In this example, we consider a three-mode Chua's circuit given by
{dx1(t)=[ai(x2(t)−m1x1(t)+(m1−m0)ψ1(x1(t)))−cix1(t−τ(t))]dt+di(x2(t)−m1x1(t))dϖ(t),dx2(t)=[x1(t)−x2(t)+x3(t)−cix1(t−τ(t))]dt+0.1(x1(t)−x2(t)+x3(t))dϖ(t),dx3(t)=[−bix2(t)+ci(2x1(t−τ(t))−x3(t−τ(t)))]dt−m3x2(t)dϖ(t), |
where parameters m0=−17, m1=27, m3=0.1, and ai, bi, ci, di (i=1,2,3) are listed in Table 1. The nonlinear characteristics ψ1(x1(t))=12(|x1(t)+1|−|x1(t)−1|) belonging to sector [0,1], and ψ2(x2(t))=ψ3(x3(t))=0. The circuit model can be re-expressed as LS (2.1) with
Ai=[−aim1ai01−110−bi0],Bi=[−ci00−ci002ci0−ci],Di=[−dim1di00.1−0.10.10−m30],Ci=[−1000−1000−1],Wi=[ai(m1−m0)00000000],Ei=[0.100]T. |
i | ai | bi | ci | di |
1 | 9 | 14.28 | 0.1 | 0.01 |
2 | 8 | 10 | 0.05 | 0.01 |
3 | 9 | 14 | 0.15 | 0.01 |
The delay parameters are specified as τ1=0.1, τ2=0.18, μ1=0.1 and μ2=0.26, the parameters related to the adaptive law are given by ρ1=0.1, ρ2=0.9, κ=0.5 and the TR and CTP matrices are chosen as
Π=[−5233−6341−5],Φ=[0.40.30.30.20.30.50.40.50.1]. |
By solving the LMIs in Theorem 2, the optimal LDSP is found to be γ∗=0.0553, and the controller gains and adaptive ETM weight matrices are calculated as
K1=[−2.1803−3.4217−0.2840−0.3775−0.17680.07480.2038−1.8311−2.1877],K2=[−2.1223−3.3641−0.3704−0.4417−0.4562−0.00720.2660−0.9016−2.0248],K3=[−2.1969−2.9252−0.3438−0.4544−0.06310.04530.2441−1.2244−2.1906],Ψ1=[12.35816.0393−0.00596.039324.55615.5930−0.00595.593012.6577],Ψ2=[12.31879.03771.02799.037722.23124.17521.02794.175212.0248],Ψ3=[12.00079.91280.66699.912824.47704.44050.66694.440512.1092]. |
We set the initial states as xm(t)=[−0.2−0.30.2]T, xs(t)=[0.250.350.35]T (t∈[−τ2,0]) and the disturbance as v(t)=0.1sint(t). The sampling period is chosen to be h=0.05s. A possible mode evolution of system and AAET controller is drawn in Figure 2. When there is no controller applied, we can find from Figure 3 that the system is unstable. By utilizing the devised AAET controller shown in Figure 4, the state response curves of the SES (2.6) are exhibited in Figure 5. It can be seen that the synchronization error between the master and slave LSs approaches zero over time, indicating that the master and slave LSs can successfully achieve synchronization under the presented AAET controller. The trajectory of the adaptive law and release time intervals between two trigger moments are depicted in Figures 6 and 7, respectively. Based on the simulation results, it can be observed that as the SES (2.6) stabilizes, the threshold function gradually converges to a fixed value. Define the function γ(t)=√E{supt⩾0{‖y(t)‖2}}/E{∫t0‖v(s)‖2ds} for LDSP. Then the trajectory of γ(t) under zero initial condition is depicted in Figure 8. It is evident from Figure 8 that the maximum value of γ(t) is 0.0047, which is lower than γ∗=0.0553.
Table 2 presents the data transmission rates under different triggering mechanisms in the same conditions. The comparison demonstrates that the adaptive ETM employed in this study can effectively reduce data transmission to achieve the goal of conserving channel resources.
SDM in [14] | PETM in [53] | Adaptive ETM in this paper | |
Number of transmitted data | 500 | 236 | 194 |
Data transmission rates | 100% | 47.20% | 38.80% |
The master-slave chaos synchronization of stochastic time-delay LSs (2.1) and (2.2) within a networked environment has been considered. To tackle the challenges posed by potential mode-mismatch behavior and limited networked channel resources, the AAET controller in (2.5) has been employed. A criterion on the SS and LDSP of the SES (2.6) has been proposed in Theorem 1 using a LKF, a Wirtinger-type inequality, the Itô formula, as well as a CCI. Then, a method for determining the desired AAET controller gains has been proposed in Theorem 2 by decoupling the nonlinearities that arise from the Lyapunov matrices and controller gains. Finally, simulation results have confirmed that the designed controller can achieve chaos synchronization between the master LS (2.1) and slave LS (2.2), while significantly reducing data transmission.
The authors declare they have not used Artificial Intelligence (AI) tools in the creation of this article.
This work was supported by the Key Research and Development Project of Anhui Province (Grant No. 202004a07020028).
All authors declare no conflicts of interest in this paper.
[1] |
Ong KC, Ng AWK, Lee LSU, et al. (2004) Pulmonary function and exercise capacity in survivors of severe acute respiratory syndrome. Eur Respir J 24: 436-442. doi: 10.1183/09031936.04.00007104
![]() |
[2] |
Gombar S, Chang M, Hogan CA, et al. (2020) Persistent detection of SARS-CoV-2 RNA in patients and healthcare workers with COVID-19. J Clin Virol 129: 104477. doi: 10.1016/j.jcv.2020.104477
![]() |
[3] |
Li N, Wang X, Lv T (2020) Prolonged SARS-CoV-2 RNA shedding: Not a rare phenomenon. J Med Virol 92: 2286-2287. doi: 10.1002/jmv.25952
![]() |
[4] |
Simmonds P, Tuplin A, Evans DJ (2004) Detection of genome-scale ordered RNA structure (GORS) in genomes of positive-stranded RNA viruses: implications for virus evolution and host persistence. RNA 10: 1337-1351. doi: 10.1261/rna.7640104
![]() |
[5] |
Lucchese G, Flöel A (2020) Molecular mimicry between SARS-CoV-2 and respiratory pacemaker neurons. Autoimmun Rev 19: 102556. doi: 10.1016/j.autrev.2020.102556
![]() |
[6] |
Angileri F, Legare S, Gammazza AM, et al. (2020) Molecular mimicry may explain multi-organ damage in COVID-19. Autoimmun Rev 19: 102591. doi: 10.1016/j.autrev.2020.102591
![]() |
[7] |
Gheblawi M, Wang K, Viveiros A, et al. (2020) Angiotensin-converting enzyme 2: SARS-CoV-2 receptor and regulator of the renin-angiotensin system: celebrating the 20th anniversary of the discovery of ACE2. Circ Res 126: 1456-1474. doi: 10.1161/CIRCRESAHA.120.317015
![]() |
[8] |
Kamo T, Akazawa H, Komuro I (2015) Pleiotropic effects of angiotensin II receptor signaling in cardiovascular homeostasis and aging. Int Heart J 56: 249-254. doi: 10.1536/ihj.14-429
![]() |
[9] |
Verdecchia P, Cavallini C, Spanevello A, et al. (2020) The pivotal link between ACE2 deficiency and SARS-CoV-2 infection. Eur J Intern Med 76: 14-20. doi: 10.1016/j.ejim.2020.04.037
![]() |
[10] |
Tseng YH, Yang RC, Lu TS (2020) Two hits to the renin-angiotensin system may play a key role in severe COVID-19. Kaohsiung J Med Sci 36: 389-392. doi: 10.1002/kjm2.12237
![]() |
[11] |
Nieto-Torres JL, Verdiá-Báguena C, Jimenez-Guardeño JM, et al. (2015) Severe acute respiratory syndrome coronavirus E protein transports calcium ions and activates the NLRP3 inflammasome. Virology 485: 330-339. doi: 10.1016/j.virol.2015.08.010
![]() |
[12] |
Hoffman HM, Wanderer AA, Broide DH (2001) Familial cold autoinflammatory syndrome: phenotype and genotype of an autosomal dominant periodic fever. J Allergy Clin Immun 108: 615-620. doi: 10.1067/mai.2001.118790
![]() |
[13] | Muckle TJ, Wells M (1962) Urticaria, deafness, and amyloidosis: a new heredo-familial syndrome. QJM-Int J Med 31: 235-248. |
[14] |
Prieur AM, Griscelli C, Lampert F, et al. (1987) A chronic, infantile, neurological, cutaneous and articular (CINCA) syndrome. A specific entity analysed in 30 patients. Scand J Rheumatol 16: 57-68. doi: 10.3109/03009748709102523
![]() |
[15] |
Wang C, Xie J, Zhao L, et al. (2020) Alveolar macrophage dysfunction and cytokine storm in the pathogenesis of two severe COVID-19 patients. EBioMedicine 57: 102833. doi: 10.1016/j.ebiom.2020.102833
![]() |
[16] |
Liao M, Liu Y, Yuan J, et al. (2020) Single-cell landscape of bronchoalveolar immune cells in patients with COVID-19. Nat Med 26: 842-844. doi: 10.1038/s41591-020-0901-9
![]() |
[17] |
Hou J, Shi J, Chen L, et al. (2018) M2 macrophages promote myofibroblast differentiation of LR-MSCs and are associated with pulmonary fibrogenesis. Cell Commun Signaling 16: 89. doi: 10.1186/s12964-018-0300-8
![]() |
[18] | Zuo Y, Yalavarthi S, Shi H, et al. (2020) Neutrophil extracellular traps (NETs) as markers of disease severity in COVID-19. JCI Insight 5: e138999. |
[19] |
Gupta S, Kaplan MJ (2016) The role of neutrophils and NETosis in autoimmune and renal diseases. Nat Rev Nephrol 12: 402-413. doi: 10.1038/nrneph.2016.71
![]() |
[20] |
Diao B, Wang C, Tan Y, et al. (2020) Reduction and functional exhaustion of T cells in patients with coronavirus disease 2019 (COVID-19). Front Immunol 11: 827. doi: 10.3389/fimmu.2020.00827
![]() |
[21] |
Lopes-Paciencia S, Saint-Germain E, Rowell MC, et al. (2019) The senescence-associated secretory phenotype and its regulation. Cytokine 117: 15-22. doi: 10.1016/j.cyto.2019.01.013
![]() |
[22] |
Weyand CM, Yang Z, Goronzy JJ (2014) T cell aging in rheumatoid arthritis. Curr Opin Rheumatol 26: 93-100. doi: 10.1097/BOR.0000000000000011
![]() |
[23] |
Ichinohe T, Yamazaki T, Koshiba T, et al. (2013) Mitochondrial protein mitofusin 2 is required for NLRP3 inflammasome activation after RNA virus infection. P Natl Acad Sci USA 110: 17963-17968. doi: 10.1073/pnas.1312571110
![]() |
[24] |
Park S, Juliana C, Hong S, et al. (2013) The mitochondrial antiviral protein MAVS associates with NLRP3 and regulates its inflammasome activity. J Immunol 191: 4358-4366. doi: 10.4049/jimmunol.1301170
![]() |
[25] |
Thompson EA, Cascino K, Ordonez AA, et al. (2021) Metabolic programs define dysfunctional immune responses in severe COVID-19 patients. Cell Rep 34: 108863. doi: 10.1016/j.celrep.2021.108863
![]() |
[26] |
Kim J, Gupta R, Blanco LP, et al. (2019) VDAC oligomers form mitochondrial pores to release mtDNA fragments and promote lupus-like disease. Science 366: 1531-1536. doi: 10.1126/science.aav4011
![]() |
[27] |
Camara AKS, Zhou Y, Wen PC, et al. (2017) Mitochondrial VDAC1: a key gatekeeper as potential therapeutic target. Front Physiol 8: 460. doi: 10.3389/fphys.2017.00460
![]() |
[28] |
Lood C, Blanco LP, Purmalek MM, et al. (2016) Neutrophil extracellular traps enriched in oxidized mitochondrial DNA are interferogenic and contribute to lupus-like disease. Nat Med 22: 146. doi: 10.1038/nm.4027
![]() |
[29] |
Vernochet C, Kahn CR (2012) Mitochondria, obesity and aging. Aging (Albany NY) 4: 859. doi: 10.18632/aging.100518
![]() |
[30] |
Hamming I, Timens W, Bulthuis MLC, et al. (2004) Tissue distribution of ACE2 protein, the functional receptor for SARS coronavirus. A first step in understanding SARS pathogenesis. J Pathol 203: 631-637. doi: 10.1002/path.1570
![]() |
[31] |
Combet M, Pavot A, Savale L, et al. (2020) Rapid onset honeycombing fibrosis in spontaneously breathing patient with Covid-19. Eur Respir J 56: 2001808. doi: 10.1183/13993003.01808-2020
![]() |
[32] |
Verdoni L, Mazza A, Gervasoni A, et al. (2020) An outbreak of severe Kawasaki-like disease at the Italian epicentre of the SARS-CoV-2 epidemic: an observational cohort study. Lancet 395: 1771-1778. doi: 10.1016/S0140-6736(20)31103-X
![]() |
[33] | Rajpal S, Tong MS, Borchers J, et al. (2021) Cardiovascular magnetic resonance findings in competitive athletes recovering from COVID-19 infection. JAMA Cardiol 6: 116-118. |
1. | Dandan Zuo, Wansheng Wang, Lulu Zhang, Jing Han, Ling Chen, Non-fragile sampled-data control for synchronizing Markov jump Lur'e systems with time-variant delay, 2024, 32, 2688-1594, 4632, 10.3934/era.2024211 |
i | ai | bi | ci | di |
1 | 9 | 14.28 | 0.1 | 0.01 |
2 | 8 | 10 | 0.05 | 0.01 |
3 | 9 | 14 | 0.15 | 0.01 |