
Citation: Vera Reitsema, Hjalmar Bouma, Jan Willem Kok. Sphingosine-1-phosphate transport and its role in immunology[J]. AIMS Molecular Science, 2014, 1(4): 183-201. doi: 10.3934/molsci.2014.4.183
[1] | Tian Xu, Jin-E Zhang . Intermittent control for stabilization of uncertain nonlinear systems via event-triggered mechanism. AIMS Mathematics, 2024, 9(10): 28487-28507. doi: 10.3934/math.20241382 |
[2] | Tao Xie, Xing Xiong . Finite-time synchronization of fractional-order heterogeneous dynamical networks with impulsive interference via aperiodical intermittent control. AIMS Mathematics, 2025, 10(3): 6291-6317. doi: 10.3934/math.2025287 |
[3] | Siyue Yao, Jin-E Zhang . Exponential input-to-state stability of nonlinear systems under impulsive disturbance via aperiodic intermittent control. AIMS Mathematics, 2025, 10(5): 10787-10805. doi: 10.3934/math.2025490 |
[4] | Huiling Li, Jin-E Zhang, Ailong Wu . Finite-time stabilization of nonlinear systems with partially known states via aperiodic intermittent control and event-triggered impulsive control. AIMS Mathematics, 2025, 10(2): 3269-3290. doi: 10.3934/math.2025152 |
[5] | Linni Li, Jin-E Zhang . Input-to-state stability of nonlinear systems with delayed impulse based on event-triggered impulse control. AIMS Mathematics, 2024, 9(10): 26446-26461. doi: 10.3934/math.20241287 |
[6] | Zhaohui Chen, Jie Tan, Yong He, Zhong Cao . Decentralized observer-based event-triggered control for an interconnected fractional-order system with stochastic Cyber-attacks. AIMS Mathematics, 2024, 9(1): 1861-1876. doi: 10.3934/math.2024091 |
[7] | Yidan Wang, Li Xiao, Yanfeng Guo . Finite-time stability of singular switched systems with a time-varying delay based on an event-triggered mechanism. AIMS Mathematics, 2023, 8(1): 1901-1924. doi: 10.3934/math.2023098 |
[8] | Jiaqi Liang, Zhanheng Chen, Zhiyong Yu, Haijun Jiang . Fixed-time consensus of second-order multi-agent systems based on event-triggered mechanism under DoS attacks. AIMS Mathematics, 2025, 10(1): 1501-1528. doi: 10.3934/math.2025070 |
[9] | Zuo Wang, Hong Xue, Yingnan Pan, Hongjing Liang . Adaptive neural networks event-triggered fault-tolerant consensus control for a class of nonlinear multi-agent systems. AIMS Mathematics, 2020, 5(3): 2780-2800. doi: 10.3934/math.2020179 |
[10] | Biwen Li, Yujie Liu . Quasi-synchronization of nonlinear systems with parameter mismatch and time-varying delays via event-triggered impulsive control. AIMS Mathematics, 2025, 10(2): 3759-3778. doi: 10.3934/math.2025174 |
Due to human interference and environmental noise, stochastic disturbances increase the complexity and unpredictability of system dynamics[1]. Since the stochastic effects of the system are taken into account, the dynamics of industrial processes can be characterized more precisely. In recognition of this, stochastic nonlinear systems have drawn more attention and been thoroughly examined by numerous academics from a variety of disciplines, including mechanical systems, economics, and bioengineering[2,3,4,5,6].
The majority of stability-related issues are managed by state feedback, which necessitates constant decision-making and state observation on the part of the controller. This operation has limits and is costly for real-world applications. In order to conserve resources, time-triggered control in conjunction with event-triggered control (ETC) is suggested as a transmission or communication technique. Time-triggered control, as a traditional control scheme, has a preset control transmission and control time, but it often leads to an inefficient use of communication width and computational resources, so an effective alternative, ETC, is proposed on this basis[7,8,9]. Because ETC maintains the necessary closed-loop performance while updating control only when the state of the system at a given moment is above the threshold of the predetermined triggering mechanism, it further improves communication efficiency. A key concern in ETC design is ensuring a positive lower bound, which is the minimum time interval between consecutive events. Without this constraint, an infinite number of triggers could occur in a finite time, leading to undesirable Zeno behavior. In recent years, there has been a continuous increase in research related to ETC. For instance, [10] investigated the exponential stability of stochastic nonlinear systems using double-event-triggering mechanisms. In[11], the design of event-triggered control schemes for nonlinear systems subject to external disturbances and dynamic uncertainties was investigated. Despite these advancements, the ETC still has limitations, and further resource optimization remains an important research direction.
Intermittent control (IC) was first proposed as a discontinuous control method and has attracted increasing attention[12,13,14,15,16,17]. For example, [14] investigated the input-to-state stability of stochastic nonlinear systems under different event-triggering mechanisms—continuous, dynamic, and periodic—in combination with IC, providing valuable insights for further research. Unlike continuous control, fully controlling these systems in real-world applications is impractical, as it would impose a heavy communication burden on the controller and waste resources; therefore, the emergence of IC is of great significance. IC divides each control interval into 'working time' with operational control and 'rest time' without operational control. Additionally, IC limits the amount of transmitted information and extends the lifespan of the control equipment by allowing control signals to be applied only at predetermined time intervals. Periodically intermittent control (PIC) and aperiodically intermittent control (APIC) are two classifications of IC that depend on whether the control interval and control periods are fixed. However, the conditions might be conservative because PIC's control and free intervals must be fixed. The advantage of APIC is that it is no longer necessary to fix the length of the working time and rest time, which increases the randomness of the control intervals and therefore has a good application prospect. Therefore, with the advantages of APIC, many scholars have combined ETC with APIC to achieve better research results[18,19,20,21]. Reference[20] realized finite-time stabilization of nonlinear delayed systems under impulsive disturbance by designing time-triggered aperiodic intermittent control with event-triggered aperiodic intermittent control.
Quantization strategies as a control scheme not only ensure sufficient accuracy but also reduce the amount of transmitted information[22,23,24,25,26]. Quantizers perform a discontinuous mapping from a continuous space to a finite set. However, due to the precision and range limitations of quantization, numerical discrepancies arise between the behavior of the ideal system and the calculated values.
The concept of stability studies the asymptotic behavior of states that tend to infinity with time. However, a state's properties in the finite time domain must be considered in practical engineering, so finite-time stability (FTS) has been widely studied as one of the concepts describing the state in the finite time domain[27,28,29,30,31,32,33,34]. FTS due to the transient properties in the finite time sense can be divided into two categories of concepts: one is for a given initial value of the upper bound with a finite time interval, which is maintained within a finite time domain within another larger threshold value. The second concept states that the system's state reaches equilibrium in finite time. To avoid confusion, only the first concept is considered in this paper. However, finite-time stabilization alone is insufficient. A more practical approach is finite-time contraction stabilization (FTCS), which not only ensures boundedness but also requires that the system's state at the termination time must remain within a smaller bound compared with the initial upper limit. This makes FTCS particularly relevant for real-world applications. In[35,36], FTS is investigated in a stochastic sense, where, unlike stochastic finite-time stability under probability[37,38], such stability has states under expectation. Reference[39] investigated the FTS of linear systems combined with state quantization.
However, little research has focused on nonlinear stochastic systems that integrate these three aspects, since stochastic state fluctuations are a primary cause of the system's instability and poor performance. Therefore, using ETC with APIC, and combining ETC with APIC and state quantization enables a more effective assessment of a system's performance through well-designed triggering mechanisms while conserving control resources.
On the basis of the motivation and inspiration of the abovementioned research, this paper presents the FTS and FTCS of stochastic nonlinear systems with two ETMs under APIC. The control system follows established ISS control laws and provides two settings for QbE and QaE, where paired quantizers are taken into consideration. By integrating ETC with quantization control, the approach aims to minimize the communication overhead. The Zeno phenomenon, in which the control is updated infinitely in finite time, is then avoided by designing a static ETM. In addition, aperiodically intermittent controllers are introduced to reduce the computational burden on controllers and mitigate reliance on continuous transmission. There are relatively few papers on stochastic nonlinear systems in ETC with IC to achieve FTS, so the theoretical results of our study are of interest. The results show that (1) under APIC, both ETMs significantly reduce the number of trigger events, and the control interval length can be adjusted according to the specific objectives of the ETMs; (2) both ETMs can achieve FTS and FTCS of stochastic nonlinear systems, and the relevant sufficient conditions are obtained. Therefore, the main innovation of this paper lies in the combination of intermittent state quantization and an event-triggered mechanism, which further reduces the computational costs and communication burdens. Compared with [14,26], this paper employs an aperiodically intermittent controller to further alleviate the controller's burden and achieve finite-time stability. In contrast to [20,39], this work extends the general nonlinear system to a stochastic nonlinear system setting and employs intermittent quantization control to achieve finite-time stability and Lyapunov stability.
The rest of the paper is structured as follows: Section 2 describes the model and provides background information, Section 3 presents the primary results, Section 4 provides numerical examples, and finally, Section 5 summarizes the key conclusions and outlines directions for future research.
Notations: In the whole paper, we have used $ \mathcal{N} $ to represent the set of natural numbers, $ \mathcal{R^+} = [0, +\infty) $ denotes the set of positive real numbers. $ V(x, t)\in \mathcal{C}^{2, 1} $ denotes the family of all non-negative functions in $ \mathcal{R}^d\times [0, +\infty) $ and is quadratically continuously differentiable with respect to $ x $ and once continuously differentiable with respect to $ t $. $ \mathbb{E}(\cdot) $ stands for the expectation operator. $ I_\mathcal{A}(x) $ represents the characteristic function. When $ x\in \mathcal{A} $, $ I_\mathcal{A}(x) = 1 $, and when $ x\notin \mathcal{A} $, $ I_\mathcal{A}(x) = 0 $. Define $ \mathcal{Z_+} $ as the set of positive integers and $ \mathbb{N} $ as the set of integers.
Let $ (\Omega, \mathcal{F}, \mathrm{Pr\{\cdot\}}) $ be a complete probability space with a filtration $ \{\mathcal{F}_t\}_{t \geq 0} $ that meets the normal conditions. Study the following nonlinear stochastic system, which has a dynamical expression of the form
$ dx(t)=(f(x(t),t)+u(t))dt+g(x(t),t)dω(t) $ | (2.1) |
on $ t \geq 0 $ with the initial state $ x(t_0) = x_0 $, where $ x(t) \in \mathbb{R}^n $, $ f $, $ g \in \mathbb{R}^n \times \mathbb{R}_+ \rightarrow \mathbb{R}^n $ and satisfies $ f(0, t) = g(0, t) = 0 $, where $ u(t) \in \mathbb{R}^n $ is control input and $ \omega(t) $ is defined as an $ n $-dimensional Wiener process on the probability space satisfying the general conditions. Next, we define the intermittent control law as follows:
$ u(t)={α(q(x(tm,i))),t∈[tm,i,tm,i+1)∩[tm,tm+sm),0,t∈[tm+sm,tm+1), $ | (2.2) |
which is affected by state quantization and is event-triggered, where $ [t_m, t_{m+1}) $ represents the $ m+1 $th control period, $ [t_m, t_m+s_m) $ represents the $ m+1 $th working interval, and $ [t_m+s_m, t_{m+1}) $ represents the rest interval; $ t_{m, i} $ is the time at which the $ i $th event is activated in the $ m+1 $th work interval. This strategy has the advantage of allowing the controller to work for a while and then take a break to lessen the strain on communication. $ \alpha: \mathbb{R}^n \rightarrow \mathbb{R}^n $ stands for the controller function. Thus, with an intermittent control law $ u(t) $, the system's dynamic can be represented as follows:
$ dx(t)={(f(x(t),t)+u(t))dt+g(x(t),t)dω(t),t∈[tm,i,tm,i+1)∩[tm,tm+sm),f(x(t),t)dt+g(x(t),t)dω(t),t∈[tm+sm,tm+1), $ | (2.3) |
where $ q:\mathbb{R}^n \rightarrow \Xi $, $ n \in \mathbb{Z_+} $ represents the logarithmic quantization function, $ \Xi $ is a discrete set of quantization values, and $ \{t_{m, i}\} $ indicates a time series consisting of the instant of event triggering. Next, we give a number of significant assumptions.
Assumption 2.1. [18] There are two constants $ \theta $, $ \omega $, satisfying $ 0 < \theta < \omega $ and for $ k = 1, 2, 3 \ldots $, such that the following holds true:
$ {infk(sk)=θ>0,supk(tk+1−tk)=ω<+∞. $ |
Remark 2.1. Here, $ \theta $ is the minimum work interval and $ \omega-\theta $ is the maximum rest interval, where the duration of the work interval will not be less than $ \theta $ and the duration of the rest interval will not be greater than $ \omega-\theta $. This prevents the controller from exerting control for long periods of time and ensures that the work interval alternates with the rest interval. The framework of the APIC strategy is shown in Figure 1.
Assumption 2.2. [22,39] The logarithmic quantizer $ q(\cdot) $ is defined as follows:
$ q(v)={ξi,if11+δξi<v≤11−δξi,0,ifv=0,−q(−v),ifv<0, $ |
where $ q(v) $, $ v $ $ \in \mathbb{R} $, without taking the finite quantization level into account $ \Xi = \{\pm\xi:\xi_i = \rho^i\xi_0; i\in \mathbb{N}\}\cup\{0\}; $ $ 0 < \rho < 1; $ and $ \xi_0 > 0 $, where $ \delta = \frac{1-\rho}{1+\rho} \in (0, 1) $ is linked to the quantizer density $ \rho $ and is referred to as the sector bound. If $ q $ is a logarithmic quantization function and $ q(x) = \Gamma[q(\zeta_{x, 1}), q(\zeta_{x, 2}), \cdots, q(\zeta_{x, n})]^T $, where $ \zeta_x = \Gamma^{-1}x = [\zeta_{x, 1}, \zeta_{x, 2}, \cdots, \zeta_{x, n}]^T $, $ x\in \mathbb{R}^n $. The nature of the quantizer is as follows:
$ |q(x)−x|≤δ|x|. $ |
Assumption 2.3. The following equation holds true for every $ x $, $ \overline{x} \in \mathbb{R}^n $, $ t \in \mathbb{R_+} $, assuming there are positive constants $ L_1 $, $ L_2 $, and $ L_3: $
$ (i)|f(x,t)|≤L1|x|,|g(x,t)|≤L2|x|,(ii)|α(x)−α(¯x)|≤L3|x−¯x|. $ |
Assumption 2.4. Positive definite functions $ V(x, t)\in \mathcal{C}^{2, 1}(\mathbb{R}^n \times \mathbb{R_+}; \mathbb{R_+}) $ exist that are continuously differentiable in x twice and in t once. Positive variables $ c_1 $, $ c_2 $ also exist, so that for every $ x \in \mathbb{R}^n $, the equation that follows holds:
$ c1|x|2≤V(x,t)≤c2|x|2. $ | (2.4) |
The operator $ \mathcal{L}V(x, t) $ is defined by
$ LV(x,t)≤φ(t)V(x,t), $ | (2.5) |
where $ \varphi(t) = \varphi_1 > 0 $ for $ t \in [t_m+s_m, t_{m+1}) $, $ \varphi(t) = \varphi_2 < 0 $ for $ t \in [t_m, t_m+s_m) $, and $ \mathrm{d}V(x, t) = \mathcal{L}V(x, t)\mathrm{d}t+V_x(x, t)\mathrm{d}\omega(t) $.
Assumption 2.5. [16] A positive definite function $ V(x, t)\in \mathcal{C}^{2, 1}(\mathbb{R}^n \times \mathbb{R_+}) $ and a positive constant $ L_4 $ exist, such that any $ x \in \mathbb{R}^n $ $ \frac{\partial V(x, t)}{\partial x} \leq L_4|x| $ holds.
Definition 2.1. For the given constants T, $ \varepsilon_1 $, and $ \varepsilon_2 $ with $ 0 < \varepsilon_1 < \varepsilon_2 $ and any trajectory $ x(t) $, if there is a control law such that $ \mathbb{E}|x_0| \leq \varepsilon_1 $ implies $ \mathbb{E}|x(t)| \leq \varepsilon_2 $, $ t \in [0, T] $, then the system (2.3) is called FTS with respect to $ (w.r.t) $ $ (T, \varepsilon_1, \varepsilon_2) $.
Definition 2.2. For the given constants T, $ \varepsilon_1 $, $ \varepsilon_2 $, $ \varrho $, and $ \tau $, where $ 0 < \varrho < \varepsilon_1 < \varepsilon_2 $ and $ \tau\in (0, T) $, the system (2.3) is FTCS with respect to $ (w.r.t) $ $ (T, \varepsilon_1, \varepsilon_2, \varrho, \tau) $. If there is a control law such that $ \mathbb{E}|x_0| \leq \varepsilon_1 $ implies $ \mathbb{E}|x(t)| \leq \varepsilon_2 $ for all $ t \in [0, T] $, for all $ t\in [T-\tau, T] $, there is $ \mathbb{E}|x(t)| \leq \varrho $.
Remark 2.2. (ⅰ) In Definition 2.1, all parameters $ \varepsilon_1 $, $ \varepsilon_2 $, and $ T $ are predesigned, and $ FTS $ indicates that the average value of the states from the initial data of the systems is within a predetermined initial bound and subsequently reaches another set bound after a finite amount of time. The $ FTS $ describes a kind of boundedness of the state of the system, whose state trajectory is depicted in Figure 2a.
(ⅱ) According to Definition 2.2, the trajectory of the system state reaches, within a small time interval $ [T-\tau, T] $ of the terminal time, another threshold $ \varrho $ that is smaller than the initial threshold, as shown in Figure 2b. Thus, we can see that the conditions for $ FTCS $ are much more restrictive than $ FTS $.
Lemma 2.1. [16] Consider stochastic nonlinear systems satisfying Assumptions 2.2, 2.4, and 2.5. When $ t \in [t_1, t_2) $, assuming the existence of some positive constants $ \hat{\beta_1} < 0 $, $ \check{\beta_1} > 0 $, and $ -\hat{\beta_1} > \check{\beta_1} > 0 $, for a positive definite function $ V(x(t), t) $, the following conditions are satisfied:
$ ELV(x(t),t)≤^β1EV(x(t),t)+ˇβ1supt1≤η<t2EV(x(η),η). $ |
Then, we can derive
$ supt1≤η<t2EV(x(η),η)=EV(x(t1),t1). $ |
To further investigate the connection between state quantization and ETMs under APIC, we designed the following two ETMs.
(Ⅰ). QbE: If the system's state is quantized before a trigger, the following ETM is available:
$ tm,i+1=inf{t≥tm,i+ϵ||q(x(tm,i))−x(t)|2≥λ|x(t)|2}. $ | (3.1) |
(Ⅱ). QaE: If the system's state is quantized after a trigger, the following ETM is available:
$ tm,i+1=inf{t≥tm,i+ϵ||(x(tm,i))−x(t)|2≥λ|x(t)|2}, $ | (3.2) |
where $ t_0 = 0 $, $ \epsilon $, and $ \lambda $ are all constants, and (3.1) and (3.2) mean that the ETM will be suspended for a period of time $ \epsilon $ after execution; after that, it will continue to execute the current predesigned trigger mechanism until the next trigger threshold condition is met. Since the stopping time $ \epsilon $ is set in the ETM, the system (2.1) naturally avoids the Zeno behavior. Compared with traditional time-triggered, the event-triggered strategy used can further increase the time interval between events on this basis, due to the fact that the defined time sequence of event-triggered is determined by the current state of the system, thus reducing the network's communication burden. The description of ETM (3.1) and ETM (3.2) can be represented by the block diagrams in Figures 3 and 4. In addition, the utilization of APIC (2.2) can further save communication resources on this basis. Next, we give the following two error estimates $ e_1(t) = q(x(t_{m, i}))-x(t) $ and $ e_2(t) = x(t_{m, i})-x(t) $.
Lemma 3.1. Under Assumptions 2.1–2.3, $ \epsilon \geq 0 $, $ 0 \leq \delta \leq 1 $, and $ \epsilon < \sqrt{\frac{1}{12L_3^2(2\delta^2+1)}} $ exist, and for the system (2.1), the following holds:
$ E|e1(t)|2≤κ1E∫tm,i+ϵtm,i|x(s)|2ds+κ2E|x(t)|2, $ | (3.3) |
where $ \kappa_1 = \frac{4(2\delta^2+1)(2\epsilon L_1^2+L_2^2)}{1-12\epsilon^2L_3^2(2\delta^2+1)} $, $ \kappa_2 = \frac{24\epsilon^2 L_3^2(2\delta^2+1)^2}{1-12\epsilon^2L_3^2(2\delta^2+1)}+4\delta^2+\lambda $.
Proof. For any fixed $ t $, define the set of time series $ \Lambda_i = \{\gamma_t = t_{m, i}\} $, $ \Lambda_{i, \epsilon} = \{\gamma_t = t_{m, i}, \; \mathrm{and} \; t \leq t_{m, i}+\epsilon\} $. We estimate the error $ e_1(t) $ in two separate cases.
Case 1: If $ t\in \Lambda_i \setminus \Lambda_{i, \epsilon} $, at this point, by ETM (3.1), we have $ |q(x(t_{m, i}))-x(t)|^2 \leq \lambda|x(t)|^2 $ a.s.(almost sure) on $ \Lambda_i \setminus \Lambda_{i, \epsilon} $, which implies
$ E(IΛi∖Λi,ϵ|q(x(tm,i))−x(t)|2)≤E(IΛi∖Λi,ϵλ|x(t)|2)≤E(IΛi|x(t)|2). $ | (3.4) |
Case 2: If $ t \in \Lambda_{i, \epsilon} $, for the error $ e_1(t) $, we have
$ E(IΛi,ϵ|q(x(tm,i))−x(t)|2)≤2E(IΛi,ϵ|q(x(tm,i))−x(tm,i)|2)+2E(IΛi,ϵ|x(tm,i)−x(t)|2)≤2δ2E(IΛi,ϵ|x(tm,i)|2)+2E(IΛi,ϵ|e2(t)|2)≤(4δ2+2)E(IΛi,ϵ|e2(t)|2)+4δ2E(IΛi,ϵ|x(t)|2). $ | (3.5) |
Next, we estimate $ e_2(t) $ conditional on ETM (3.1). Based on the system (2.3), we have
$ E(IΛi,ϵ|e2(t)|2)=E(IΛi,ϵ|∫ttm,if(x(s),s)+u(s)ds+∫ttm,ig(x(s),s)dω(s)|2)≤4E(|IΛi,ϵ∫ttm,if(x(s),s)ds|2)+4E(|IΛi,ϵ∫ttm,iu(s)ds|2)+2E(|IΛi,ϵ∫ttm,ig(x(s),s)dω(s)|2). $ | (3.6) |
From H$ \mathrm{\ddot{o}} $lder's inequality and Assumption 2.3, we get
$ E(|IΛi,ϵ∫ttm,if(x(s),s)ds|2)≤ϵL21E(|IΛi,ϵ∫ttm,i|x(s)|2ds). $ | (3.7) |
From Assumptions 2.2 and 2.3
$ E(|IΛi,ϵ∫ttm,iu(s)ds|2)=E(|IΛi,ϵ∫ttm,iα(q(x(tm,i)))ds|2)≤ϵ2L23(EIΛi,ϵ|q(x(tm,i))−x(tm,i)+x(tm,i)−x(t)+x(t)|2)≤3ϵ2L23E(IΛi,ϵ|q(x(tm,i))−x(tm,i)|2)+3ϵ2L23E(IΛi,ϵ|x(tm,i)−x(t)|2)+3ϵ2L23E(IΛi,ϵ|x(t)|2)≤(6ϵ2L23δ2+3ϵ2L23)E(IΛi,ϵ|x(t)|2+IΛi,ϵ|e2(t)|2). $ | (3.8) |
Furthermore, from the $ It\hat{o} $ isometry and Assumption 2.3, we obtain
$ E(|IΛi,ϵ∫ttm,ig(x(s),s)dω(s)|2)≤L22E(IΛi,ϵ∫ttm,i|x(s)|2ds). $ | (3.9) |
Then, substituting (3.7), (3.8), and (3.9) into (3.6) yields
$ E(IΛi,ϵ|e2(t)|2)≤(4ϵL21+2L22)E(IΛi,ϵ∫ttm,i|x(s)|2ds)+(24ϵ2L23δ2+12ϵ2L23)E(IΛi,ϵ|x(t)|2)+(24ϵ2L23δ2+12ϵ2L23)E(IΛi,ϵ|e2(t)|2). $ |
Since $ \epsilon < \sqrt{\frac{1}{12L_3^2(2\delta^2+1)}} $, shifting the terms gives
$ E(IΛi,ϵ|e2(t)|2)≤4ϵL21+2L221−12ϵ2L23(2δ2+1)E(IΛi,ϵ∫ttm,i|x(s)|2ds)+24ϵ2L23δ2+12ϵ2L231−12ϵ2L23(2δ2+1)E(IΛi,ϵ|x(t)|2). $ | (3.10) |
Substituting the result of (3.10) into (3.5) gives
$ E(IΛi,ϵ|q(x(tm,i))−x(t)|2)≤(4δ2+24ϵ2L23(2δ2+1)21−12ϵ2L23(2δ2+1))E(IΛi,ϵ|x(t)|2)+4(2ϵL21+L22)(2δ2+1)1−12ϵ2L23(2δ2+1)E(IΛi,ϵ∫ttm,i|x(s)|2ds). $ | (3.11) |
Thus, combining (3.4) and (3.11), we get
$ E(IΛi|q(x(tm,i))−x(t)|2)=E(IΛi,ϵ|q(x(tm,i))−x(t)|2)+E(IΛi∖Λi,ϵ|q(x(tm,i))−x(t)|2)≤4(2ϵL21+L22)(2δ2+1)1−12ϵ2L23(2δ2+1)E(IΛi,ϵ∫ttm,i|x(s)|2ds)+(4δ2+24ϵ2L23(2δ2+1)21−12ϵ2L23(2δ2+1)+λ)E(IΛi|x(t)|2)≤4(2ϵL21+L22)(2δ2+1)1−12ϵ2L23(2δ2+1)E(IΛi∫tm,i+ϵtm,i|x(s)|2ds)+(4δ2+24ϵ2L23(2δ2+1)21−12ϵ2L23(2δ2+1)+λ)E(IΛi|x(t)|2). $ |
Therefore, when $ t \in [t_m, t_m+s_m) $, there are up to $ \lceil \frac{s_m}{\epsilon} \rceil $ communication times on $ [t_m, t_m+s_m) $, $ m \in \mathbb{N}^+ $. As a result, we can arrive at
$ E|q(x(tm,i))−x(t)|2=⌈smϵ⌉∑i=0E(IΛi|q(x(tm,i))−x(t)|2)≤4(2ϵL21+L22)(2δ2+1)1−12ϵ2L23(2δ2+1)⌈smϵ⌉∑i=0E(IΛi∫tm,i+ϵtm,i|x(s)|2ds)+(4δ2+24ϵ2L23(2δ2+1)21−12ϵ2L23(2δ2+1)+λ)⌈smϵ⌉∑i=0E(IΛi|x(t)|2)=4(2ϵL21+L22)(2δ2+1)1−12ϵ2L23(2δ2+1)E(∫tm,i+ϵtm,i|x(s)|2ds)+(4δ2+24ϵ2L23(2δ2+1)21−12ϵ2L23(2δ2+1)+λ)E(|x(t)|2), $ |
let $ \kappa_1 = \frac{4(2\delta^2+1)(2\epsilon L_1^2+L_2^2)}{1-12\epsilon^2L_3^2(2\delta^2+1)} $, $ \kappa_2 = \frac{24\epsilon^2 L_3^2(2\delta^2+1)^2}{1-12\epsilon^2L_3^2(2\delta^2+1)}+4\delta^2+\lambda $, we conclude that
$ E|e1(t)|2≤κ1E∫tm,i+ϵtm,i|x(s)|2ds+κ2E|x(t)|2, $ |
and the proof is completed. Next, we analyze the FTS and FTCS of the system (2.3) under APIC in terms of ETM (3.1) with state quantization.
Theorem 3.1. Under Assumptions 2.1–2.5 and Lemmas 2.1 and 3.1, there are $ \epsilon < \sqrt{\frac{1}{12L_3^2(2\delta^2+1)}} $ and some positive constants $ \lambda, \epsilon, \delta, \omega, \theta, \tilde{\mu}_1 $ that satisfy
$ −ˆβ1>ˇβ1>0, $ | (3.12) |
and
$ N(0,t)[φ1(ω−θ)−˜μ1θ]−lnc1ε22+lnc2ε21≤0, $ | (3.13) |
where $ \mathcal{N}(0, t) $ delegates the number of the control period on $ (0, T] $ and $ T\neq t_n $, $ \check{\beta}_1 = \frac{L_3L_4\epsilon}{2c_1}\kappa_1 $, and $ \hat{\beta}_1 = \frac{L_3L_4}{2c_1}\kappa_2+\frac{L_3L_4}{2c_1}+\varphi_2 $, where $ \kappa_1 $ and $ \kappa_2 $ are the same as in Lemma 3.1. $ 0 < \tilde{\mu}_1 < \mu_1 $ and $ \mu_1 $ is the sole positive real root of equation $ \mu_1+\check{\beta}_1e^{\mu_1\Delta_1}+\hat{\beta}_1 = 0 $. The upper bound on the inter-event interval can be expressed as $ \underset{m, i\in \mathbb{N}}{sup}\{t_{m, i+1}-t_{m, i}\}\leq \Delta_1 $. We can then claim that the system (2.1) is capable of FTS $ (w.r.t) $ $ (T, \varepsilon_1, \varepsilon_2) $ under APIC with ETM (3.1).
Moreover, if for all $ t\in [T-\tau, T] $, there are
$ N(0,t)[φ1(ω−θ)−˜μ1θ]−lnc1ϱ2+lnc2ε21≤0. $ | (3.14) |
Then, we claim that system (2.1) is capable of FTCS $ (w.r.t) $ $ (T, \varepsilon_1, \varepsilon_2, \varrho, \tau) $ under APIC with ETM (3.1).
Proof. For $ 0 < |x_0|\leq \varepsilon_1 $, assume $ x(t) = x(t, 0, x_0) $ is a solution of the system (2.2) at $ (0, x_0) $, when $ t \in [t_m+s_m, t_{m+1}) $, from Assumption 2.4, we have
$ ELV(x(t),t)≤Eφ1V(x(t),t). $ | (3.15) |
Integrating (3.15) over the interval $ [t_m+s_m, t) $ gives
$ EV(x(t),t)≤Eeφ1(t−tm−sm)V(x(tm+sm),tm+sm). $ | (3.16) |
When $ t \in [t_m, t_m+s_m) $, from Assumptions 2.4 and 2.5 and Condition (ⅱ) in Assumption 2.2, we obtain
$ ELV(x(t),t)≤Eφ2V(x(t),t)+E∂V(x,t)∂x|α(q(x(tm,i)))−αx(t)|≤φ2EV(x(t),t)+L3L42E(|x(t)|2+|q(x(tm,i))−x(t)|2). $ | (3.17) |
Substituting the result of Lemma 3.1 into (3.17) yields
$ ELV(x(t),t)≤φ2EV(x(t),t)+L3L42E(|x(t)|2)+L3L42E(|q(x(tm,i))−x(t)|2)≤φ2EV(x(t),t)+L3L42E(|x(t)|2)+L3L42E(κ1∫tm,i+ϵtm,i|x(s)|2ds+κ2|x(t)|2)≤L3L42c1κ1E∫tm,i+ϵtm,iV(x(s),s)ds+(L3L42c1κ2+L3L42c1+φ2)EV(x(t),t)≤L3L4ϵ2c1κ1suptm,i≤η<tm,i+ϵEV(x(η),η)+(L3L42c1κ2+L3L42c1+φ2)EV(x(t),t). $ | (3.18) |
Substituting the result of Lemma 2.1, $ \check{\beta}_1 = \frac{L_3L_4\epsilon}{2c_1}\kappa_1 $, and $ \hat{\beta}_1 = \frac{L_3L_4}{2c_1}\kappa_2+\frac{L_3L_4}{2c_1}+\varphi_2 $ into Eq (3.18) yields
$ ELV(x(t),t)≤ˇβ1EV(x(tm,i),tm,i)+ˆβ1EV(x(t),t). $ | (3.19) |
Further, let $ \dot{z}(t) = \check{\beta}_1z(t_{m, i})+\hat{\beta}_1z(t) $ and $ y(t) = z(t)e^{\tilde{\mu}_1(t-t_{m, i})} $ and assume that $ z(t) = \mathbb{E}V(x(t), t) $. Since $ z(t_{m, i}) > 0 $, we assert that $ \phi > 1 $ exists such that $ y(t) < \phi z(t_{m, i}) $. Otherwise, $ t > t_{m, i} $ exists such that $ y(t) > \phi z(t_{m, i}) $, and we define $ \hat{t} = \inf\{t > t_{m, i}\vert y(t) = \phi z(t_{m, i})\} $. Thus, we can derive $ y(\hat{t}) = \phi z(t_{m, i}) $, which means that $ \dot{y}(\hat{t})\geq 0 $. In this cases,
$ ˙y(t)=e˜μ1(t−tm,i)(˜μ1z(t)+˙z(t))=e˜μ1(t−tm,i)(˜μ1z(t)+ˇβ1z(tm,i)+ˆβ1z(t))≤˜μ1y(t)+ˆβ1y(t)+ˇβ1e˜μ1(t−tm,i)y(tm,i)=(˜μ1+ˆβ1)y(t)+ˇβ1e˜μ1(t−tm,i)y(tm,i). $ |
When $ t = \hat{t} $, the following equation holds:
$ ˙y(ˆt)≤(˜μ1+ˆβ1)y(ˆt)+ˇβ1e˜μ1(ˆt−tm,i)y(tm,i)≤(˜μ1+ˆβ1+ˇβ1e˜μ1(ˆt−tm,i))y(ˆt)≤(˜μ1+ˆβ1+ˇβ1e˜μ1(tm,i+1−tm,i))y(ˆt)≤(˜μ1+ˆβ1+ˇβ1e˜μ1Δ1)y(ˆt). $ |
Next, we define $ \vartheta(\mu_1) = \mu_1+\hat{\beta}_1+\check{\beta}_1e^{\mu_1\Delta_1} $. We then have $ \vartheta(\mu_1)' $ and, by $ \vartheta(0) < 0 $ and $ \vartheta(-\hat{\beta}_1) > 0 $, a unique positive root $ {\mu}_1 $ exists such that $ \mu_1+\hat{\beta}_1+\check{\beta}_1e^{\mu_1\Delta_1} = 0 $. Further, for $ 0 < \tilde{\mu}_1 < \mu_1 $, we have $ \tilde{\mu}_1+\hat{\beta}_1+\check{\beta}_1e^{\tilde{\mu}_1\Delta_1} < 0 $. In summary, we conclude that $ \dot{y}(\hat{t})\leq 0 $. This is contradictory to the above. Thus, $ y(t) < \phi z(t_{m, i}) $ holds. Therefore, when $ t \in [t_{m, i}, t_{m, i+1}) $ and when $ \phi\rightarrow 1 $, by the comparison principle, we have
$ EV(x(t),t)≤Ee−˜μ1(t−tm,i)V(x(tm,i),tm,i). $ | (3.20) |
When $ t\in[t_m, t_{m, 1}) $, Eq (3.20) becomes
$ EV(x(t),t)≤Ee−˜μ1(t−tm)V(x(tm),tm). $ |
If we let $ t = t_{m, 1} $, then we have
$ EV(x(tm,1),tm,1)≤Ee−˜μ1(tm,1−tm)V(x(tm),tm). $ | (3.21) |
When $ t\in[t_{m, 1}, t_{m, 2}) $, we have
$ EV(x(t),t)≤Ee−˜μ1(t−tm,1)V(x(tm,1),tm,1). $ | (3.22) |
Substituting (3.21) into (3.22) yields
$ EV(x(t),t)≤Ee−˜μ1(t−tm)V(x(tm),tm),t∈[tm,1,tm,2). $ | (3.23) |
Suppose that the following equation still holds when $ t\in[t_{m, k}, t_{m, k+1}) $:
$ EV(x(t),t)≤Ee−˜μ1(t−tm)V(x(tm),tm),t∈[tm,k,tm,k+1), $ |
and when $ t = t_{m, k+1} $
$ EV(x(tm,k+1),tm,k+1)≤Ee−˜μ1(tm,k+1−tm)V(x(tm,k+1),tm,k+1),t∈[tm,k,tm,k+1). $ | (3.24) |
When $ t\in[t_{m, k+1}, t_{m, k+2}) $, we have
$ EV(x(t),t)≤Ee−˜μ1(t−tm,k+1)V(x(tm,k+1),tm,k+1). $ | (3.25) |
Substituting (3.24) into (3.25) gives
$ EV(x(t),t)≤Ee−˜μ1(t−tm)V(x(tm),tm),t∈[tm,k+1,tm,k+2). $ | (3.26) |
The assumption still holds when $ t\in[t_{m, k+1}, t_{m, k+2}) $. Hence, for any $ t\in [t_{m, i}, t_{m, i+1}) $ and $ 0 \leq i \leq \lceil \frac{s_m}{\epsilon} \rceil $, we have $ \mathbb{E}V(x(t), t)\leq \mathbb{E}e^{-\tilde{\mu}_1(t-t_m)}V(x(t_m), t_m) $ holds true. Then for $ t\in [t_m, t_m+s_m) $, we still have $ \mathbb{E}V(x(t), t)\leq \mathbb{E}e^{-\tilde{\mu}_1(t-t_m)}V(x(t_m), t_m) $.
In summary, we have
$ EV(x(t),t)≤Ee−˜μ1(t−tm)V(x(tm),tm),t∈[tm,tm+sm),EV(x(t),t)≤Eeφ1(t−tm−sm)V(x(tm+sm),tm+sm),t∈[tm+sm,sm+1), $ |
for $ 0\leq t\leq T $, $ 0 < \varepsilon_1 < \varepsilon_2 $, and $ 0 < |x_0|\leq \varepsilon_1 $.
When $ t\in [t_0, t_0+s_0) $, we have
$ EV(x(t),t)≤Ee−˜μ1(t−t0)V(x(t0),t0), $ | (3.27) |
and
$ EV(x(t0+s0),t0+s0)≤Ee−˜μ1s0V(x(t0),t0), $ | (3.28) |
for $ t \in [t_0+s_0, t_1) $. Combining with (3.27) and (3.28), one has
$ EV(x(t),t)≤Eeφ1(t−t0−s0)V(x(t0+s0),t0+s0)≤Eeφ1(t−t0−s0)−˜μ1s0V(x(t0),t0), $ |
and
$ EV(x(t1),t1)≤Eeφ1(t1−t0−s0)−˜μ1s0V(x(t0),t0). $ | (3.29) |
When $ t\in [t_1, t_1+s_1) $, we have
$ EV(x(t),t)≤Ee−˜μ1(t−t1)V(x(t1),t1), $ |
and
$ EV(x(t1+s1),t1+s1)≤Ee−˜μ1s1V(x(t1),t1). $ | (3.30) |
For $ t \in [t_1+s_1, t_2) $, combining (3.27), (3.29), and (3.30), one has
$ EV(x(t),t)≤Eeφ1(t−t1−s1)V(x(t1+s1),t1+s1)≤Eeφ1(t−t1−s1)−˜μ1s1V(x(t1),t1)≤Eeφ1(t−t1−s1+t1−t0−s0)−˜μ1(s0+s1)V(x(t0),t0), $ |
and
$ EV(x(t2),t2)≤Eeφ1(t2−t1−s1+t1−t0−s0)−˜μ1(s0+s1)V(x(t0),t0). $ | (3.31) |
When $ t\in [t_2, t_2+s_2) $, we have
$ EV(x(t),t)≤Ee−˜μ1(t−t2)V(x(t2),t2), $ |
and
$ EV(x(t2+s2),t2+s2)≤Ee−˜μ1s2V(x(t2),t2). $ | (3.32) |
For $ t \in [t_2+s_2, t_3) $, combining (3.27), (3.31), and (3.32), one has
$ EV(x(t),t)≤Eeφ1(t−t2−s2)V(x(t2+s2),t2+s2)≤Eeφ1(t−t2−s2)−˜μ1s2V(x(t2),t2)≤Eeφ1(t−t2−s2+t2−t1−s1+t1−t0−s0)−˜μ1(s0+s1+s2)V(x(t0),t0), $ |
and
$ EV(x(t2),t2)≤Eeφ1(t3−t2−s2+t2−t1−s1+t1−t0−s0)−˜μ1(s0+s1+s2)V(x(t0),t0). $ |
In the same way, for $ t \in [t_n+s_n, t_{n+1}) $ and using Assumption 2.1, we have
$ EV(x(t),t)≤Eeφ1[t−tn−sn+n−1∑i=0(ti+1−ti−si)]−˜μ1n∑i=0siV(x(t0),t0)≤Eeφ1[n∑i=0(ti+1−ti−si)]−˜μ1n∑i=0siV(x(t0),t0)≤Ee(n+1)φ1(ω−θ)−(n+1)˜μ1θV(x(t0),t0)≤EeN(0,t)(φ1(ω−θ)−˜μ1θ)V(x(t0),t0). $ |
From Condition (2.4) in Assumption 2.4 and (3.13), we can derive
$ |x(t)|2≤c2c1eN(0,t)(φ1(ω−θ)−˜μ1θ)|x0|2≤c2c1ε21eN(0,t)(φ1(ω−θ)−˜μ1θ)≤ε22, $ | (3.33) |
which means that $ |x(t)|\leq \varepsilon_2 $, and thus $ \mathbb{E}|x(t)|\leq \varepsilon_2 $ holds on $ [0, T] $. As described, it can be concluded that the system (2.3) can achieve FTS on $ [0, T] $. The system (2.1) is FTS $ ($w, r, t$) $ $ (T, \varepsilon_1, \varepsilon_2) $ under APIC (2.2) with ETM (3.1).
When $ t\in [T-\tau, T] $, if Condition (3.14) in Theorem 3.1 is satisfied, from (3.33) we have
$ |x(t)|2≤c2c1eN(0,t)(φ1(ω−θ)−˜μ1θ)|x0|2≤c2c1ε21eN(0,t)(φ1(ω−θ)−˜μ1θ)≤ϱ2, $ | (3.34) |
which shows that $ |x(t)|\leq \varrho $, and thus $ \mathbb{E}|x(t)|\leq \varrho $ hold on $ t\in [T-\tau, T] $. Then the system (2.1) can achieve FTCS $ ($w, r, t$) $ $ (T, \varepsilon_1, \varepsilon_2, \varrho, \tau) $ under APIC (2.2) with ETM (3.1).
The proof is complete.
Lemma 3.2. Under Assumptions 2.1–2.3 and Lemma 3.1, $ \epsilon \geq 0 $, $ 0 \leq \delta \leq 1 $, and $ \epsilon < \sqrt{\frac{1}{12L_3^2(2\delta^2+1)}} $ exists, and for the system (2.1), the following holds:
$ E|e2(t)|2≤κ3E∫tm,i+ϵtm,i|x(s)|2ds+κ4E|x(t)|2, $ | (3.35) |
where $ \kappa_3 = \frac{2(2\epsilon L_1^2+L_2^2)}{1-12\epsilon^2L_3^2(2\delta^2+1)} $ and $ \kappa_4 = \frac{12\epsilon^2 L_3^2(2\delta^2+1)}{1-12\epsilon^2L_3^2(2\delta^2+1)}+\lambda $.
Proof. Similarly to Lemma 3.1, we discuss the same in two cases.
Case 1: If $ t\in \Lambda_i \setminus \Lambda_{i, \epsilon} $, at this point, by ETM (3.2), we have $ |(x(t_{m, i})-x(t)|^2 \leq \lambda|x(t)|^2 $ a.s. on $ \Lambda_i \setminus \Lambda_{i, \epsilon} $, which implies
$ E(IΛi∖Λi,ϵ|x(tm,i)−x(t)|2)≤E(IΛi∖Λi,ϵλ|x(t)|2)≤E(IΛiλ|x(t)|2). $ | (3.36) |
Case 2: If $ t \in \Lambda_{i, \epsilon} $, using the results of (3.10) in Lemma 3.1, we have
$ E(IΛi,ϵ|e2(t)|2)≤4ϵL21+2L221−12ϵ2L23(2δ2+1)E(IΛi,ϵ∫ttm,i|x(s)|2ds)+12ϵ2L23(2δ2+1)1−12ϵ2L23(2δ2+1)E(IΛi,ϵ|x(t)|2). $ | (3.37) |
Thus, combining (3.36) and (3.37), we get
$ E(IΛi|x(tm,i)−x(t)|2)=E(IΛi,ϵ|x(tm,i)−x(t)|2)+E(IΛi∖Λi,ϵ|x(tm,i)−x(t)|2)≤2(2ϵL21+L22)1−12ϵ2L23(2δ2+1)E(IΛi∫tm,i+ϵtm,i|x(s)|2ds)+(12ϵ2L23(2δ2+1)1−12ϵ2L23(2δ2+1)+λ)E(IΛi|x(t)|2). $ |
The latter steps of the proof are similar to those in Lemma 3.1, so we omit this part of the proof process. In the end, we arrive at
$ E|e2(t)|2≤κ3E∫tm,i+ϵtm,i|x(s)|2ds+κ4E|x(t)|2. $ |
The proof is complete.
Theorem 3.2. Under Assumptions 2.1–2.5 and Lemmas 2.1 and 3.2, we have $ \epsilon < \sqrt{\frac{1}{12L_3^2(2\delta^2+1)}} $ and some positive constants $ \lambda, \epsilon, \delta, \omega, \theta, \tilde{\mu}_2 $ that satisfy
$ −ˆβ2>ˇβ1>0, $ | (3.38) |
and
$ N(0,t)[φ1(ω−θ)−˜μ2θ]−lnc1ε22+lnc2ε21≤0, $ | (3.39) |
where $ \mathcal{N}(0, t) $ delegates the number of the control period on $ (0, T] $ and $ T\neq t_k $, $ \check{\beta}_1 = \frac{L_3L_4\kappa_3\epsilon(2\delta^2+1)}{c_1} $, $ \hat{\beta}_2 = \varphi_2+\frac{L_3L_4}{2c_1}+\frac{2\delta^2L_3L_4}{c_1}+ \frac{L_3L_4(2\delta^2+1)\kappa_4}{c_1} $, $ \kappa_3 $, and $ \kappa_4 $ are the same as in the Lemma 3.2. Moreover, $ \kappa_3 = \frac{\kappa_1}{2\delta^2+1} $, $ 0 < \tilde{\mu}_2 < \mu_2 $, where $ \mu_2 $ is the sole positive real root of the equation $ \mu_2+\check{\beta}_1e^{\mu_2\Delta_2}+\hat{\beta}_2 = 0 $. The upper bound on the execution time between events can be expressed as $ \underset{m, i\in \mathbb{N}}{sup}\{t_{m, i+1}-t_{m, i}\}\leq \Delta_2 $. We then claim that the system (2.1) is capable of FTS $ (w.r.t) $ $ (T, \varepsilon_1, \varepsilon_2) $ under APIC with ETM (3.2).
Moreover, for all $ t\in [T-\tau, T] $, there are
$ N(0,t)[φ1(ω−θ)−˜μ2θ]−lnc1ϱ2+lnc2ε21≤0. $ | (3.40) |
Then, we claim that the system (2.1) is capable of FTCS $ (w.r.t) $ $ (T, \varepsilon_1, \varepsilon_2, \varrho, \tau) $ under APIC with ETM (3.2).
Proof. For $ 0 < |x_0|\leq \varepsilon_1 $, assume that $ x(t) = x(t, 0, x_0) $ is a solution of the system (2.2) at $ (0, x_0) $. When $ t \in [t_m+s_m, t_{m+1}) $, from Assumption 2.4, we have
$ ELV(x(t),t)≤Eφ1V(x(t),t). $ |
Integrating the equation above over the interval $ [t_m+s_m, t) $ gives
$ EV(x(t),t)≤Eeφ1(t−tm−sm)V(x(tm+sm),tm+sm). $ |
When $ t \in [t_m, t_m+s_m) $, from Assumptions 2.2, 2.4, and 2.5 and Condition (ⅱ) in Assumption 2.3, we obtain
$ ELV(x(t),t)≤Eφ2V(x(t),t)+E∂V(x,t)∂x|α(q(x(tm,i)))−αx(t)|≤φ2EV(x(t),t)+L3L42E(|x(t)|2+|q(x(tm,i))−x(t)|2)≤φ2EV(x(t),t)+L3L42E|x(t)|2+L3L4E(|q(x(tm,i))−x(tm,i)|2+|x(tm,i)−x(t)|2)≤φ2EV(x(t),t)+(L3L42+2δ2L3L4)E|x(t)|2+L3L4(2δ2+1)E|e2(t)|2. $ | (3.41) |
If we substitute the result of Lemma 3.2, the equation above becomes
$ ELV(x(t),t)≤φ2EV(x(t),t)+(L3L42+2δ2L3L4)E|x(t)|2+L3L4(2δ2+1)(κ3E∫tm,i+ϵtm,i|x(s)|2ds+κ4E|x(t)|2)≤(φ2+L3L42c1+2δ2L3L4c1+L3L4(2δ2+1)κ4c1)E|x(t)|2+L3L4κ3(2δ2+1)E∫tm,i+ϵtm,i|x(s)|2ds≤(φ2+L3L42c1+2δ2L3L4c1+L3L4(2δ2+1)κ4c1)EV(x(t),t)+L3L4κ3ϵ(2δ2+1)c1suptm,i≤η<tm+ϵV(x(η),η). $ | (3.42) |
Substituting the result of Lemma 2.1, $ \check{\beta}_1 = \frac{L_3L_4\kappa_3\epsilon(2\delta^2+1)}{c_1} $, and $ \hat{\beta}_2 = \varphi_2+\frac{L_3L_4}{2c_1}+\frac{2\delta^2L_3L_4}{c_1}+\frac{L_3L_4(2\delta^2+1)\kappa_4}{c_1} $ into Eq (3.42) yields
$ ELV(x(t),t)≤ˇβ1EV(x(tm,i),tm,i)+ˆβ2EV(x(t),t). $ |
The latter steps are omitted because they closely resemble those in Theorem 3.1.
Remark 3.1. The proofs of Theorems 3.1 and 3.2 rely on the upper bound condition of the execution time between events. However, due to the arbitrariness of $ t_{m, i+1}-t_{m, i} $, determining the roots of the equation $ \mu_1+\hat{\beta}_1+\check{\beta}_1e^{\mu_1\Delta_1} = 0 $ is not straightforward. Nevertheless, it can be seen from the equation that if $ t_{m, i+1}-t_{m, i} $ is larger, then the roots of the equation $ \mu_1 $ can be appropriately small to satisfy $ 0 < \tilde{\mu}_1 < \mu_1 $. Therefore, we have the existence of $ 0 < \tilde{\mu}_1^{*} < \mu_1\leq{\mu}_1^{*} $ for an arbitrary $ t_{m, i+1}-t_{m, i} $, whose corresponding equation has the solution $ {\mu}_1^{*} $, such that $ \tilde{\mu}_1^{*}+\hat{\beta}_1+\check{\beta}_1e^{\tilde{\mu}_1^{*}\Delta_1} < 0 $ holds.
Remark 3.2. Theorem 3.1 is obtained from the trigger mechanism (3.1) on the basis of the error estimate (3.3), and Theorem 3.2 is obtained from the trigger mechanism (3.2) on the basis of the error estimate (3.35). Since (3.1) is based on quantization first and then event-triggered determination, the scheme is applicable to the overall quantization nature of the state trajectories, while (3.2) is based on event-triggered of the system's state and then realizing the quantization, which is more suitable for exploring the local quantization nature of the state trajectories under intermittent control. Therefore, according to (3.14) in Theorem 3.1, $ \varrho $ can be reduced with the change in $ \theta $ by increasing $ \theta $, which can better realize the 'contraction' in FTCS. By Eq (3.40) of Theorem 3.2, it can be seen that by decreasing $ \theta $ appropriately, $ \varrho $ can increase relatively with a change in $ \theta $, which makes it easier to achieve FTCS. See Section 4 for details.
This section illustrates our design approach using two examples of real process simulation and numerical simulation.
Example 1. Consider the following stochastic nonlinear system:
$ dx(t)=f(x(t),t)dt+g(x(t),t)dω(t) $ | (4.1) |
on $ t \geq 0 $, where
$ f(x(t),t)=[x2(t)−dx1(t)−csinx1(t)−ax2(t)] $ |
and
$ g(x(t),t)=[0−(b+e)x2(t)]. $ |
Consider the initial state $ x_0 = (0.4, 0, 3)^T $, where $ x(t) $ denotes the system's state vector and $ x_1(t) $, $ x_2(t) $ are the state components of $ x(t) $. Parameters $ a = 0.08 $, $ b = 0.03 $, $ c = 0.01 $, $ d = 0.99 $, and $ e = 0.03 $. We select the Lyapunov function $ V(x) = x_1^2+x_2^2+0.1x_1x_2 $. Then we define the aperiodically intermittent controller as follows:
$ u(t)=[0−x1(tm,i)−x2(tm,i)]. $ | (4.2) |
Then, from Assumptions 2.2 and 2.5, we can obtain
$ |f(x(t),t)|2≤x22(t)+3d2x21(t)+3c2x21(t)+3a2x22(t);|g(x(t),t)|2≤(b+e)2x22(t);|α(q(x(tm,i)))−α(x(t))|2≤2|−q(x1(tm,i))+x1(t)|2+2|−q(x2(tm,i))+x2(t)|2;∂V(x,t)∂x≤2.1|x|. $ |
Hence, according to Assumptions 2.3 and 2.5, we choose the appropriate parameters $ L_1 = 1.8 $, $ L_2 = 0.15 $, $ L_3 = 1.42 $, and $ L_4 = 2.1 $. Then, from Assumption 2.4, $ \varphi_1 $ and $ \varphi_2 $ can be set as $ 0.5 $ and $ -2.8 $. Next, we select the appropriate parameters on the basis of the results of Lemma 3.1 and Theorem 3.1: $ \delta = 0.01 $, $ \epsilon = 0.01 $, $ \lambda = 0.01 $, and $ \Delta_1 = 0.14 $. This makes it possible to calculate the roots of the equation $ \mu_1+\check{\beta}_1e^{\mu_1\Delta_1}+\hat{\beta}_1 = 0 $ in Theorem 3.1, selecting the appropriate $ \tilde{\mu}_1 $. Assume the maximum control interval $ \omega = 2.5 $ and the minimum working interval $ \theta = 1.9 $. From Definitions 2.1 and 2.2, let $ \varepsilon_1 = 0.51 $ and $ \varepsilon_2 = 0.55 $. Substituting into Eq (3.13) in Theorem 3.1 yields
$ −1.6665N(0,t)−ln0.2723+ln0.2861≤0,N(0,t)≥1. $ |
Further, by Definition 2.2, let $ \varrho = 0.07 $ and $ \tau = 1 $, and use Formula (3.14) from Theorem 3.1
$ −1.6665N(0,t)−ln0.0009+ln0.2861≤0,N(0,t)≥3. $ |
In summary, we can see that the system is not only FTS $ (w.r.t) $ $ (7.3, 0.51, 0.55) $ when $ t\in [0, 7.3] $ under the aperiodically intermittent ETM (3.1) with state quantization, but is also FTCS $ (w.r.t) $ $ (7.3, 0.51, 0.55, 0.07, 0.5) $ when $ t\in [6.8, 7.3] $ as shown in Figure 5. The state trajectory of the system, the ETM (3.1), the state quantization trajectory, and the intermittent controller are shown in Figures 6–9. As can be seen from Figures 5 and 6, the system $ (4.1) $ is not only FTCS but also has Lyapunov stability. Figure 6 shows the intermittent state quantization curve trajectory implemented on the basis of Figure 5. The ETM (3.1) is represented by Figure 7. The controller (4.2) is represented by Figure 8.
Similarly, we choose the maximum control interval $ \omega = 2.5 $, the minimum working interval $ \theta = 1.6 $, and the other parameters are the same as in Theorem 3.1, then we can find the solution to equation $ \mu_2+\check{\beta}_1e^{\mu_2\Delta_2}+\hat{\beta}_2 = 0 $ in Theorem 3.2, selecting the appropriate $ \tilde{\mu}_2 $. Further we set $ \varepsilon_1 = 0.51 $ and $ \varepsilon_2 = 0.55 $, replacing Eq (3.39) in Theorem 3.2 yields
$ −1.1381N(0,t)−ln0.2723+ln0.2861≤0,N(0,t)≥1. $ |
Further by Definition 2.2, let $ \varrho = 0.09 $ and $ \tau = 1 $, use formula (3.40) from Theorem 3.2
$ −1.1381N(0,t)−ln0.0109+ln0.2861≤0,N(0,t)≥3. $ |
Therefore, it can be obtained that the system (4.1) is FTS $ (w.r.t) $ $ (7.3, 0.51, 0.55) $ when $ t\in [0, 7.3] $ under aperiodically intermittent ETM (3.2) with state quantization and is FTCS $ (w.r.t) $ $ (7.3, 0.51, 0.55, 0.09, 0.5) $ when $ t\in [6.8, 7.3] $, as shown in Figure 10. Figures 11–14 represent the state quantization trajectory, the ETM (3.2), the intermittent controller, and the system state trajectory, respectively. Similarly, as shown in Figures 10 and 14, it can be seen that in Theorem 3.2, the system (4.1) is not only FTS but also has Lyapunov stability.
If we compare Figure 7 with Figure 12, it is clear that the number of ETM (3.1) communications is 118 and the number of ETM (3.2) communications is 100. Thus by decreasing $ \theta $, the number of communications is reduced to some extent. According to Remark 3.2, due to the different schemes of the two ETMs, the first scheme is chosen if all the states of the system are to be quantized in a finite time, and the second scheme is chosen if the states of the system are to be quantized in a certain part of the system in a finite time, as shown in Figures 6 and 11. Since we use intermittent state quantization, if the first scheme is chosen, $ \theta $ can be increased appropriately to achieve better quantization. If the second scheme is chosen, $ \theta $ can be decreased appropriately as a way to reduce the work burden of the controller and achieve a local quantization effect.
Furthermore, in Example 1, the number of communications under different control methods and trigger mechanisms is investigated, as shown in Table 1, and it can be clearly seen that there is a significant reduction in the number of communications under the effect of APIC and ETMs. In addition, by adjusting the suspension time $ \epsilon $ and the triggering parameter $ \lambda $, the number of communications can also be affected, as shown in Table 2.
Different trigger mechanisms | Theorem 3.1 | Theorem 3.2 | |
Continuous control | Time-triggered mechanism | 655 | 658 |
Event-triggered mechanism | 128 | 122 | |
Intermittent control | Time-triggered mechanism | 594 | 554 |
Event-triggered mechanism | 118 | 100 |
$ \epsilon $ | $ \lambda $ | Theorem 3.1 | Theorem 3.2 |
0.1 | 0.01 | 82 | 48 |
0.01 | 0.01 | 118 | 100 |
0.001 | 0.01 | 124 | 114 |
0.1 | 0.05 | 47 | 32 |
0.01 | 0.05 | 55 | 50 |
0.001 | 0.05 | 57 | 52 |
Example 2. To further verify the validity of the proposed theory, we consider the following stochastic nonlinear system whose parameters contain:
$ f(x(t),t)=[0.1sin(x1(t))+0.1x2(t)+0.2u(t)0.1x1(t)−0.2x2(t)] $ |
and
$ g(x(t),t)=[0.1x1(t)0]. $ |
Where $ t \geq 0 $, consider the initial state $ x_0 = (0.5, -0, 5)^T $ and $ x(t) $ is defined as the state vector and $ x_1(t) $, $ x_2(t) $ as the state components of $ x(t) $. We select the Lyapunov function $ V(x) = 0.1x_1^2+0.1x_2^2 $. Then we define the aperiodically intermittent controller as follows:
$ u(t)=[−2x1(t)0]. $ | (4.3) |
Similarly, according to Assumptions 2.3 and 2.5, we choose the appropriate parameters $ L_1 = 0.6 $, $ L_2 = 0.11 $, $ L_3 = 2.1 $, and $ L_4 = 0.21 $. Then, from Assumption 2.4, $ \varphi_1 $, $ \varphi_2 $ can be set as $ 0.5 $ and $ -3.4 $. We select the appropriate parameters according to the results of Lemma 3.1 and Theorem 3.1, $ \delta = 0.01 $, $ \epsilon = 0.01 $, $ \lambda = 0.01 $, and $ \Delta_1 = 0.45 $. Similar to Example 1, we can also calculate the roots of equation $ \mu_1+\check{\beta}_1e^{\mu_1\Delta_1}+\hat{\beta}_1 = 0 $ according to the above parameters. Assume the maximum control interval $ \omega = 2.5 $ and the minimum working interval $ \theta = 2 $. From Definitions 2.1 and 2.2, let $ \varepsilon_1 = 0.75 $ and $ \varepsilon_2 = 0.8 $, then substituting into Eq (3.13) in Theorem 3.1 yields
$ −1.5412N(0,t)−ln0.0576+ln0.0619≤0,N(0,t)≥1. $ |
Furthermore, by Definition 2.2, let $ \varrho = 0.083 $ and $ \tau = 0.7 $, use formula (3.14) from Theorem 3.1
$ −1.5412N(0,t)−ln0.0007+ln0.2861≤0,N(0,t)≥3. $ |
In summary, we can see that the system is not only FTS $ (w.r.t) $ $ (8.5, 0.75, 0.8) $ when $ t\in [0, 8.5] $ under the aperiodically intermittent ETM (3.1) with state quantization, but also FTCS $ (w.r.t) $ $ (8.5, 0.75, 0.8, 0.083, 0.7) $ when $ t\in [7.8, 8.5] $, as shown in Figure 15. The state trajectory of the system, the ETM (3.1), the state quantization trajectory, and the intermittent controller are shown in Figures 16–19. As can be seen from Figures 15 and 19, the system $ (4.1) $ is not only FTCS but also has Lyapunov stability. Figure 16 shows the intermittent state quantization curve trajectory implemented on the basis of Figure 15. The ETM (3.1) is represented by Figure 17. The controller (4.2) is represented by Figure 18.
Similarly, choose the maximum control interval $ \omega = 2.5 $ and the minimum working interval $ \theta = 1.8 $, and the other parameters are the same as in Theorem 3.1. Furthermore, we set $ \varepsilon_1 = 0.75 $ and $ \varepsilon_2 = 0.8 $, and then replacing Eq (3.39) in Theorem 3.2 yields
$ −1.1658N(0,t)−ln0.0576+ln0.2861≤0,N(0,t)≥1. $ |
Furthermore, by Definition 2.2, let $ \varrho = 0.15 $ and $ \tau = 0.8 $, and use formula (3.40) from Theorem 3.2
$ −1.1381N(0,t)−ln0.0109+ln0.2861≤0,N(0,t)≥3. $ |
Therefore, it can be seen that the system (4.1) is FTS $ (w.r.t) $ $ (7.8, 0.75, 0.8) $ when $ t\in [0, 7.8] $ under aperiodically intermittent ETM (3.2) with state quantization and is FTCS $ (w.r.t) $ $ (7.8, 0.75, 0.8, 0.15, 0.8) $ when $ t\in [7.0, 7.8] $ as shown in Figure 20. Figures 21–24 represent the state quantization trajectory, the ETM (3.2), the intermittent controller, and the system state trajectory, respectively. Similarly, as shown in Figures 10 and 14, it can be seen that in Theorem 3.2, the system (4.1) is not only FTS but also has Lyapunov stability. Comparing Figure 7 with Figure 12, it is clear that the number of ETM (3.1) communications is 33 and the number of ETM (3.2) communications is 50. If we set the controller to $ u(t) = 0 $, the system is unstable, as shown in Figure 25.
This study uses ETC and APIC to investigate the FTS of stochastic nonlinear systems. First, the Zeno behavior is avoided by designing the hover time in ETM. After that, the state quantization strategy is introduced to implement the two triggering schemes, and quantization error estimation and sampling error estimation are used to further implement the FTS and the FTCS. The viability and efficacy of the theoretical results of state quantization and APIC are confirmed in two numerical examples, as are the feasibility and validity of the two ETMs that have been proposed. Finally, different triggering schemes can be selected by adjusting the size of the working interval to achieve different effects within a finite time, which further saves resources. However, since the logarithmic quantizer in Assumption 2.1 of this paper becomes more error-prone as the quantization level increases, exploring alternative quantization methods, such as dynamic quantization, could be a promising direction for future research. In addition, Assumptions 2.3 and 2.5 are more applicable to cases without time delay; therefore, these assumptions may no longer hold when studying a stochastic nonlinear time delay system. However, a similar approach is provided in [14]. Future research work on stochastic nonlinear systems containing delays with dynamic ETC is also needed.
Biwen Li: Supervision, writing–review and editing; Guangyu Wang: Writing–original draft. Both authors have read and approved the final version of the manuscript for publication.
The authors declare that they have not used artificial intelligence (AI) tools in the creation of this paper.
The authors would like to thank the editors and referees for their very helpful comments and suggestions.
The authors declare no conflicts of interest.
Parameters | |
$ t_{m, i} $ | Event-triggered sampling instants, where $ 0\leq i\leq \lceil \frac{s_m}{\epsilon} \rceil $, $ \lceil \frac{s_m}{\epsilon} \rceil $ is the maximum number of communications on the interval $ [t_m, t_m+s_m) $ |
$ t_m $ | Starting point of the workspace |
$ s_m $ | Length of the working interval |
$ \theta $ | Minimum working interval length |
$ \omega $ | Maximum control interval length |
$ q(v) $ | System state quantization |
$ \delta $ | Constant related to the quantization density $ \rho $ and |
$ L_i $ | Positive constants in Assumptions 2.3 and 2.5 $ (i = 1, 2, 3, 4) $ |
$ \varepsilon_1 $ | Upper bound on the initial state of the system |
$ \varepsilon_2 $ | An upper bound on the state $ E|x(t)| $ of the system in finite time $ T $ |
$ \varrho $ | During the time interval $ [T-\tau, T] $, the state $ E|x(t)| $ of the system does not exceed $ \varrho $ |
$ \epsilon $ | Suspension time, indicating that the next trigger moment is executed after at least $ \epsilon $ |
$ \lambda $ | Event-trigger related parameters for adjusting the trigger thresholds |
$ \kappa_i $ | The coefficients in Lemmas 3.1 and 3.2, consisting of $ \delta $, $ \epsilon $, $ \lambda $, $ L_1 $, $ L_2 $, and $ L_3 $ |
$ \mathcal{N}(0, t) $ | Number of control intervals on interval $ (0, T] $ |
$ \hat{\beta_i} $, $ \check{\beta_i} $ | The correlation coefficients in Theorems 3.1 and 3.2, consisting of $ L_1 $, $ L_2 $, $ L_3 $, $ L_4 $, $ \epsilon $, $ c_1 $, $ \varphi_2 $, $ \kappa_1 $, and $ \kappa_2 $, where $ \varphi_1 $, $ \varphi_2 $ and $ c_1 $, $ c_2 $ are given by Assumption 2.4 $ (i = 1, 2) $ |
$ \Delta_i $ | Upper bound on the execution time between events in Theorems 3.1 and 3.2 $ (i = 1, 2) $ |
[1] |
Schwab SR, Pereira JP, Matloubian M, et al. (2005) Lymphocyte sequestration through S1P lyase inhibition and disruption of S1P gradients. Science 309: 1735-1739. doi: 10.1126/science.1113640
![]() |
[2] |
Matloubian M, Lo CG, Cinamon G, et al. (2004) Lymphocyte egress from thymus and peripheral lymphoid organs is dependent on S1P receptor 1. Nature 427: 355-360. doi: 10.1038/nature02284
![]() |
[3] | Tarling EJ, de Aguiar Vallim TQ, Edwards PA (2013) Role of ABC transporters in lipid transport and human disease. Trends Endocrinol Metab 4: 342-350. |
[4] |
Takabe K, Spiegel S (2014) Export of sphingosine-1-phosphate and cancer progression. J Lipid Res 55: 1839-1846. doi: 10.1194/jlr.R046656
![]() |
[5] |
Kornhuber J, Müller CP, Becker KA, et al. (2014) The ceramide system as a novel antidepressant target. Trends Pharmacol Sci 35: 293-304. doi: 10.1016/j.tips.2014.04.003
![]() |
[6] |
Ito M, Okino N, Tani M. (2014) New insight into the structure, reaction mechanism, and biological functions of neutral ceramidase. Biochim Biophys Acta 1841: 682-691. doi: 10.1016/j.bbalip.2013.09.008
![]() |
[7] |
Kumar A, Saba JD (2009) Lyase to live by: sphingosine phosphate lyase as a therapeutic target. Expert Opin Ther Targets 13: 1013-1025. doi: 10.1517/14728220903039722
![]() |
[8] |
Pyne S, Kong K-C, Darroch PI (2004) Lysophosphatidic acid and sphingosine 1-phosphate biology: the role of lipid phosphate phosphatases. Semin Cell Dev Biol 15: 491-501. doi: 10.1016/j.semcdb.2004.05.007
![]() |
[9] |
Blaho VA, Hla T (2014) An update on the biology of sphingosine 1-phosphate receptors. J Lipid Res 55: 1596-1608. doi: 10.1194/jlr.R046300
![]() |
[10] |
Nishi T, Kobayashi N, Hisano Y, et al. (2014) Molecular and physiological functions of sphingosine 1-phosphate transporters. Biochim Biophys Acta 1841: 759-765. doi: 10.1016/j.bbalip.2013.07.012
![]() |
[11] |
Hisano Y, Nishi T, Kawahara A (2012) The functional roles of S1P in immunity. J Biochem 152: 305-311. doi: 10.1093/jb/mvs090
![]() |
[12] |
Mitra P, Oskeritzian CA, Payne SG, et al. (2006) Role of ABCC1 in export of sphingosine-1-phosphate from mast cells. Proc Natl Acad Sci USA 103: 16394-16399. doi: 10.1073/pnas.0603734103
![]() |
[13] |
Tanfin Z, Serrano-Sanchez M, Leiber D (2011) ATP-binding cassette ABCC1 is involved in the release of sphingosine 1-phosphate from rat uterine leiomyoma ELT3 cells and late pregnant rat myometrium. Cell Signal 23: 1997-2004. doi: 10.1016/j.cellsig.2011.07.010
![]() |
[14] |
Nieuwenhuis B, Lüth A, Chun J, et al. (2009) Involvement of the ABC-transporter ABCC1 and the sphingosine 1-phosphate receptor subtype S1P(3) in the cytoprotection of human fibroblasts by the glucocorticoid dexamethasone. J Mol Med (Berl) 87: 645-657. doi: 10.1007/s00109-009-0468-x
![]() |
[15] |
Cartwright TA, Campos CR, Cannon RE, et al. (2013) Mrp1 is essential for sphingolipid signaling to p-glycoprotein in mouse blood-brain and blood-spinal cord barriers. J Cereb Blood Flow Metab 33: 381-388. doi: 10.1038/jcbfm.2012.174
![]() |
[16] |
Takabe K, Kim RH, Allegood JC, et al. (2010) Estradiol induces export of sphingosine 1-phosphate from breast cancer cells via ABCC1 and ABCG2. J Biol Chem 285: 10477-10486. doi: 10.1074/jbc.M109.064162
![]() |
[17] | Sato K, Malchinkhuu E, HoriuchiY, et al. (2007) Critical role of ABCA1 transporter in sphingosine 1-phosphate release from astrocytes. J Neurochem 103: 2610-2619. |
[18] |
Lee Y-M, Venkataraman K, Hwang S-I, et al. (2007) A novel method to quantify sphingosine 1-phosphate by immobilized metal affinity chromatography (IMAC). Prostaglandins Other Lipid Mediat 84: 154-162. doi: 10.1016/j.prostaglandins.2007.08.001
![]() |
[19] |
Hisano Y, Kobayashi N, Kawahara A, et al. (2011) The sphingosine 1-phosphate transporter, SPNS2, functions as a transporter of the phosphorylated form of the immunomodulating agent FTY720. J Biol Chem 286: 1758-1766. doi: 10.1074/jbc.M110.171116
![]() |
[20] |
Hänel P, Andréani P, Gräler MH (2007) Erythrocytes store and release sphingosine 1-phosphate in blood. FASEB J 21: 1202-1209. doi: 10.1096/fj.06-7433com
![]() |
[21] |
Venkataraman K, Lee Y-M, Michaud J, et al. (2008) Vascular endothelium as a contributor of plasma sphingosine 1-phosphate. Circ Res 102: 669-676. doi: 10.1161/CIRCRESAHA.107.165845
![]() |
[22] |
Yatomi Y, Igarashi Y, Yang L, et al. (1997) Sphingosine 1-phosphate, a bioactive sphingolipid abundantly stored in platelets, is a normal constituent of human plasma and serum. J Biochem 121: 969-973. doi: 10.1093/oxfordjournals.jbchem.a021681
![]() |
[23] | Yatomi Y, Ruan F, Hakomori S, et al. (1995) Sphingosine-1-phosphate: a platelet-activating sphingolipid released from agonist-stimulated human platelets. Blood 86: 193-202. |
[24] | Maceyka M, Milstien S, Spiegel S. (2009) Sphingosine-1-phosphate: the Swiss army knife of sphingolipid signaling. J Lipid Res 50: S272-S276. |
[25] | Bode C, Sensken S-C, Peest U, et al. (2010) Erythrocytes serve as a reservoir for cellular and extracellular sphingosine 1-phosphate. J Cell Biochem 109: 1232-1243. |
[26] |
Pappu R, Schwab SR, Cornelissen I, et al. (2007) Promotion of lymphocyte egress into blood and lymph by distinct sources of sphingosine-1-phosphate. Science 316: 295-298. doi: 10.1126/science.1139221
![]() |
[27] | Kobayashi N, Nishi T, Hirata T, et al. (2006) Sphingosine 1-phosphate is released from the cytosol of rat platelets in a carrier-mediated manner. J Lipid Res 47: 614-621. |
[28] |
Kobayashi N, Kobayashi N, Yamaguchi A, et al. (2009) Characterization of the ATP-dependent sphingosine 1-phosphate transporter in rat erythrocytes. J Biol Chem 284: 21192-21200. doi: 10.1074/jbc.M109.006163
![]() |
[29] |
Bouma HR, Kroese FGM, Kok JW, et al. (2011) Low body temperature governs the decline of circulating lymphocytes during hibernation through sphingosine-1-phosphate. Proc Natl Acad Sci USA 108: 2052-2057. doi: 10.1073/pnas.1008823108
![]() |
[30] |
Lamkanfi M, Mueller JL, Vitari AC, et al. (2009) Glyburide inhibits the cryopyrin/Nalp3 inflammasome. J Cell Biol 187: 61-70. doi: 10.1083/jcb.200903124
![]() |
[31] | Ancellin N, Colmont C, Su J, et al. (2002) Extracellular export of sphingosine kinase-1 enzyme. Sphingosine 1-phosphate generation and the induction of angiogenic vascular maturation. J Biol Chem 277: 6667-6675. |
[32] |
Venkataraman K, Thangada S, Michaud J, et al. (2006) Extracellular export of sphingosine kinase-1a contributes to the vascular S1P gradient. Biochem J 397: 461-471. doi: 10.1042/BJ20060251
![]() |
[33] |
Rosen H, Stevens RC, Hanson M, et al. (2013) Sphingosine-1-phosphate and its receptors: structure, signaling, and influence. Annu Rev Biochem 82: 637-662. doi: 10.1146/annurev-biochem-062411-130916
![]() |
[34] |
Osborne N, Brand-Arzamendi K, Ober EA, et al. (2008) The spinster homolog, two of hearts, is required for sphingosine 1-phosphate signaling in zebrafish. Curr Biol 18: 1882-1888. doi: 10.1016/j.cub.2008.10.061
![]() |
[35] |
Kawahara A, Nishi T, Hisano Y, et al. (2009) The sphingolipid transporter spns2 functions in migration of zebrafish myocardial precursors. Science 323: 524-527. doi: 10.1126/science.1167449
![]() |
[36] |
Mandala S, Hajdu R, Bergstrom J, et al. (2002) Alteration of lymphocyte trafficking by sphingosine-1-phosphate receptor agonists. Science 296: 346-349. doi: 10.1126/science.1070238
![]() |
[37] |
Nagahashi M, Kim EY, Yamada A, et al. (2013) Spns2, a transporter of phosphorylated sphingoid bases, regulates their blood and lymph levels, and the lymphatic network. FASEB J 27: 1001-1011. doi: 10.1096/fj.12-219618
![]() |
[38] | Fukuhara S, Simmons S, Kawamura S, et al. (2012) The sphingosine-1-phosphate transporter Spns2 expressed on endothelial cells regulates lymphocyte trafficking in mice. J Clin Invest 122 : 1416-1426. |
[39] | Hisano Y, Kobayashi N, Yamaguchi A, et al. (2012) Mouse SPNS2 functions as a sphingosine-1-phosphate transporter in vascular endothelial cells. PLoS One 7: e38941. |
[40] |
Mendoza A, Bréart B, Ramos-Perez WD, et al. (2012) The transporter Spns2 is required for secretion of lymph but not plasma sphingosine-1-phosphate. Cell Rep 2: 1104-1110. doi: 10.1016/j.celrep.2012.09.021
![]() |
[41] |
Nijnik A, Clare S, Hale C, et al. (2012) The role of sphingosine-1-phosphate transporter Spns2 in immune system function. J Immunol 189: 102-111. doi: 10.4049/jimmunol.1200282
![]() |
[42] |
Brizuela L, Martin C, Jeannot P, et al. (2014) Osteoblast-derived sphingosine 1-phosphate to induce proliferation and confer resistance to therapeutics to bone metastasis-derived prostate cancer cells. Mol Oncol 8: 1181-1195. doi: 10.1016/j.molonc.2014.04.001
![]() |
[43] |
Zachariah MA, Cyster JG (2010) Neural crest-derived pericytes promote egress of mature thymocytes at the corticomedullary junction. Science 328: 1129-1135. doi: 10.1126/science.1188222
![]() |
[44] |
Ansel KM, Cyster JG (2001) Chemokines in lymphopoiesis and lymphoid organ development. Current Opinion in Immunology 13: 172-179. doi: 10.1016/S0952-7915(00)00201-6
![]() |
[45] |
Luo ZJ, Tanaka T, Kimura F, et al. (1999) Analysis of the mode of action of a novel immunosuppressant FTY720 in mice. Immunopharmacology 41: 199-207. doi: 10.1016/S0162-3109(99)00004-1
![]() |
[46] | Chiba K, Yanagawa Y, Masubuchi Y, et al. (1998) FTY720, a novel immunosuppressant, induces sequestration of circulating mature lymphocytes by acceleration of lymphocyte homing in rats. I. FTY720 selectively decreases the number of circulating mature lymphocytes by acceleration of lymphocyte homing. J Immunol 160: 5037-5044. |
[47] |
Schwab SR, Cyster JG (2007) Finding a way out: lymphocyte egress from lymphoid organs. Nat Immunol 8: 1295-1301. doi: 10.1038/ni1545
![]() |
[48] |
Ito K, Anada Y, Tani M, et al. (2007) Lack of sphingosine 1-phosphate-degrading enzymes in erythrocytes. Biochem Biophys Res Commun 357: 212-217. doi: 10.1016/j.bbrc.2007.03.123
![]() |
[49] |
Murata N, Sato K, Kon J, et al. (2000) Interaction of sphingosine 1-phosphate with plasma components, including lipoproteins, regulates the lipid receptor-mediated actions. Biochem J 352: 809-815. doi: 10.1042/0264-6021:3520809
![]() |
[50] |
Allende ML, Sasaki T, Kawai H, et al. (2004) Mice deficient in sphingosine kinase 1 are rendered lymphopenic by FTY720. J Biol Chem 279: 52487-52492. doi: 10.1074/jbc.M406512200
![]() |
[51] |
Bréart B, Ramos-Perez WD, Mendoza A, et al. (2011) Lipid phosphate phosphatase 3 enables efficient thymic egress. J Exp Med 208: 1267-1278. doi: 10.1084/jem.20102551
![]() |
[52] |
Pham THM, Baluk P, Xu Y, et al. (2010) Lymphatic endothelial cell sphingosine kinase activity is required for lymphocyte egress and lymphatic patterning. J Exp. Med 207: 17-27. doi: 10.1084/jem.20091619
![]() |
[53] |
Mildner A, Yona S, Jung S (2013) A close encounter of the third kind: monocyte-derived cells. Adv Immunol 120: 69-103. doi: 10.1016/B978-0-12-417028-5.00003-X
![]() |
[54] |
Kolaczkowska E, Kubes P (2013) Neutrophil recruitment and function in health and inflammation. Nat Rev Immunol 13: 159-175. doi: 10.1038/nri3399
![]() |
[55] |
Roviezzo F, Brancaleone V, De Gruttola L, et al. (2011) Sphingosine-1-phosphate modulates vascular permeability and cell recruitment in acute inflammation in vivo. J Pharmacol Exp Ther 337: 830-837. doi: 10.1124/jpet.111.179168
![]() |
[56] |
Olivera A, Rivera J (2011) An emerging role for the lipid mediator sphingosine-1-phosphate in mast cell effector function and allergic disease. Ad Exp Med Biol 716: 123-142. doi: 10.1007/978-1-4419-9533-9_8
![]() |
[57] | Finley A, Chen Z, Esposito E, et al. (2013) Sphingosine 1-phosphate mediates hyperalgesia via a neutrophil-dependent mechanism. PLoS One 8: e55255. |
[58] |
Florey O, Haskard DO (2009) Sphingosine 1-phosphate enhances Fc gamma receptor-mediated neutrophil activation and recruitment under flow conditions. J Immunol 183: 2330-2336. doi: 10.4049/jimmunol.0901019
![]() |
[59] |
Sun WY, Abeynaike LD, Escarbe S, et al. (2012) Rapid histamine-induced neutrophil recruitment is sphingosine kinase-1 dependent. Am J Pathol 180: 1740-1750. doi: 10.1016/j.ajpath.2011.12.024
![]() |
[60] |
Lewis ND, Haxhinasto SA, Anderson SM, et al. (2013) Circulating monocytes are reduced by sphingosine-1-phosphate receptor modulators independently of S1P3. J Immunol 190: 3533-3540. doi: 10.4049/jimmunol.1201810
![]() |
[61] |
Zemann B, Urtz N, Reuschel R, et al. (2007) Normal neutrophil functions in sphingosine kinase type 1 and 2 knockout mice. Immunol Lett 109: 56-63. doi: 10.1016/j.imlet.2007.01.001
![]() |
[62] |
Linke B, Schreiber Y, Zhang DD, et al. (2012) Analysis of sphingolipid and prostaglandin synthesis during zymosan-induced inflammation. Prostaglandins Other Lipid Mediat. 99: 15-23. doi: 10.1016/j.prostaglandins.2012.06.002
![]() |
[63] | Gräler MH (2012) The role of sphingosine 1-phosphate in immunity and sepsis. Am J Clin Exp Immunol 1: 90-100. |
[64] |
Ogle ME, Sefcik LS, Awojoodu AO, et al. (2014) Engineering in vivo gradients of sphingosine-1-phosphate receptor ligands for localized microvascular remodeling and inflammatory cell positioning. Acta Biomater 10: 4704-4714. doi: 10.1016/j.actbio.2014.08.007
![]() |
[65] |
Allende ML, Bektas M, Lee BG, et al. (2011) Sphingosine-1-phosphate lyase deficiency produces a pro-inflammatory response while impairing neutrophil trafficking. J Biol Chem 286: 7348-7358. doi: 10.1074/jbc.M110.171819
![]() |
[66] |
Belz GT, Heath WR, Carbone FR (2002) The role of dendritic cell subsets in selection between tolerance and immunity. Immunol Cell Biol 80: 463-468. doi: 10.1046/j.1440-1711.2002.01116.x
![]() |
[67] |
Singer II, Tian M, Wickham LA, et al. (2005) Sphingosine-1-phosphate agonists increase macrophage homing, lymphocyte contacts, and endothelial junctional complex formation in murine lymph nodes. J Immunol 175: 7151-7161. doi: 10.4049/jimmunol.175.11.7151
![]() |
[68] | Lan YY, De Creus A, Colvin BL, et al. (2005). The sphingosine-1-phosphate receptor agonist FTY720 modulates dendritic cell trafficking in vivo. Am J Transplant 2649-2659. |
[69] | Idzko M, Panther E, Corinti S, et al. (2002) Sphingosine 1-phosphate induces chemotaxis of immature and modulates cytokine-release in mature human dendritic cells for emergence of Th2 immune responses. FASEB J 16: 625-627. |
[70] |
Czeloth N, Bernhardt G, Hofmann F, et al. (2005) Sphingosine-1-phosphate mediates migration of mature dendritic cells. J Immunol 175: 2960-2967. doi: 10.4049/jimmunol.175.5.2960
![]() |
[71] |
Oskeritzian CA (2015) Mast cell plasticity and sphingosine-1-phosphate in immunity, inflammation and cancer. Mol Immunol 63:104-112. doi: 10.1016/j.molimm.2014.03.018
![]() |
[72] |
Jolly PS, Bektas M, Olivera A, et al. (2004) Transactivation of sphingosine-1-phosphate receptors by FcepsilonRI triggering is required for normal mast cell degranulation and chemotaxis. J Exp Med 199: 959-970. doi: 10.1084/jem.20030680
![]() |
[73] |
Olivera A, Mizugishi K, Tikhonova A, et al. (2007) The sphingosine kinase-sphingosine-1-phosphate axis is a determinant of mast cell function and anaphylaxis. Immunity 26: 287-297. doi: 10.1016/j.immuni.2007.02.008
![]() |
[74] |
Oskeritzian CA, Price MM, Hait NC, et al. (2010) Essential roles of sphingosine-1-phosphate receptor 2 in human mast cell activation, anaphylaxis, and pulmonary edema. J Exp Med 207: 465-474. doi: 10.1084/jem.20091513
![]() |
Different trigger mechanisms | Theorem 3.1 | Theorem 3.2 | |
Continuous control | Time-triggered mechanism | 655 | 658 |
Event-triggered mechanism | 128 | 122 | |
Intermittent control | Time-triggered mechanism | 594 | 554 |
Event-triggered mechanism | 118 | 100 |
$ \epsilon $ | $ \lambda $ | Theorem 3.1 | Theorem 3.2 |
0.1 | 0.01 | 82 | 48 |
0.01 | 0.01 | 118 | 100 |
0.001 | 0.01 | 124 | 114 |
0.1 | 0.05 | 47 | 32 |
0.01 | 0.05 | 55 | 50 |
0.001 | 0.05 | 57 | 52 |
Different trigger mechanisms | Theorem 3.1 | Theorem 3.2 | |
Continuous control | Time-triggered mechanism | 655 | 658 |
Event-triggered mechanism | 128 | 122 | |
Intermittent control | Time-triggered mechanism | 594 | 554 |
Event-triggered mechanism | 118 | 100 |
$ \epsilon $ | $ \lambda $ | Theorem 3.1 | Theorem 3.2 |
0.1 | 0.01 | 82 | 48 |
0.01 | 0.01 | 118 | 100 |
0.001 | 0.01 | 124 | 114 |
0.1 | 0.05 | 47 | 32 |
0.01 | 0.05 | 55 | 50 |
0.001 | 0.05 | 57 | 52 |