
Citation: Stefan G. Hofmann, Elizabeth A. Mundy, Joshua Curtiss. Neuroenhancement of Exposure Therapy in Anxiety Disorders[J]. AIMS Neuroscience, 2015, 2(3): 123-138. doi: 10.3934/Neuroscience.2015.3.123
[1] | B. Spagnolo, D. Valenti, A. Fiasconaro . Noise in ecosystems: A short review. Mathematical Biosciences and Engineering, 2004, 1(1): 185-211. doi: 10.3934/mbe.2004.1.185 |
[2] | Meng Fan, Bingbing Zhang, Michael Yi Li . Mechanisms for stable coexistence in an insect community. Mathematical Biosciences and Engineering, 2010, 7(3): 603-622. doi: 10.3934/mbe.2010.7.603 |
[3] | Yanjie Hong, Wanbiao Ma . Sufficient and necessary conditions for global attractivity and stability of a class of discrete Hopfield-type neural networks with time delays. Mathematical Biosciences and Engineering, 2019, 16(5): 4936-4946. doi: 10.3934/mbe.2019249 |
[4] | Yun Kang, Sourav Kumar Sasmal, Amiya Ranjan Bhowmick, Joydev Chattopadhyay . Dynamics of a predator-prey system with prey subject to Allee effects and disease. Mathematical Biosciences and Engineering, 2014, 11(4): 877-918. doi: 10.3934/mbe.2014.11.877 |
[5] | Yufei Wang, Huidong Cheng, Qingjian Li . Dynamic analysis of wild and sterile mosquito release model with Poincaré map. Mathematical Biosciences and Engineering, 2019, 16(6): 7688-7706. doi: 10.3934/mbe.2019385 |
[6] | N. H. AlShamrani, A. M. Elaiw . Stability of an adaptive immunity viral infection model with multi-stages of infected cells and two routes of infection. Mathematical Biosciences and Engineering, 2020, 17(1): 575-605. doi: 10.3934/mbe.2020030 |
[7] | Tainian Zhang, Zhixue Luo, Hao Zhang . Optimal harvesting for a periodic $ n $-dimensional food chain model with size structure in a polluted environment. Mathematical Biosciences and Engineering, 2022, 19(8): 7481-7503. doi: 10.3934/mbe.2022352 |
[8] | Balázs Boros, Stefan Müller, Georg Regensburger . Complex-balanced equilibria of generalized mass-action systems: necessary conditions for linear stability. Mathematical Biosciences and Engineering, 2020, 17(1): 442-459. doi: 10.3934/mbe.2020024 |
[9] | Salvatore Rionero . A nonlinear $L^2$-stability analysis for two-species population dynamics with dispersal. Mathematical Biosciences and Engineering, 2006, 3(1): 189-204. doi: 10.3934/mbe.2006.3.189 |
[10] | Shuixian Yan, Sanling Yuan . Critical value in a SIR network model with heterogeneous infectiousness and susceptibility. Mathematical Biosciences and Engineering, 2020, 17(5): 5802-5811. doi: 10.3934/mbe.2020310 |
Population dynamics is one of the main issues of theoretical biomathematics and has aroused the interest of many scholars in the fields of mathematical biology. A lot of methods have been presented and developed to study the evolution of population dynamics. It is clear that establishing mathematical models is the prerequisite for analysis of population dynamics. Until now, researchers have proposed a variety of models, represented by difference equations or differential equations [1,2,3].
As is well known, no species can exist in isolation, all populations must be related to the others directly or indirectly, and mutualism, parasitism, competition and predation are the four most widespread direct relationships in the ecosystem [4]. Based on these four relationships, researchers have established a variety of models to study the dynamics of the population, such as the Lotka-Volterra models, Leslie-Gower models and predator-prey models [5,6,7,8]. In recent years, many researchers began to study more complex and realistic population models and have got some interesting results [9,10,11,12,13,14]. In [15], a predator-prey system with Beddington-DeAngelis functional response was considered, and global asymptotical stability of the positive equilibrium was investigated by using divergency criterion. In [16], a ratio-dependent prey-predator model with the Allee effect was proposed, and bifurcation and stability analysis were carried out. Moreover, all possible non-degenerated phase portraits have been displayed. In [17], a simple predator-prey interaction where predator population is subjected to harvesting was considered, and different outcomes including switching of stability, oscillation and deterministic extinction were demonstrated.
On the other hand, with the development of fractional calculus, researchers have applied fractional derivatives to various fields [18,19,20,21,22,23,24,25,26,27,28,29]. Compared with the classical integer-order counterpart, fractional derivative is an outstanding instrument to describe memory and hereditary properties of various materials and processes [30]. In [31], the fractional-order predator-prey model and the fractional-order rabies model were firstly established. Moreover, existence and uniqueness of solutions, and stability of equilibrium points were studied. A comparison between the proposed fractional-order model and its integer-order counterpart was made. Since then, fractional population models have received extensive attention, and numerous results have been reported in the literature. Some different fractional Lotka-Volterra models are studied in [32,33,34]. For more details, see [35,36,37,38] and the references cited therein. In [39], stability of fractional-order nonlinear systems was studied by using Lyapunov direct method with the introduction of generalized Mittag-Leffler stability definition. It provided a new instrument to investigate the dynamics of the fractional population model. After that, the Lyapunov direct method has been widely applied to stability analysis of the fractional population model [40,41,42]. For instance, dynamics of a fractional-order predator-prey model incorporating a prey refuge was discussed in [40]. Stability of a fractional-order prey-predator system with time-delay and Monod-Haldane functional response was considered in [41]. Stability of a fractional-order two-species facultative mutualism model with harvesting was addressed in [42]. Some sufficient conditions to ensure the stability of the considered models were obtained in the aforementioned references based on the the Lyapunov direct method. Recent years, variety of interesting fractional-order population models are studied and some significant results were obtained [43,44,45].
Due to factors such as reproduction, most of the population systems have memory and hereditary effects. Thus, the fractional-order population system is more realistic than integer-order counterpart. Moreover, the integer-order system can be seemed as a special form of fractional-order system. So the analysis of fractional-order model is more general. Based on the above advantages, a new fractional-order $ N $ species model is established in this paper. In order to find general theories, the general functions are used in this model. It can be said that most of the population model can be seemed as a special form of this model. Therefore, it is valuable to analyze the stability of this model. The main contributions of this paper are as follows: First of all, a new generalized fractional order $ N $ species network is established to describe the relationship between species in an ecosystem. In addition, the existence, uniqueness and non-negativity of the solution are discussed. Moreover, the algebraic criteria for local stability and global stability are established by using the eigenvalue method and the Lyapunov direct method, respectively. Finally, the theoretical analysis is demonstrate by three examples and numerical simulations.
The rest of this paper is organized as follows. In Section 2, some definitions in fractional calculus and some stability results are introduced. In Section 3, existence, uniqueness, non-negativity of the solutions, and local and global asymptotical stability of the equilibrium point are discussed in depth. In Section 4, some numerical simulation results are presented. Finally, some conclusions are drawn in Section 5.
In this section, some definitions and lemmas in fractional calculus are recalled, which will be used later.
Definition 1. [46] The Caputo fractional derivative of a function $ f(t) $ with order $ \alpha $ is defined as
$ Dαf(t)=1Γ(n−α)∫tt0f(n)(τ)(t−τ)α+1−ndτ, n−1<α<n, $
|
(1) |
where $ \alpha > 0 $, $ t_{ 0} $ is the initial time, $ n\in\mathbb{N} $, and $ \Gamma $ is the Gamma function.
Lemma 1. [47] The equilibrium points $ x^* $ of $ D^\alpha x(t) = f(x) $ are locally asymptotically stable if all eigenvalues $ \lambda_i $ of the Jacobian matrix $ J = {\partial f}/{\partial x} $ evaluated at the equilibrium points satisfy $ |\arg(\lambda_i)| > \frac{\alpha\pi}{2} $.
Lemma 2. [48] Let $ x(t)\in\mathbb{R}^+ $ be a differentiable function. Then, for any time instant $ t\geq t_0 $
$ Dα[x(t)−x∗−x∗lnx(t)x∗]≤(1−x∗x(t))Dαx(t),x∗∈R+,∀α∈(0,1). $
|
(2) |
Lemma 3. [49] (Uniform Asymptotic Stability Theorem) Let $ x = 0 $ be an equilibrium point of $ D^\alpha x(t) = f(t, x) $, and let $ \Omega\subset R^n $ be a domain containing $ x = 0 $. Let $ V(t, x) : [t, \infty) \times \Omega\rightarrow \mathbb{R} $ be a continuously differentiable function such that
$ W1(x)≤V(t,x)≤W2(x), $
|
(3) |
and
$ DαV(t,x)≤−W3(x), $
|
(4) |
for $ t\geq0, x\in\Omega $ and $ 0 < \alpha < 1 $, where $ W_1(x), W_2(x) $ and $ W_3(x) $ are continuous positive definite functions on $ \Omega $, then $ x = 0 $ is uniformly asymptotically stable.
Remark 1. [39] If $ x = x^\ast $ is the equilibrium point of $ D^\alpha x(t) = f(t, x) $ and satisfies the conditions of Lemma 3, then $ x = x^\ast $ is uniformly asymptotically stable.
In [50], the following model is considered.
$ u′i(t)=ui(t)[ai(t)−N∑j=1bij(t)uj(t)], i=1,2,…,N, $
|
(5) |
where the functions $ a_i(t), b_{ij}(t) $ are assumed to be nonnegative and continuous for $ t\in(-\infty, \infty) $. This system is commonly called the Volterra-Lotka system for $ N $-competing species. Because of the complex relations between the species, it would be more realistic to change the functions $ b_{ij}(t)u_j(t) $ to $ f_{ij}(u_j(t)) $, so one can build a new population model.
This paper considers the following generalized fractional-order ecosystem model:
$ Dαxi(t)=Fi(x1,x2,…,xn)=xi(t)N∑j=1aijfij(xj(t)), $
|
(6) |
$ xi(t0)=xit0,i=1,2,3,…,N, $
|
where $ t_0\geq0 $ is the initial time, $ x_i(t) $ for $ i = 1, 2, 3, \ldots, N $ denotes population density of the species $ x_i $ at time $ t $, $ a_{ij} = \pm 1, 0 $. $ f_{ij}(x_j(t)) $ are continuous, non-negative and differentiable functions.
$ f_{ii}(x_i) $ are the specific growth rate of $ x_i $ in the absence of other species for $ i = 1, 2, 3, \ldots, N $. If $ x_i $ represents a producer in ecosystems, one can see that the specific growth rate of $ x_i $ is positive, so one makes $ a_{ii} > 0( = 1) $. If $ x_i $ represents a consumer in ecosystems, one can see that the specific growth rate of $ x_i $ is negative, so one makes $ a_{ii} < 0( = -1) $. The greater the number of species is, the greater the intra-specific competition will be. So $ {df_{ii}(x_i)}/{dx_i} < 0 $, if $ x_i $ represents a producer and $ {df_{ii}(x_i)}/{dx_i}\geq0 $, if $ x_i $ represents a consumer.
$ f_{ij}(x_j) $ are the effect of $ x_j $ on $ x_i $ in a time unit for $ i = 1, 2, 3, \ldots, N $, $ i\neq j $. The greater $ x_j $ is the greater the impact on $ x_i $ will be, so one makes $ {df_{ij}(x_j)}/{dx_j} > 0 $. It is easy to see that when $ x_j = 0 $, there is no effect on $ x_i $. That is $ f_{ij}(x_j) = 0 $ for $ x_j = 0 $.
One can describe the relationship between $ x_i $ and $ x_j $ by determining the sign of $ a_{ij} $ and $ a_{ji} $. If $ a_{ij} > 0( = 1) $ and $ a_{ji} > 0( = 1) $, then the relationship between $ x_i $ and $ x_j $ is mutualism. If $ a_{ij} > 0( = 1) $ and $ a_{ji} < 0( = -1) $, then the relationship between $ x_i $ and $ x_j $ is predation(parasitism) and it can be seen that $ x_i $ is the predator(parasite) and $ x_j $ is the prey (host). If $ a_{ij} < 0( = -1) $ and $ a_{ji} < 0( = -1) $, then the relationship between $ x_i $ and $ x_j $ is competition. If $ a_{ij} = 0 $ and $ a_{ji} = 0 $, there is no direct relationship between $ x_i $ and $ x_j $.
One should consider the significance of system (6), that is the boundedness of $ x_i $. So the function $ f_{ij}(x_j(t)) $ for $ i, j = 1, 2, 3, \ldots, n $ should give the restriction of making $ x_i $ to be bounded.
Remark 2. If $ x_i $ represents a producer, since $ {df_{ii}(x_i)}/{dx_i} < 0 $ and $ f_{ii}(x_i) > 0 $, then $ f_{ii}(x_i) = b+g(x_i) $ ($ g(x_i) $ does not contain a constant term and b is a constant), where $ b > 0 $ represents growth and $ {dg(x_i)}/{dx_i} < 0 $. In addition, if the time dependence of coefficients is ignored, Eq (5) can be regarded as a special form of Eq (6) (just set all $ x_i $ as a producer, $ a_{ii} = 1 $, $ a_{ij} = -1 $, $ f_{ij}(x_j) = b_{ij}x_j $ and $ \alpha = 1 $).
Remark 3. Moreover, let all $ x_i $ as a producer, $ a_{ii} = 1 $, $ a_{ij} = -1 $, $ f_{ii} = k_i-k_ic_{ii}x_i $, $ f_{ij} = k_ic_{ij}x_j $ for $ i, j = 1, 2, 3 $ and $ i\neq j $, then Eq (6) is same as the model in [32]. Let $ x_1 $ as a producer and $ x_2 $ as a consumer, $ a_{11}, a_{21} = 1 $, $ a_{12}, a_{22} = -1 $, $ f_{11} = r-kx_1 $, $ f_{12} = x_2 $, $ f_{21} = \beta x_1 $ and $ f_{22} = 1 $, then Eq (6) is same as system (5) in [33]. Let $ x_1 $ as a producer and $ x_2, x_3 $ as consumers, $ a_{i1} = 1 $, $ a_{ij} = -1 $, $ f_{1j} = c_{1j}x_j $, $ f_{j1} = c_{j1}x_j $, , $ f_{11} = b_1-c_{11}x_1 $, $ f_{jj} = b_j+c_{jj}x_j $ for $ i = 1, 2, 3, j = 2, 3 $, $ f_{23} = c_{23}x_3 $ and $ f_{32} = c_{32}x_2 $, then Eq (6) is same as system (1) in [34]. Just let $ a_{23} = a_{32} = 0 $, then Eq (6) is same as system (19) in [34]. So the models in [32,33,34] are special forms of Eq (6).
Theorem 1. If $ x_i(t_0) > 0, $ for $ i = 1, \cdots, N $, then is a unique solution $ x(t) $ of system (6) in $ \mathbb{R}_+^N $ for $ t\geq t_0 $.
Proof. We study the existence and uniqueness of the solution of system (6) in the region $ \Omega\times[0, T] $, where $ \Omega = \{(x_1, x_2, \ldots, x_N)\in\mathbb{R}^3:max\{\mid x_1\mid, \mid x_2\mid, \ldots, \mid x_N\mid < M\}\} $ and $ T < +\infty $. Denote $ X = (x_1(t_1), x_2(t_1), \ldots, x_N(t_1)) $ and $ \bar{X} = (x_1(t_2), x_2(t_2), \ldots, x_N(t_2)) $. Consider a mapping $ H(X) = (H_1(X), H_2(X), \ldots, H_N(X)) $ where
$ Hi(X)=xi(t)N∑j=1aijfij(xj(t)) $
|
For any $ X, \bar{X}\in\Omega $
$ ‖H(X)−H(ˉX)‖=N∑i=1|xi(t1)N∑j=1aijfij(xj(t1))−xi(t2)N∑j=1aijfij(xj(t2))|=N∑i=1|xi[N∑j=1aijfij(xj(t1))−N∑j=1aijfij(xj(t2))]+[xi(t1)−xi(t2)]N∑j=1aijfij(xj(t2))|≤N∑i=1|M[N∑j=1aijfij(xj(t1))−N∑j=1aijfij(xj(t2))]+[xi(t1)−xi(t2)]N∑j=1aijfij(xj(t2))|≤N∑i=1|MN∑j=1aijfij(xj(t))[xj(t1)−(xj(t2))]+[xi(t1)−xi(t2)]N∑j=1aijfij(xj(t2))|≤|MN∑i=1N∑j=1aijfij(xj(t))[xj(t1)−(xj(t2))]+N∑i=1N∑j=1[xi(t1)−xi(t2)]aijfij(xj(t2))|≤N∑i=1N∑j=1|Mfji(xi(t))[xi(t1)−(xi(t2))]|+N∑i=1N∑j=1|[xi(t1)−xi(t2)]fij(xj(t2))|≤L‖X−ˉX‖ $
|
where $ t\in[t_1, t_2] $ and $ L = \max\{M \sum_{j = 1}^N[f_{ji}(x_i(t))-f_{ij}(x_j(t_2))]\} $ for $ i = 1, 2, \ldots, n $. Obviously, $ H(Z) $ satisfies the Lipschitz condition. Thus, system (6) has a unique solution $ x(t) $.
Theorem 2. If $ x_i(t_0) > 0, $ for $ i = 1, \cdots, N $, then solutions of system (6) are non-negative.
Proof. Let $ x_i(t_0) > 0, i = 1, \cdots, N $ in $ R_+^N $ be the initial solution of system (6). By contradiction, suppose that there exists a solution $ x(t) $ that lies outside of $ R_+^N $. The consequence is that $ x(t) $ crosses the $ x_i $ axis for $ i = 1, 2, 3, \ldots, N $.
Assume that $ x(t) $ crosses $ x_k = 0 $, then there exists $ t^* $ such that $ t^* > t_0 $ and $ x_k(t^*) = 0 $, and there exists $ t_1 $ sufficiently close to $ t^* $ such that $ t_1 > t^* $, and $ x_k(t) < 0 $ for all $ t \in(t^*, t_1] $. Based on the $ k $-th equation of system (6), one obtains
$ Dαxk(t)=xk(t)N∑j=1akjfkj(xj(t)). $
|
(8) |
Since $ x(t) $ and $ f_{kj}(x_j(t)) $ are continuous, one can see that $ f_{kj}(x_j(t)) $ is bounded on $ t\in[t^*, t_1] $.
Assume that $ \max |a_{kj}f_{kj}(x_j(t))| = M $. Then
$ Dαxk(t)≥xk(t)(nM). $
|
(9) |
By using the Laplace transform on both sides, one gets
$ xk(t)≥xk(t∗)Eα(nM(t−t∗)α),t∈[t∗,t1], $
|
(10) |
where $ E_\alpha $ is the Mittag-Leffler function. Thus, $ x(t)\geq 0 $ for any $ t \geq t_0 $, which contradicts the assumption. By using the same method, one gets $ x_i(t) $ are non-negative for $ i = 1, 2, \ldots, N $.
In this section, the stability of the equilibrium points will be investigated by using the Lyapunov direct method. The equilibrium points of the model can be obtained from the following equations.
$ xi(t)N∑j=1aijfij(xj(t))=0i=1,2,3,…,N. $
|
(11) |
In the following, we will only consider the stability of a certain equilibrium point, for the other equilibrium points can be discussed by the same way.
Assume that $ x^* $ is the equilibrium point of system (6), then it has k ($ 0\leq k\leq N $) components of vector $ x^* $ that are not 0. By the operations of row and column, $ x^* $ can be written as $ x^* = (x_1^*, x_2^*, \ldots, x_k^*, 0, \ldots, 0) $. The Jacobian matrix at $ x^* $ is
$ J(x^*) = [b11b12b13⋯ b1kb1k+1b1k+2⋯b1nb21b22b23⋯ b2kb2k+1b2k+2⋯b2nb31b32b33⋯ b3kb3k+1b3k+2⋯b3n⋮⋮⋮⋱⋮⋮⋮⋱⋮bk1bk2bk3⋯ bkkbkk+1bkk+2⋯bkn000⋯ 0∑nj=1ak+1′jfk+1′j(x∗j)0⋯0000⋯ 00∑nj=1ak+2′jf(k+2′j)(x∗j)⋯0⋮⋮⋮⋱⋮⋮⋮⋱⋮000⋯ 000⋯∑nj=1anjfnj(x∗j)] , $
|
(12) |
where $ b_{ij} = a_{ij}f^{'}_{ij}(x^*_j)x_i^* $.
Solving the characteristic equation $ det(\lambda I-J(x^*)) = 0 $ for $ \lambda $ to find the eigenvalues of $ J(x^*) $, one gets
$ [λk+a1λk−1+a2λk−2+⋯+ak−1λ+ak][(λ−n∑j=1ak+1′jfk+1′j(x∗j))⋯(λ−n∑j=1anjfnj(x∗j))]=0. $
|
(13) |
Let
$ A = [b11b12b13⋯ b1kb21b22b23⋯ b2kb31b32b33⋯ b3k⋮⋮⋮⋱⋮bk1bk2bk3⋯ bkk] , $
|
(14) |
$ M(i, j) $ is the $ j-th $ $ i-order $ principal minor of $ A $ and $ a_i = (-1)^i\sum_{j = 1}^{C_k^i}M(i, j) $.
For the sake of discussion, we define $ H_j $ as follows
$ H_j = |a1a3a5⋯ a2j−11a2a4⋯ a2j−20a1a3⋯ a2j−301a2⋯ a2j−4⋮⋮⋮⋱⋮000⋯ aj| , $
|
(15) |
Theorem 3. Suppose that $ x^* = (x_1^*, x_2^*, \ldots, x_k^*, 0, \ldots, 0) $ is the equilibrium point of the system (6), then the equilibrium point is locally asymptotically stable, if the following algebraic conditions hold:
1). $ \sum_{j = 1}^k a_{ij}f_{ij}(x_j^*)+a_{ii}f_{ii}(x_j^*)\leq0 $, for $ i = k+1, k+2, \ldots, N $.
2). $ a_i $ for $ i = 1, 2, \ldots, k $ satisfy $ H_j > 0 $ for $ j = 1, 2, \ldots, k $.
Proof. According to the Hurwitz criterion, if $ H_j > 0 $ for $ j = 1, 2, \ldots, k $, then all eigenvalues of $ \lambda^k+a_{1}\lambda^{k-1}+a_{2}\lambda^{k-2}+\cdots+a_{k-1}\lambda+a_k = 0 $ have negative real part.
According to $ \sum_{j = 1}^k a_{ij}f_{ij}(x_j^*)+a_{ii}f_{ii}(x_j^*)\leq0 $, one can see that all eigenvalues of $ [(\lambda-\sum_{j = 1}^n a_{k+1'j}f_{k+1'j}(x_j^*)) \cdots(\lambda-\sum_{j = 1}^n a_{nj}f_{nj}(x_j^*))] = 0 $ are negative or equal to 0.
Above all, the equilibrium point is locally asymptotically stable.
Remark 4. The conditions of Theorem 3 are sufficient conditions. If $ H_j < 0 $ and all eigenvalues of $ \lambda^k+a_{1}\lambda^{k-1}+a_{2}\lambda^{k-2}+\cdots+a_{k-1}\lambda+a_k = 0 $ satisfy the condition in Lemma 1, the equilibrium point is also locally asymptotically stable.
Theorem 4. Suppose that $ x^* = (x_1^*, x_2^*, \ldots, x_k^*, 0, \ldots, 0) $ is the equilibrium point of system (6), then $ x^* $ is globally asymptotically stable, if the following algebraic conditions hold:
1). $ x^* $ satisfy $ \sum_{j = 1}^k a_{ij}f_{ij}(x_j^*)+a_{ii}f_{ii}(x_j^*)\leq0 $, for $ i = k+1, k+2, \ldots, N $.
2). $ \exists k_{ij}\geq0 $ satisfy $ \sum_{j = 1}^n k_{ij} = 1 $ for $ i, j = 1, 2, \ldots, N $ and $ i\neq j $.
3). $ \exists c_i > 0 $ and $ \exists k_{ij}\geq0 $ satisfy $ 2\sqrt{a_{ii}a_{jj}c_ic_jk_{ij}k_{ji}f^{'}_{ii}(x_i^*)f^{'}_{jj}(x_j^*)} > |a_{ij}c_if^{'}_{ij}(x_j^*)+a_{ji}c_jf^{'}_{ji}(x_i^*)| $ for $ i, j = 1, 2, \ldots, N $.
Proof. If $ \sum_{j = 1}^k a_{ij}f_{ij}(x_j^*)+a_{ii}f_{ii}(x_j^*)\leq 0 $, for $ i = k+1, k+2, \ldots, N $, that is
$ {n∑j=1aijfij(x∗j)=0,fori=1,2,…,k,n∑j=1aijfij(x∗j)≤0,fori=k+1,k+2,…,N. $
|
Let us consider the following positive definite function about $ x^* $
$ V(x1,x2,…,xn)=k∑i=1ci(xi−x∗i−x∗ilnxix∗i)+n∑i=k+1cixi. $
|
(16) |
One can subtly choose $ c_i > 0 $ such that $ V $ is a Lyapunov function. By Lemma 2, one obtains
$ DαV(x1,x2,…,xn)≤k∑i=1n∑j=1ci(xi−x∗i)(aijfij(xj(t)))+n∑i=k+1n∑j=1cixi(aijfij(xj(t)))≤k∑i=1n∑j=1ci(xi−x∗i)(aijfij(xj)−aijfij(x∗j))+n∑i=k+1n∑j=1ci(xi−x∗i)(aijfij(xj)−aijfij(x∗j)). $
|
(17) |
For arbitrary $ \varepsilon > 0 $, since functions $ f_{ij} $ for $ i, j = 1, 2, \ldots, n $ are differentiable functions, there exists $ \delta > 0 $ such that $ |x_i -x_i^{\ast}| < \delta $ for $ i = 1, 2, \ldots, N $, it implies
$ |fij(xj)−fij(x∗j)xj−x∗j−f′ij(x∗j)|<εfori,j=1,2,…,n. $
|
(18) |
Thus
$ DαV(x1,x2,…,xn)≤n∑i=1n∑j=1ci(xi−x∗i)(xj−x∗j)(aijf′ij(x∗j)+ε) $
|
(19) |
By the arbitrariness of $ \varepsilon $, one has
$ DαV(x1,x2,…,xn)≤n∑i=1n∑j=1ci(xi−x∗i)(xj−x∗j)aijf′ij(x∗j)=n∑i=1n∑j=1[(kijaiici(xi−x∗i)2f′ii(x∗i)+(xi−x∗i)(xj−x∗j)(ciaijf′ij(x∗j)+cjajif′ji(x∗i))2]. $
|
(20) |
For $ i\neq j $, then one has
$ DαV(x1,x2,…,xn)≤−n∑i=1n∑j>i[2|xi−x∗i||xj−x∗j|√aiiajjcicjkijkjif′ii(x∗i)f′jj(x∗j)−(xi−x∗i)(xj−x∗j)(ciaijf′ij(x∗j)+cjajif′ji(x∗i))]. $
|
(21) |
According to the condition $ 2\sqrt{a_{ii}a_{jj}c_ic_jk_{ij}k_{ji}f^{'}_{ii}(x_i^*)f^{'}_{jj}(x_j^*)} > |a_{ij}c_if^{'}_{ij}(x_j^*)+a_{ji}c_jf^{'}_{ji}(x_i^*)| $, and $ a_{ii}f^{'}_{ii}(x_i) < 0 $ for $ i = 1, 2, \ldots, n $. So the conditions in Lemma 3 are satisfied, where $ W_3(x) = \sum_{i = 1}^n\sum_{j > i}^n\bigg[2|x_i-x_i^*||x_j-x_j^*|\sqrt{a_{ii}a_{jj}c_ic_jk_{ij}k_{ji}f^{'}_{ii}(x_i^*)f^{'}_{jj}(x_j^*)}-(x_i-x_i^*)(x_j-x_j^*)(c_ia_{ij}f_{ij}^{'}(x_j^*)+c_ja_{ji}f_{ji}^{'}(x_i^*))\bigg] > 0 $.
Thus, $ x^* $ is a globally asymptotically stable equilibrium point for the system (6).
Remark 5. According to theorem 4, one can see that N-order system should have $ N(N-1)/2 $ conditions at least. So if $ N $ is large enough, it is difficult to find the suitable $ c_i, k_{ij} $ for $ i, j = 1, 2, 3, \ldots, n $ and $ i\neq j $.
In this section, we will give some examples to demonstrate the theoretical analysis.
Example 1:
Let us consider the functions of the system (6) as follow
$ f11(x1(t))=2(2−x1(t)),f12(x2(t))=x2(t),f13(x3(t))=x3(t),a11=1,a12=−1,a13=−1,f21(x1(t))=x1(t),f22(x2(t))=2(2−x2(t)),f23(x3(t))=x3(t),a21=−1,a22=1,a23=−1,f31(x1(t))=x1(t),f32(x2(t))=x2(t),f33(x3(t))=2(2−x3(t)),a31=−1,a32=−1,a33=1. $
|
(22) |
Therefore, the system (6) can be denoted by the following Volterra-Lotka competition system:
$ Dαx1(t)=x1(t)(4−2x1(t)−x2(t)−x3(t)),Dαx2(t)=x2(t)(4−x1(t)−2x2(t)−x3(t)),Dαx3(t)=x3(t)(4−x1(t)−x2(t)−2x3(t)). $
|
(23) |
From the parameters of the system, it can be seen that the equilibrium points of the system are $ (1, 1, 1) $, $ (1, 1, 0) $ and $ (1, 0, 0) $. One can see that when $ k_{ij} = 0.5 $ and $ c_i = 1 $ for $ i, j = 1, 2, 3, i\neq j $, the equilibrium point $ x^* = (1, 1, 1) $ can satisfy three conditions in Theorem 4. Other equilibrium points can not satisfy condition 1 in Theorem 4. One selects the initial values as $ (0.8, 0.6, 0.4) $, $ (1.6, 1.2, 0.8) $, $ (2.4, 1.8, 1.2) $ and $ (3.2, 2.4, 1.6) $ respectively, and the numerical results are shown in Figure 1. From Figure 1, one can see that the positive equilibrium point (1, 1, 1) of system (23) is globally asymptotically stable.
Example 2:
In this example, one considers the functions $ f_{ij} $ of system (6) as nonlinear form:
$ f11(x1(t))=2(2−x21(t)),f12(x2(t))=x22(t),f13(x3(t))=x23(t),a11=1,a12=−1,a13=−1,f21(x1(t))=x21(t),f22(x2(t))=2(2−x22(t)),f23(x3(t))=x23(t),a21=−1,a22=1,a23=−1,f31(x1(t))=x21(t),f32(x2(t))=x22(t),f33(x3(t))=2(2−x23(t)),a31=−1,a32=−1,a33=1. $
|
(24) |
Therefore, the system (6) can be denoted by the following competition system:
$ Dαx1(t)=x1(t)(4−2x21(t)−x22(t)−x23(t)),Dαx2(t)=x2(t)(4−x21(t)−2x22(t)−x23(t)),Dαx3(t)=x3(t)(4−x21(t)−x22(t)−2x23(t)). $
|
(25) |
From the parameters of the system, it can be seen that the equilibrium points of the system are $ (1, 1, 1) $ and $ (0, 0, 0) $. One can see that when $ k_{ij} = 0.5 $ and $ c_i = 2 $ for $ i, j = 1, 2, 3, i\neq j $, the equilibrium point $ x^* = (1, 1, 1) $ can satisfy three conditions in Theorem 4 and the other can not satisfy all conditions in Theorem 4. One selects the initial values as $ (0.4, 0.6, 0.5) $, $ (0.8, 1.2, 1) $, $ (1.2, 1.8, 1.5) $ and $ (1.6, 2.4, 2) $ respectively, and the numerical results are shown in Figure 2. From Figure 2, one can see that the positive equilibrium point (1, 1, 1) of system (25) is globally asymptotically stable.
Example 3:
The new example will consider the complex relationships between the species, one selects the functions of the system (6) as follow.
$ f11(x1(t))=0.5(1−x1(t)),f12(x2(t))=x2(t),f13(x3(t))=x3(t),a11=1,a12=−1,a13=−1,f21(x1(t))=x1(t),f22(x2(t))=x2(t),f23(x3(t))=x3(t),a21=1,a22=−1,a23=−1,f31(x1(t))=x1(t),f32(x2(t))=0.5x2(t),f33(x3(t))=2x3(t).a31=1,a32=−1,a33=−1. $
|
Therefore, the system (6) can be denoted by the following prey-predator system with interspecific competition:
$ Dαx1(t)=x1(t)(0.5(1−x1(t))−x2(t)−x3(t)),Dαx2(t)=x2(t)(x1(t)−x2(t)−x3(t)),Dαx3(t)=x3(t)(x1(t)−0.5x2(t)−2x3(t)). $
|
(26) |
From the parameters of the system, it can be seen that the equilibrium points of the system are $ (1/3, 2/9, 1/9) $, $ (1/3, 1/3, 0) $ and $ (1, 0, 0) $. One can see that when $ k_{12} = k_{21} = 0.5 $, $ k_{32} = k_{23} = 0.8 $, $ k_{21} = k_{31} = 0.2 $ and $ c_i = 1 $ for $ i, j = 1, 2, 3, i\neq j $, the equilibrium point $ (1/3, 2/9, 1/9) $ can satisfy three conditions in Theorem 4. One takes initial values $ (0.2, 0.2, 0.3) $, $ (0.4, 0.4, 0.6) $, $ (0.6, 0.6, 0.9) $ and $ (0.8, 0.8, 1.2) $ respectively, and the numerical results are shown in Figure 3. From Figure 3, one can see that the positive equilibrium point $ (1/3, 2/9, 1/9) $ of system (26) is globally asymptotically stable.
In this paper, one considers a class of generalized fractional population model. Firstly, the existence, uniqueness and non-negative of solutions of the system are proved. Secondly, one provides a sufficient conditions for local stability and globally stability of the equilibrium points. Finally, three examples are given to demonstrate the theoretical analysis. This paper not only extends the integer population models to fractional-order form, but also extends the dimension to n-dimension. The new model can be used to simulate the relationships between various populations in a complex ecosystem. Compared with other population models, our model is more general.
Time delay stays in the biological system widely and may effect the stability of the biological system. Thus, system (6) with time delay is of great research value. It will be our future work.
This work was supported by the National Natural Science Foundation of China (Nos. 61573008, 61973199), the Natural Science Foundation of Shandong Province (No. ZR2018MF005), and the SDUST graduate innovation project (No. SDKDYC190353).
The author declares no conflicts of interest in this paper.
[1] |
Hofmann SG, Asnaani A, Vonk JJ, et al. (2012) The efficacy of cognitive behavioral therapy: A review of meta-analyses. Cognitive Ther Res 36: 427-440. doi: 10.1007/s10608-012-9476-1
![]() |
[2] |
Hofmann SG, Smits JA (2008) Cognitive-behavioral therapy for adult anxiety disorders: a meta-analysis of randomized placebo-controlled trials. J Clin Psychiatry 69: 621-632. doi: 10.4088/JCP.v69n0415
![]() |
[3] | Hofmann SG, Otto MW, Pollack MH, et al. (2015) D-Cycloserine Augmentation of Cognitive Behavioral Therapy for Anxiety Disorders: an Update. Curr Psychiatry Rep 17(1): 1-5. |
[4] |
Hofmann SG (2008) Cognitive processes during fear acquisition and extinction in animals and humans: Implications for exposure therapy of anxiety disorders. Clin Psychol Rev 28: 199-210. doi: 10.1016/j.cpr.2007.04.009
![]() |
[5] |
Singewald N, Schmuckermair C, Whittle N, et al. (2015) Pharmacology of cognitive enhancers for exposure—based therapy for fear, anxiety, and trauma-related disorder. Pharmacol Ther 149:150-190. doi: 10.1016/j.pharmthera.2014.12.004
![]() |
[6] |
Hofmann SG, Meuret AE, Smits JA, et al. (2006) Augmentation of exposure therapy with D-cycloserine for social anxiety disorder. Arch Gen Psychiatry 63: 298-304. doi: 10.1001/archpsyc.63.3.298
![]() |
[7] |
Smits JA, Rosenfield D, Davis ML, et al. (2014) Yohimbine enhancement of exposure therapy for social anxiety disorder: A randomized controlled trial. Biol Psychiatry 75: 840-846. doi: 10.1016/j.biopsych.2013.10.008
![]() |
[8] |
Davis M, Ressler K, Rothbaum BO, et al. (2006) Effects of D-cycloserine on extinction: translation from preclinical to clinical work. Biol Psychiatry 60: 369-375. doi: 10.1016/j.biopsych.2006.03.084
![]() |
[9] |
Richardson R, Ledgerwood L, Cranney J (2004) Facilitation of fear extinction by D-cycloserine: theoretical and clinical implications. Learn Mem 11: 510-516. doi: 10.1101/lm.78204
![]() |
[10] |
Bouton ME, Vurbic D, Woods AM (2008) D-cycloserine facilitates context-specific fear extinction learning. Neurobiol Learn Mem 90: 504-510. doi: 10.1016/j.nlm.2008.07.003
![]() |
[11] |
Ressler KJ, Rothbaum BO, Tannenbaum L, et al. (2004) Cognitive enhancers as adjuncts to psychotherapy: Use of D-cycloserine in phobic individuals to facilitate extinction of fear. Arch Gen Psychiatry 61: 1136-1144. doi: 10.1001/archpsyc.61.11.1136
![]() |
[12] |
Otto MW, Tolin DF, Simon NM, et al. (2010) Efficacy of D-cycloserine for enhancing response to cognitive-behavior therapy for panic disorder. Biol Psychiatry 67: 365-370. doi: 10.1016/j.biopsych.2009.07.036
![]() |
[13] |
Hofmann SG (2014) D-cycloserine for treating anxiety disorders: making good exposures better and bad exposures worse. Depress Anxiety 31: 175-177. doi: 10.1002/da.22257
![]() |
[14] |
Hofmann SG, Hüweler R, Mackillop J, et al. (2012) Effects of d-cycloserine on craving to alcohol cues in problem drinkers: Preliminary findings. Am J Drug Alcohol Abuse 38: 101-107. doi: 10.3109/00952990.2011.600396
![]() |
[15] |
Lee JL, Milton AL, Everitt BJ (2006) Reconsolidation and extinction of conditioned fear: inhibition and potentiation. J Neurosci 26: 10051-10056. doi: 10.1523/JNEUROSCI.2466-06.2006
![]() |
[16] |
Hofmann SG, Smits JA, Rosenfield D, et al. (2013) D-Cycloserine as an augmentation strategy with cognitive-behavioral therapy for social anxiety disorder. Am J Psychiatry 170: 751-758. doi: 10.1176/appi.ajp.2013.12070974
![]() |
[17] |
Smits JAJ, Rosenfield D, Otto MW, et al. (2013) D-cycloserine enhancement of exposure therapy for social anxiety disorder depends on the success of exposure sessions. J Psychiat Res 47: 1455-1461. doi: 10.1016/j.jpsychires.2013.06.020
![]() |
[18] |
Holmes A, Quirk GJ (2010) Pharmacological facilitation of fear extinction and the search for adjunct treatments for anxiety disorders—the case of yohimbine. Trends Pharmacol Sci 31: 2-7. doi: 10.1016/j.tips.2009.10.003
![]() |
[19] |
Cain CK, Blouin AM, Barad M (2004). Adrenergic transmission facilitates extinction of conditional fear in mice. Learn Mem 11: 179-187. doi: 10.1101/lm.71504
![]() |
[20] |
O'Carroll RE, Drysdale E, Cahill L, et al. (1999) Stimulation of the noradrenergic system enhances and blockade reduces memory for emotional material in man. Psychol Med 29: 1083-1088. doi: 10.1017/S0033291799008703
![]() |
[21] |
Powers MB, Smits JAJ, Otto MW, et al. (2009) Facilitation of fear extinction in phobic participants with a novel cognitive enhancer: A randomized placebo controlled trial of yohimbine augmentation. J Anxiety Disord 23: 350-356. doi: 10.1016/j.janxdis.2009.01.001
![]() |
[22] |
Lupien SJ, McEwen BS, Gunnar MR, et al. (2009) Effects of stress throughout the lifespan on the brain, behavior and cognition. Nat Rev Neurosci 10: 434-445. doi: 10.1038/nrn2639
![]() |
[23] | De Quervain DJF, Aerni A, Schelling G, et al. (2009) Glucocorticoids and the regulation of memory in health and disease. J Epidemiol commu H 30(3): 358-370. |
[24] | Roozendaal B, McGaugh JL (1997) Glucocorticoid receptor agonist and antagonist administration into the basolateral but not central amygdala modulates memory storage, Neurobiol Learn Mem 67: 176-179. |
[25] | Lupien SJ, Fiocco A, Wan N, et al. (2005) Stress hormones and human memory function across the lifespan. Psychoneuroendocrinol 30(3): 225-242. |
[26] | Otto MW, McHugh Rk, Kantak KM (2010) Combined pharmacotherapy and cognitive-behavioral therapy for anxiety disorders: Medication effects, glucocorticoids, and attenuated treatment outcomes. Clin Psychol 17(2): 91-103. |
[27] | Andreano JM, Cahill L (2006) Glucocorticoid release and memory consolidation in men and women. Psychol Sci 17(6): 466-470. |
[28] | Roozendaal B, Williams CL, McGaugh JL (1999) Glucocorticoid receptor activation in the rat nucleus of the solitary tract facilitates memory consolidation: Involvement of the basolateral amygdala. Eur J Neurosci 11(4): 1317-1323. |
[29] | Cai WH, Blundell J, Han J, et al. (2006) Postreactivation glucocorticoids impair recall of established fear memory. J Neurosci 26(37): 9560-9566. |
[30] | Pakdel R, Rashidy-Pour A (2007) Microinjections of the dopamine D2 receptor antagonist sulpiride into the medial prefrontal cortex attenuate glucocorticoid-induced impairment of long-term memory retrieval in rats. Neurobiol Learn Mem 87(3): 385-390. |
[31] | Barrett D, Gonzalez-Lima F (2004) Behavioral effects of metyrapone on Pavlovian extinction. Neurosci Lett 371(2-3): 91-96. |
[32] | Bohus B, Lissak K (1968) Adrenocortical hormones and avoidance behavior of rats. Int J Neuropharmacol 7(4): 301-306. |
[33] | Yang YL, Chao PK, Lu KT (2006) Systemic and intra-amygdala administration of glucocorticoid agonist and antagonist modulate extinction of conditioned fear. Neuropsychopharmacol 31(5): 912-924. |
[34] |
Lass-Hennemann J, Michael T (2014) Endogenous cortisol levels influence exposure therapy in spider phobia. Behav Res Ther 60: 39-45. doi: 10.1016/j.brat.2014.06.009
![]() |
[35] | Soravia LM, Heinrichs M, Aerni A, et al. (2006) Glucocorticoids reduce phobic fear in humans. Proc Natl Acad Sci USA 103(14): 5585-5590. |
[36] |
Soravia LM, Heinrichs M, Winzeler L, et al. (2014) Glucocorticoids enhance in vivo exposure-based therapy if spider phobia. Depress Anxiety 31: 429-435. doi: 10.1002/da.22219
![]() |
[37] | De Quervain DJ, Bentz D, Michael T, et al. (2011) Glucocorticoids enhance extinction-based psychotherapy. Proc Natl Acad Sci USA 108(16): 6621-6625. |
[38] |
Meuret AE, Trueba AF, Abelson JL, et al. (2015) High cortisol awakening response and cortisol levels moderate exposure-based psychotherapy success. Psychoneuroendocrinol 51: 331-340. doi: 10.1016/j.psyneuen.2014.10.008
![]() |
[39] | Siegmund A, Koster L, Meves AM, et al. (2011) Stress hormones during flooding therapy and their relationship to therapy outcome in patients with panic disorder and agoraphobia. J Psychiatr Res 45(3): 339-346. |
[40] | Suris A, North C, Adinoff B, et al. (2010) Effects of exogenous glucocorticoid on combat-related PTSD symptoms. Ann Clin Psychiatry 22: 274-279. |
[41] | Aerni A, Traber R, Hock C, et al. (2004) Low-dose cortisol for symptoms of posttraumatic stress disorder. Am J Psychiatry 161(8): 1488-1490. |
[42] | Fries E, Hellhammer DH, Hellhammer J (2006) Attenuation of the hypothalamic-pituitary-adrenal axis responsivity to the Trier Social Stress Test by the benzodiazepine alprazolam. Psychoneuroendocrinol 31(10): 1278-1288. |
[43] | Pomara N, Willoughby LM, Sidtis JJ, et al. (2005) Cortisol response to diazepam: Its relationship to age, dose, duration of treatment, and presence of generalized anxiety disorder. Psychopharmacol 178(1): 1-8. |
[44] |
Brown RM, Crane AM, Goldman PS (1979) Regional distribution of monoamines in the cerebral cortex and subcortical structures of rhesus monkey: concentrations and in vivo synthesis. Brain Res 168: 133-150. doi: 10.1016/0006-8993(79)90132-X
![]() |
[45] | Goldman-Rakic PS (1991) Prefrontal cortical dysfunction in schizophrenia: the relevance of working memory. In: Psychopathology and the Brain, edited by B. Carroll, New York: Raven, 1-23. |
[46] | Sawaguchi T, Goldman-Rakic PS (1994) The role of D1-dopamine receptor in working memory: Local injections of dopamine antagonists into the prefrontal cortex of rhesus monkeys performing an oculomotor delayed-response task. J Neurophysiol 71(2): 515-528. |
[47] | Seamans JK, Yang CR (2004) The principal features and mechanisms of dopamine modulation in the prefrontal cortex. Prog Neurobiol 74(1): 1-58. |
[48] | Bromberg-Martin ES, Matsumoto M, Hikosaka O (2010) Dopamine in motivational control: rewarding, aversive, and alerting. Neuron 68(5): 815-834. |
[49] | Nikolaus S, Antke C, Beu M, et al. (2010) Cortical GABA, striatal dopamine and midbrain serotonin as the key players in compulsive and anxiety disorders: Results from in vivo imaging studies. Rev Neurosci 21(2): 119-139. |
[50] | Olver JS, O'Keefe G, Jones GR, et al. (2009) Dopamine D1 receptor binding in the striatum of patients with obsessive-compulsive disorder. J Affect Disord 114(1-3): 321-326. |
[51] | De la Mora MP, Gallegos-Cari A, Arizmendi-Garcia Y, et al. (2010) Role of dopamine receptor mechanisms in the amygdaloid modulation of fear and anxiety: Structural and functional analysis. Prog Neurobiol 90(2): 198-216. |
[52] | Koo MS, Kim EJ, Roh D, et al. (2010) Role of dopamine in the pathophysiology and treatment of obsessive-compulsive disorder. Expert Rev Neurother 10(2): 275-290. |
[53] | Insel TR (2010) The challenge of translation in social neuroscience: A review of oxytocin, vasopressin, and affiliative behavior. Neuron 65(6): 768-779. |
[54] | Kosfeld M, Heinrichs M, Zak PJ, et al. (2005) Oxytocin increases trust in humans. Nat 435(7042): 673-676. |
[55] |
Meyer-Lindenberg A, Domes G, Kirsch P, et al. (2011). Oxytocin and vasopressin in the human brain: Social neuropeptides for translational medicine. Nat Rev Neurosci 12(9): 524-538. doi: 10.1038/nrn3044
![]() |
[56] |
Frith CD (2008) Social Cognition. Philos Trans R Soc Biol Sci, 363: 2033-2039. doi: 10.1098/rstb.2008.0005
![]() |
[57] |
Eisenberg N, Miller PA (1987) The relation of empathy to prosocial and related behaviors. Psycholog Bull, 101: 91-119. doi: 10.1037/0033-2909.101.1.91
![]() |
[58] |
Perez-Rodriguez MM, Mahon K, Russo M, et al. (2015) Oxytocin and social cognition in affective and psychotic disorders. Eur Neuropsychopharmacol 25: 265-282. doi: 10.1016/j.euroneuro.2014.07.012
![]() |
[59] | Zak PJ, Kurzban R & Matzner WT (2005) Oxytocin is associated with human trustworthiness. Horm Behav 48(5): 522-527. |
[60] | Grewen KM, Girdler SS, Amico J, et al. (2005) Effects of partner support on resting oxytocin, cortisol, norepinephrine, and blood pressure before and after warm partner contact. Psychosom Med 67(4): 531-538. |
[61] | Scantamburlo G, Hansenne M, Fuchs S, et al. (2007). Plasma oxytocin levels and anxiety in patients with major depression. Psychoneuroendocrinol 32(4): 407-410. |
[62] | Goldman M, Marlow-O'Connor M, Torres I, et al. (2008) Diminished plasma oxytocin in schizophrenic patients with neuroendocrine dysfunction and emotional deficits. Schizophr Res 98(1-3): 247-255. |
[63] | Green L, Fein D, Modahl C, et al. (2001) Oxytocin and autistic disorder: Alterations in peptide forms. Biol Psychiatry 50(8): 609-613. |
[64] | Cyranowski JM, Hofkens TL, Frank E, et al. (2008) Evidence of dysregulated peripheral oxytocin release among depressed women. Psychosom Med 70(9): 967-975. |
[65] | Taylor SE, Gonzaga GC, Klein LC, et al. (2006) Relation of oxytocin to psychological stress responses and hypothalamic-pituitary-adrenocortical axis activity in older women. Psychosom Med 68(2): 238-245. |
[66] | Hoge EA, Pollack MH, Kaufman RE, et al. (2008) Oxytocin levels in social anxiety disorder. CNS Neurosci Ther 14(3): 165-170. |
[67] | Born J, Lange T, Kern W, et al. (2002) Sniffing neuropeptides: A transnasal approach to the human brain. Nat Neurosci 5(6): 514-516. |
[68] | Mikolajczak M, Gross JJ, Lane A, et al. (2010) Oxytocin makes people trusting, not gullible. Psychol Sci 21(8): 1072-1074. |
[69] | Mikolajczak M, Pinon N, Lane A, et al. (2010) Oxytocin not only increases trust when money is at stake, but also when confidential information is in the balance. Biol Psychol 85(1): 182-184. |
[70] | Baumgartner T, Heinrichs M, Vonlanthen A, et al. (2008) Oxytocin shapes the neural circuitry of trust and trust adaptation in humans. Neuron 58(4): 639-650. |
[71] | Hofmann S G, Fang A, Brager D N (in press). Effect of intranasal oxytocin administration on psychiatric symptoms: A meta-analysis of placebo-controlled studies.Psychiatry Res. |
[72] | Guastella AJ, Howard AL, Dadds MR, et al. (2009) A randomized controlled trial of intranasal oxytocin as an adjunct to exposure therapy for social anxiety disorder. Psychoneuroendocrinol 34(6): 917-923. |
[73] | MacDonald E, Dadds MR, Brennan JL, et al. (2011) A review of safety, side-effects and subjective reactions to intranasal oxytocin in human research. Psychoneuroendocrinol 36(8): 1114-1126. |
[74] | Labuschagne I, Phan KL, Wood A, et al. (2010) Oxytocin attenuates amygdala reactivity to fear in generalized social anxiety disorder. Neuropsychopharmacol 35(12): 2403-2413. |
[75] |
Labuschagne I, Phan KL, Wood A, et al. (2012) Medial frontal hyperactivity to sad faces in generalized social anxiety disorder and modulation by oxytocin. Int J Neuropsychopharmacol 15: 883-896. doi: 10.1017/S1461145711001489
![]() |
[76] | Fang A, Hoge E A, Heinrichs M, et al. (2014) Attachment Style Moderates the Effects of Oxytocin on Social Behaviors and Cognitions During Social Rejection: Applying an RDoC Framework to Social Anxiety. Clin Psychol Sci 2 (6):740-747. |
[77] | Minzenberg MJ, Carter CS (2008) Modafinil: A review of neurochemical actions and effects on cognition. Neuropsychopharmacol 33(7): 1477-1502. |
[78] | Volkow ND, Fowler JS, Logan J, et al. (2009) Effects of modafinil on dopamine and dopamine transporters in the male human brain: clinical implications. JAMA 301(11): 1148-1154. |
[79] |
Madras BK, Xie Z, Lin Z, et al. (2006) Modafinil occupies dopamine and norepinephrine transporters in vivo and modulates the transporters and trace amine activity in vitro. J Pharmacol Exp Ther 319: 561-569. doi: 10.1124/jpet.106.106583
![]() |
[80] | Hermant JF, Rambert FA, Duteil J (1991) Awakening properties of modafinil: Effect on nocturnal activity in monkeys (Macacamulatta) after acute and repeated administration. Psychopharmacol 103(1): 28-32. |
[81] | Kahbazi M, Ghoreishi A, Rahiminejad F, et al. (2009) A randomized, double-blind and placebo-controlled trial of modafinil in children and adolescents with attention deficit and hyperactivity disorder. Psychiatry Res 168(3): 234-237. |
[82] | Randall DC, Shneerson JM, Plaha KK, et al. (2003) Modafinil affects mood, but not cognitive function, in healthy young volunteers. Hum Psychopharmacol 18(3): 163-173. |
[83] | Wong YN, King SP, Simcoe D, et al. (1999) Open-label, single-dose pharmacokinetic study of modafinil tablets: Influence of age and gender in normal subjects. J Clin Pharmacol 39(3): 281-288. |
[84] |
Murphy HM, Ekstrand D, Tarchick M, et al. (2015) Modafinil as a cognitive enhancer of spatial working memory in rats. Physiol Behav 142: 126-130. doi: 10.1016/j.physbeh.2015.02.003
![]() |
[85] | Rasetti R, Mattay VS, Stankevich B, et al. (2010) Modulatory effects of modafinil on neural circuits regulating emotion and cognition. Neuropsychopharmacol 35(10): 2101-2109. |
[86] | Schwartz JR, Hirshkowitz M, Erman MK, et al. (2003) Modafinil as adjunct therapy for daytime sleepiness in obstructive sleep apnea: a 12-week, open-label study. Chest 124(6): 2192-2199. |
[87] | Zifko UA, Rupp M, Schwarz S, et al. (2002) Modafinil in treatment of fatigue in multiple sclerosis. Results of an open-label study. J Neurol 249(8): 983-987. |
[88] |
Balanza-Martinez V, Fries GR, Colpo GD, et al. (2011) Therapeutic use of omega-3 fatty acids in bipolar disorder. Expert Rev Neurotherapeutics 11: 1029-1047. doi: 10.1586/ern.11.42
![]() |
[89] |
Bloch MH, Qawasmi A (2011) Omega-3 fatty acid supplementation for the treatment of children with attention-deficit/hyperactivity disorder symptomatology: Systematic review and meta-analysis. J Am Acad Child Adolesc Psychiatry 50: 991-1000. doi: 10.1016/j.jaac.2011.06.008
![]() |
[90] | Cosci F, Abrams K, Schruers KRJ, et al. (2006) Effect of nicotine on 35% CO2-induced anxiety: A study in healthy volunteers. Nicotine Tob Res 8, 511-517. |
[91] |
Gertsik L, Poland RE, Bresee C, et al. (2012) Omega-3 fatty acid augmentation of citalopram treatment for patients with major depressive disorder. J Clin Psychopharmacol 32: 61-64. doi: 10.1097/JCP.0b013e31823f3b5f
![]() |
[92] |
Lesperance FO, Frasure-Smith N, St-Andre E, et al. (2011) The efficacy of omega-3 supplementation for major depression: A randomized controlled trial. J Clin Psychiatry 72: 1054-1062. doi: 10.4088/JCP.10m05966blu
![]() |
[93] | Masdrakis VG, Papakostas YG, Vaidakis N, et al. (2008) Caffeine challenge in patients with panic disorder: Baseline differences between those who panic and those who do not. Depress Anxiety 25, E72-E79. |
[94] |
Mystkowski JL, Mineka S, Vernon LL, et al. (2003) Changes in caffeine states enhance return of fear in spider phobia. J Consult Clin Psychol 71: 243-250. doi: 10.1037/0022-006X.71.2.243
![]() |
[95] | Salin-Pascual RJ, Basanez-Villa E (2003) Changes in compulsion and anxiety symptoms with nicotine transdermal patches in non-smoking obsessive-compulsive disorder patients. Revista de Investigacion Clinica 55: 650-654. |
[96] | Culver NC, Vervliet B, Craske MG (2014). Compound Extinction Using the Rescorla–Wagner Model to Maximize Exposure Therapy Effects for Anxiety Disorders. Clin Psychol Sci 2167702614542103. |
[97] |
McNamara RK, Carlson SE (2006) Role of omega-3 fatty acids in brain development and function: potential implications for the pathogenesis and prevention of psychopathology. Prostaglandins Leukot Essent Fatty Acids 75: 329-349. doi: 10.1016/j.plefa.2006.07.010
![]() |
[98] | Timonen M, Horrobin D, Jokelainen J, et al. (2004) Fish consumption and depression: The Northern Finland 1966 birth cohort study. J Affective Disord 82: 447-452. |
[99] |
McNamara RK (2011) Omega-3 fatty acid deficiency: A preventable risk factor for schizophrenia? Schizophr Res 129: 215-216. doi: 10.1016/j.schres.2010.12.017
![]() |
[100] | Hofmann SG, Sawyer AT, Korte KJ, et al. (2009) Is it beneficial to add pharmacotherapy to cognitive-behavioral therapy when treating anxiety disorders? A meta-analytic review. Int J Cogn Ther 2: 160-175. |
1. | Yingkang Xie, Zhen Wang, Junwei Lu, Yuxia Li, Stability analysis and control strategies for a new SIS epidemic model in heterogeneous networks, 2020, 383, 00963003, 125381, 10.1016/j.amc.2020.125381 |