Psychiatric disorders may extremely impair the quality of life with patients and are important reasons of social disability. Several data have shown that psychiatric disorders are associated with an altered composition of gut microbiota. Dietary intake could determine the microbiota, which contribute to produce various metabolites of fermentation such as short chain fatty acids. Some of the metabolites could result in epigenetic alterations leading to the disease susceptibility. Epigenetic dysfunction is in fact implicated in various psychiatric and neurologic disorders. For example, it has been shown that neuroepigenetic dysregulation occurs in psychiatric disorders including schizophrenia. Several studies have demonstrated that the intestinal microbiome may influence the function of central nervous system. Furthermore, it has been proved that the alterations in the gut microbiota-composition might affect in the bidirectional communication between gut and brain. Similarly, evidences demonstrating the association between psychiatric disorders and the gut microbiota have come from preclinical studies. It is clear that an intricate symbiotic relationship might exist between host and microbe, although the practical significance of the gut microbiota has not yet to be determined. In this review, we have summarized the function of gut microbiota in main psychiatric disorders with respect to the mental health. In addition, we would like to discuss the potential mechanisms of the disorders for the practical diagnosis and future treatment by using bioengineering of microbiota and their metabolites.
Citation: Kurumi Taniguchi, Yuka Ikeda, Nozomi Nagase, Ai Tsuji, Yasuko Kitagishi, Satoru Matsuda. Implications of Gut-Brain axis in the pathogenesis of Psychiatric disorders[J]. AIMS Bioengineering, 2021, 8(4): 243-256. doi: 10.3934/bioeng.2021021
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Psychiatric disorders may extremely impair the quality of life with patients and are important reasons of social disability. Several data have shown that psychiatric disorders are associated with an altered composition of gut microbiota. Dietary intake could determine the microbiota, which contribute to produce various metabolites of fermentation such as short chain fatty acids. Some of the metabolites could result in epigenetic alterations leading to the disease susceptibility. Epigenetic dysfunction is in fact implicated in various psychiatric and neurologic disorders. For example, it has been shown that neuroepigenetic dysregulation occurs in psychiatric disorders including schizophrenia. Several studies have demonstrated that the intestinal microbiome may influence the function of central nervous system. Furthermore, it has been proved that the alterations in the gut microbiota-composition might affect in the bidirectional communication between gut and brain. Similarly, evidences demonstrating the association between psychiatric disorders and the gut microbiota have come from preclinical studies. It is clear that an intricate symbiotic relationship might exist between host and microbe, although the practical significance of the gut microbiota has not yet to be determined. In this review, we have summarized the function of gut microbiota in main psychiatric disorders with respect to the mental health. In addition, we would like to discuss the potential mechanisms of the disorders for the practical diagnosis and future treatment by using bioengineering of microbiota and their metabolites.
Alzheimer's disease;
attention deficit hyperactivity disorder;
autism spectrum disorder;
blood brain barrier;
central nervous system;
deoxyribonucleic acid;
gamma amino butyric acid;
gastrointestinal;
G protein-coupled receptor;
histone deacetylases;
lipopolysaccharide;
reactive oxygen species;
superoxide dismutase
There are many papers investigating the stochastic travelling waves of population dynamical system with multiplicative noise, most of them focus on the scaler Fisher-KPP equation. For instance, Tribe [1] studied the KPP equation with nonlinear multiplicative noise √udWt, and Müeller et al. [2,3,4] studied the KPP equation with √u(1−u)dWt. Both of their work take the Heaviside function as the initial data, and they also gave the estimates of the wave speed with an upper bound and a lower bound. Zhao et al. [5,6,7] showed that only if the strength of noise is moderately, for example the multiplicative noise k(t)dWt, the effects of noise would present or the solution would tend to be zero or converge to the deterministic travelling wave solution. Shen [8] developed a theoretical random variational framework to show the existence of random travelling waves, and then Shen and his collaborators [9,10] also studied the random travelling waves in reaction-diffusion equations with Fisher-KPP nonlinearity, Nagumo nonlinearity and ignition nonlinearity, in random media. Furthermore, Huang et al. [11,12,13,14] investigated the bifurcations of asymptotic behaviors of solution induced by strength of the dual noises for stochastic Fisher-KPP equation. Recently, Wang and Zhou [15] discovered that the same results still hold even if the decrease restrictions on the growth function are removed. Moreover, they showed that with increasing the noise intensity, the original equation with Fisher-KPP nonlinearity evolves into first the one with degenerated Fisher-KPP nonlinearity and then the one with Nagumo nonlinearity, and we refer it to [15] for details.
It is worthy to point out that the above mentioned papers mainly focus on the scalar stochastic reaction-diffusion equation. Recently, Wen et al. [16] applied the theory of random monotone dynamical systems developed by Cheushov [17] and Kolmogorov tightness criterion to obtain the existence of stochastic travelling wave solution for stochastic two-species cooperative system
{du=[uxx+u(1−a1u+b1v)]dt+ϵudWt,dv=[vxx+v(1−a2v+b2u)]dt+ϵvdWt,u(0)=u0,v(0)=v0, | (1.1) |
where W(t) is a white noise as in [11], u0,v0 are both Heaviside functions, and ai,bi are positive constants satisfying min{ai}>max{bi}. The element "1" of 1−a1u+b1v and 1−a2v+b2u in Eq (1.1) is the formal environment carrying capacity, and then by constructing upper and lower solution and applying Feynman-Kac formula they obtained the estimation of upper bound and lower bound for wave speed, respectively. Moreover, Wen et al. [18] established the existence of stochastic travelling wave solution for stochastic two-species competitive system, and they obtained the upper bound and lower bound of the asymptotic wave. To the best of our knowledge, there are few papers concerning the stochastic travelling waves for cooperative N-species systems (N≥3), which leads to the motivation of the current work.
There are some papers that study the stability and stochastic persistence for the stochastic N-species system without space diffusion. For example, Cui and Chen [19] proved that there exists a unique globally asymptotically stable positive ω-periodic solution for the N-species time dependent Lotka-Volterra periodic mutualistic system
˙xi=xi(ri(t)+n∑j=1aij(t)xj),i=1,2,⋯,n, | (1.2) |
provided with (−1)kdet(max0≤t<+∞aij(t))1≤i,j≤k>0. Subsequently, Ji et al. [20] studied the N-species Lotka-Volterra mutualism system with stochastic perturbation
dxi(t)=xi(t)[(bi−n∑j=1aijxj(t))dt+σidBi(t)],i=1,2,⋯,n, |
and proved the sufficient criteria for persistence in mean and stationary distribution of the system. Moreover, they also showed the large white noise make the system nonpersistent, we refer the readers to [20,21] for details.
In this paper, we consider the travelling wave solution of the following stochastic N-species cooperative systems,
{du(i)=[u(i)xx+u(i)(ai−biiu(i)+n∑j=1j≠ibiju(j))]dt+ϵu(i)dWt,i=1,2,⋯,n,u(i)(0,x)=u(i)0=piχ(−∞,0],i=1,2,⋯,n, | (1.3) |
where W(t) is a Brownian motion, u(i)0(i=1,2,⋯,n) are Heaviside functions, ai represents the environment carrying capacity, and bij are positive constants satisfying min{bii}>2nmaxj≠k{bjk}, rank{(bij)n×n}=n.
To study the existence of stochastic travelling wave solution for stochastic N-species cooperative systems (1.3), it needs to introduce a suitable wavefront marker for system (1.3). The comparison method is applied to prove the boundedness of the solutions based on the random monotonicity and the Feynman-Kac formula. The existence of the travelling wave solution is focused on verifying the trajectory property, connecting the two states poses the support compactness propagation (SCP) property, defined by Shiga in [22].
Denote
Y=(u(1),u(2),⋯,u(n))T,Y0=(u(1)0,u(2)0,⋯,u(n)0)T, |
and
Fi(Y)=u(i)(ai−biiu(i)+n∑j=1j≠ibiju(j)),F(Y)=(F1(Y),⋯,Fn(Y))T, |
then the stochastic cooperative system (1.3) can be rewritten as the following vector equation
{dY=[Yxx+F(Y)]dt+ϵYdWt,Y(0,x)=Y0. | (1.4) |
For any matrix M=(mij)n×m, define the norm |⋅| as |M|=n∑i=1n∑j=1|mij|, and the vector norm is defined as ||A||∞=maxi(Ai) for vector A=(ai)n×1. Let Ω be the space of temper distributions, F be the σ-algebra on Ω, and (Ω,F,P) be the white noise probability space.
In order to apply the Feynman-Kac formula in [7], we can define
βt(k):=e∫t0k(s)dWs−12∫t0k2(s)ds,0≤t<∞. |
Denote by
ϕλ(x)=e−λ|x|,||f||λ=supx∈R(|f(x)ϕλ(x)|),C+={f|f:R→[0,∞)andfiscontinuous},C+λ={f∈C+|fiscontinuous,and|f(x)ϕλ(x)|→0asx→±∞},C+tem=∩λ>0C+λ. |
C+C[0,1]={f|f:R→[0,1]} is space of nonnegative functions with compact support, Φ={f:||f||λ<∞forsomeλ<0} is the space of functions with exponential decay, and C+tem is the space of vector valued functions whose each component belongs to C+tem.
The rest of the paper is organized as follows. In Section 2, the existence of stochastic travelling wave solution is established. In Section 3, the upper and lower bound of asymptotic wave speed are obtained. An example of 3-species stochastic cooperative system is also presented in Section 4.
In this section, we establish the existence of stochastic travelling wave solution. We first provide with the definition of stochastic travelling wave solution, which is from [1]. To the end, it needs to define some state space follows as
D[0,∞)={ϕ:R→[0,∞),ϕis right continuous and decreasing,ϕ−∞=limx→−∞ϕexists}.D[0,1]={ϕ:R→[0,1],ϕis right continuous and decreasing}.D={ϕ∈D[0,1]:ϕ(−∞)=1,ϕ(∞)=0}. |
We endow D[0,∞) with the topology induced from L1loc(R) metric. Then D[0,1] and D are the measurable subset of D[0,∞). It follows from [13] that D[0,∞), D[0,1] and D are Polish spaces and compact.
Consider the following stochastic reaction diffusion equation with Heaviside data
{du=[Duxx+f(u)]dt+σ(u)dWt,u(0)=χx≤0. | (2.1) |
Definition 2.1 (Stochastic travelling wave solution). A stochastic travelling wave is a solution u=(u(t):t≥0) to (2.1) with values in D and for which the centered process (˜u(t)=u(t,⋅+R0(t)):t≥0) is a stationary process with respect to time, where R0(t) is a wave front marker. The law of a stochastic travelling wave is the law of ˜u(0) on D.
Then, we prove the following Lemmas 2.2 and 2.3 by the idea of Tribe [1].
Lemma 2.2. For any Heaviside functions Y0, and a.e. ω∈Ω, there exists a unique solution to (1.4) in law with the form
Y(t,x)=∫RG(t,x,y)Y0dy+∫t0∫RG(t−s,x,y)F(Y)dsdy+ϵ∫t0∫RG(t−s,x,y)YdWsdy, | (2.2) |
where G(t,x,y) is Green function, and Y(t,x)∈C+tem.
Lemma 2.3. All solutions to (1.4) started at Y0 have the same law which we denote by QY0,ai,bij, and the map (Y0,ai,bij)→QY0,ai,bij is continuous. The law QY0,ai,bij for Y0 as a Heaviside function forms a strong Markov family.
Next, we estimate the term Y(t,x), which is key tools to prove the existence of stochastic travelling wave solutions.
Theorem 2.4. For any Heaviside functions u(i)0, and t>0 fixed, a.e. ω∈Ω, it permits that
E[n∑i=1u(i)(t,x)]≤C(ϵ,t)(n∑i=1u(i)0+αk−ϵ22k),∀x∈R, | (2.3) |
where C(ϵ,t) is a constant, k=mini{bii}−(n−1)maxi≠j{bij}n, α=maxi{ai}.
Proof. Denote by ϕ(t,x)=n∑i=1u(i)(t,x), we have
{dϕ=[ϕxx+n∑i=1u(i)(t,x)(ai−biiu(i)+n∑j=1j≠ibiju(j))]dt+ϵϕdWt,ϕ(0,x)=ϕ0=n∑i=1u(i)0, | (2.4) |
Since min{bii}>2nmaxj≠k{bjk}, then
n∑i=1u(i)(ai−biiu(i)+n∑j=1j≠ibiju(j))≤αn∑i=1u(i)−mini{bii}n∑i=1(u(i))2+2maxi≠j{bij}n∑i,j=1i<ju(i)u(j)≤αn∑i=1u(i)−kn∑i=1(u(i))2≤n∑i=1u(i)(α−kn∑i=1u(i)). |
Let ψ be the solution of the following equation
{dψ=[ψxx+ψ(α−kψ)]dt+ϵψdWt,ψ0=n∑i=1u(i)0, | (2.5) |
then, u(i)(t,x)≤ψ(t,x) a.s., i=1,2,⋯,n.
Let ζ be a solution to the following equation
{ζt=ζxx+ζ(α−kζ)−ϵ22ζ,ζ0=ψ0. | (2.6) |
We claim that for every (t,x)∈[0,∞)×R, it follows
einf0≤r≤t∫trϵdWsζ(t,x)≤ψ(t,x)≤esup0≤r≤t∫trϵdWsζ(t,x)a.s. | (2.7) |
In fact, we prove this claim by contradiction. We suppose that there is (t0,x0)∈[0,∞)×R such that
ψ(t0,x0)>esup0≤r≤t0∫t0rϵdWsζ(t0,x0), | (2.8) |
which implies that
ψ(t0,x0)>ζ(t0,x0). |
To construct a new probability space (ˆΩ,ˆF,ˆP), and denote ˆW=(ˆW(t):t≥0) be a Brownian motion over the new probability space. Let Xt0,x0s=(t0−s,x0+√2ˆW(s)),s>0, and define a stopping time
τ=inf{s>0:ζ(Xt0,x0s)=ψ(Xt0,x0s)}, |
for each ω∈ˆΩ. Using the stochastic Feynman-Kac formula and by the strong Markov property, we have almost surely
ψ(t0,x0)=ˆE[ψ(Xt0,x0τ)exp(∫τ0(α−kψ(Xt0,x0τ))]×exp(∫t0t0−τϵdWs−12∫t0t0−τϵ2ds)≤ˆE[ζ(Xt0,x0τ)e∫τ0(α−kζ(Xt0,x0τ))ds]×e∫t0t0−τϵdWs−12∫t0t0−τϵ2ds=esup0≤r≤t0∫t0t0−rϵdWsζ(t0,x0), |
which contradicts (2.8) and the upper bound is proved.
Similarly, we have almost surely
ψ(t0,x0)≥exp(inf0≤r≤t0∫t0rϵdWs)ζ(t0,x0)a.s. |
For arbitrary t>0 fixed, for any σ>0, multiplying G(t−s+σ,x−y) in (2.6) and integrating over R, we obtain
∂∂s∫Rζ(s,y)G(t−s+σ,x−y)dy≤(α−ϵ22)∫Rζ(s,y)G(t−s+σ,x−y)dy−k(∫Rζ(s,y)G(t−s+σ,x−y)dy)2. |
Let φ(s)=∫Rζ(s,y)G(t−s+σ,x−y)dy, thus we get
{dφ(s)ds≤(α−ϵ22)φ(s)−kφ2(s),φ0=∫Rζ0G(t+σ,x−y)dy. | (2.9) |
In general, we have
φ(s)≤φ0+αk−ϵ22k, | (2.10) |
which implies
∫Rζ(t,y)G(σ,x−y)dy≤∫Rζ0G(t+σ,x−y)dy+αk−ϵ22k. | (2.11) |
Let σ→0, then
ζ(t,x)≤∫Rζ0G(t,x−y)dy+αk−ϵ22ka.s. | (2.12) |
Combining the above estimate with (2.7), we obtain
n∑i=1u(i)(t,x)≤esup0≤r≤t∫trϵdWs×(∫Rψ0G(t,x−y)dy+αk−ϵ22k)a.s. | (2.13) |
Fixing the initial data u(i)0=piχ(−∞,0], and taking the expectation, we get
E[n∑i=1u(i)(t,x)]≤C(ϵ,t)(n∑i=1u(i)0+αk−ϵ22k), | (2.14) |
where C(ϵ,t)=E[esup0≤r≤t∫trϵdWs].
Lemma 2.5. For any Heaviside functions u(i)0, a.e. ω∈Ω and t>0, one has
E[n∑i=1|u(i)(t)|2]≤E[n∑i=1|u(i)0|2]e−t+K(1−e−t), | (2.15) |
where K=(ϵ6+2α+1)3n54k2.
Proof. Let V(t):=n∑i=1|u(i)(t)|2, by Itô formula we have
dV(t)=2n∑i=1⟨u(i),△u(i)⟩dt+2n∑i=1⟨u(i),aiu(i)−bii(u(i))2+n∑j=1biju(i)u(j)⟩dt+ϵ2n∑i=1(u(i))2dt+2ϵn∑i=1(u(i))2dWt. |
Integrate both sides on [0,t] and take expectation, we have
E[V(t)]=En∑i=1(u(i)0)2+2En∑i=1∫t0⟨u(i),△u(i)⟩ds+2En∑i=1∫t0⟨u(i),aiu(i)−bii(u(i))2+n∑j=1biju(i)u(j)⟩ds+ϵ2n∑i=1E∫t0(u(i))2ds≤En∑i=1(u(i)0)2−2En∑i=1∫t0|∇u(i)|2ds+2αEn∑i=1∫t0(u(i))2ds−2kEn∑i=1∫t0(u(i))3ds+ϵ2En∑i=1∫t0(u(i))2ds≤En∑i=1(u(i)0)2−2kEn∑i=1∫t0(u(i))3ds+2αEn∑i=1∫t0(u(i))2ds+ϵ2En∑i=1∫t0(u(i))2ds+En∑i=1∫t0(u(i))2ds−En∑i=1∫t0(u(i))2ds. |
By Young inequality we have
(2α+1)E∫t0n∑i=1(u(i))2ds≤k∫t0En∑i=1(u(i))3ds+(2α+1)3n54k3t, | (2.16) |
and
ϵ2E∫t0n∑i=1(u(i))2ds≤k∫t0En∑i=1(u(i))3ds+ϵ6n54k2t. | (2.17) |
Combining (2.16) with (2.17) offers that
E[n∑i=1|u(i)(t)|2]≤E[n∑i=1|u(i)0|2]+(ϵ6+2α+1)3)n54k2t−En∑i=1∫t0(u(i))2ds. |
Thus by Gronwall inequality we have
Esup0≤t≤T[n∑i=1|u(i)(t)|2]≤E[n∑i=1|u(i)0|2]e−t+(ϵ6+2α+1)3)n54k2(1−e−t). |
Modifying the argument in Lemma 2.1 from [1], we can estimate how fast the compact support of Y(t) can spread.
Lemma 2.6. Let Y(t,x) be a solution to (1.4) started at Y0, suppose for some R>0 that Y0 is supported outside (−R−2,R+2), then for any t≥1,
P(∫t0∫R−R||Y(s,x)||∞dsdx>0)≤Cet∫√t|x|−(R+1)exp(−(|x|−(R+1))22t)||Y0||∞dx. |
Proof. From Theorem 2.4, we know the solution Y(t,x) is uniformly bounded, thus the sup-solution solves
{dv(i)=[v(i)xx+v(i)(k−bv(i))]dt+ϵv(i)dWt,v(i)(0)=u(i)0,i=1,2,⋯,n, | (2.18) |
where k>0 is a constant satisfying Fi(Y)≤u(k−bu). Refer to [1,23], the proof can be completed.
Remark 1. When R0(t) is defined as a wavefront marker as in [1], the SCP property of Y(t,x) can not hold. Additionally, we can not ensure the translational invariance of the solution Y(t,x) with respect to R0(t). However thanks to Lemma 2.6, we can choose a suitable wavefront marker to ensure the SCP property of Y(t) holds.
It is easy to verify that Y(t,x) satisfy Kolmogorov tightness criterion, and Y(t,x)∈K(C,δ,μ,γ), which helps constructing a probability measure sequence, which is convergent.
Lemma 2.7. For any Heaviside functions u(i)0, t>0, fixed p≥2 and a.e. ω∈Ω, if |x−x′|≤1, there exists positive constant C(t), such that
QY0(|Y(t,x)−Y(t,x′)|p)≤C(t)|x−x′|p/2−1. |
Proof. Referring to [1], it is not difficult to complete the proof.
Define QY0 as the law of the unique solution to Eq (1.4) with initial data Y(0)=Y0. For a probability measure ν on C+tem, we define
Qν(A)=∫C+temQY0(A)ν(dY0). |
In order to construct the travelling wave solution to Eq (1.3), we must ensure that the translation of solution with respect to a wavefront marker is stationary and the solution poses the SCP property. However, R0(Y(t)) does not satisfy this condition. So we have to choose a new suitable wavefront marker. As the solution to (1.4) with Heaviside initial condition is exponentially small almost surely as x→∞, with the stochastic Feynman-Kac formula we may turn to R1(t):C+tem→[−∞,∞] defined as
R1(f)=ln∫Rexfdx,R1(u(i)(t))=ln∫Rexu(i)(t)dx, |
and
R1(t):=R1(Y(t))=maxi{R1(u(i)(t))}. |
The marker R1(t) is an approximation to R0(Y(t))=maxi{R0(u(i)(t))}.
Let
Z(t)=Y(t,⋅+R1(t))=(Z1(t),Z2(t),⋯,Zn(t))T,Z0(t)=Y(t,⋅+R0(Y(t))), |
and define
Z(t)={(0,0,⋯,0)T,R1(t)=−∞,(u(1)(t,⋅+R1(t)),u(2)(t,⋅+R1(t))⋯,u(n)(t,⋅+R1(t)))T,−∞<R1(t)<∞(p1,p2,⋯,pn)T,R1(t)=∞. |
Hence Z(t) is the wave shifted so that the wavefront marker R1(t) lies at the origin. Note that whenever R0(Y0)<∞, the compact support property implies that R0(t)<∞, ∀t>0, QY0-a.s.
Remark 2. Here we define R1(t) in the maximum form, not only since it simplifies the discussion about boundedness, but also the asymptotic wave speed is the minimum wave speed which keeps the travelling wave solution monotonic. As mentioned before, we approximate the asymptotic wave speed via c=limt→∞R1(t)t. Therefore, the wavefront marker R1(t) defined in such form can ensure the travelling wave solutions of the two subsystems monotonic.
Define
νT=thelawof1T∫T0Z(s)dsunderQY0. |
Now we summarise the method for constructing the travelling wave solution. With the initial data (u(1)0=p1χ(−∞,0],u(2)0=p2χ(−∞,0],⋯,u(n)0=pnχ(−∞,0])∈C+tem as Heaviside function, we shall show that the sequence {νT}T∈N is tight (see Lemma 2.9) and any limit point is nontrivial (see Theorem 2.10). Hence for any limit point ν (the limit is not unique), Qν is the law of a travelling wave solution. Two parts constituting the proof of tightness are Kolmogorov tightness criterion for the unshifted waves (see Lemma 2.7) and the control on the movement of the wavefront marker R1(t) to ensure the shifting will not destroy the tightness (see Lemma 2.8).
Lemma 2.8. For any Heaviside functions u(i)0, t≥0, d>0, T≥1, and a.e. ω∈Ω there exists a positive constant C(t)<∞, such that
QνT(|R1(t)|>d)≤C(t)d. | (2.19) |
Proof. By the comparison principle proposed in [24,25], we can construct a sup-solution satisfying, for i=1,2,⋯,n,
{d˜u(i)=[˜u(i)xx+k0˜u(i)]dt+ϵ˜udWt,˜u(i)0=u(i)0, | (2.20) |
where the constant k0>0 can be obtained by Theorem 2.4 such that Fi(Y)<k0u(i). Therefore, we know that u(i)(t)≤˜u(i)(t) hold on [0,T] uniformly, and for a.e. ω∈Ω the solution ˜Y(t,x) to Eq (2.20) is
˜Y(t,x)=∫Rek0tG(t,x−y)Y0(y)dy+ϵ∫R∫t0G(t−s,x−y)˜YdWsdy. | (2.21) |
Applying the comparison method yields, for any i=1,2,⋯,n we have
Qu(i)0(∫Ru(i)(t,x)exdx)≤E[∫R˜u(i)(t,x)exdx]=ek0t+t∫Ru(i)0(x)exdx. |
Without loss of generality, we assume that R1(t)=R1(u(1)(t)), then
∫Ru(1)(t,x+R1(t))exdx=e−R1(t)∫Ru(1)(t,x)exdx=1. |
Combing with the above arguments, we deduce that
QνT(R1(t)≥d)=1T∫T0Qu(1)0(Qu(1)(s)(e−d∫Ru(1)(t,x)exdx≥1))ds≤e−dek0t+t. |
Then the Jensen's inequality gives
Qu(1)0(R1(t))≤ln(ek0t+t∫Ru(1)0(x)exdx)≤k0t+t+R1(u(1)0). |
Direct calculation implies
1TQu(1)0(∫T+ttR1(s)ds−∫T0R1(s)ds)≤1T∫T0∫∞0Qu(1)0(R1(t+s)−R1(s)≥y)dyds−dT∫T0Qu(1)0(R1(t+s)−R1(s)≤−d)ds=∫∞0QνT(R1(t)≥y)dy−dQνT(R1(t)≤−d). |
Thus, by rearranging the above inequalities
QνT(R1(t)≤−d)≤1d∫∞0QνT(R1(t)≥y)dy+1dT∫T0QνT(R1(s))ds≤C(t)d, |
which completes the proof of Lemma 2.8.
We will prove the marker R1(t) is bounded, which helps to prove the sequence {νT:T∈N} is tight and the wavefront marker R0(t) is bounded. Next, we will show the tightness of {νT:T∈N} with Y(t,x)∈K(C,δ,μ,γ).
Lemma 2.9. For any Heaviside functions u(i)0, and a.e. ω∈Ω, the sequence {νT:T∈N} is tight.
Proof. Following the idea to prove Lemma 2.8, we focus on the term u(i)(t,x). Since Y(t,x)∈K(C,δ,μ,γ) gives u(i)(t,x)∈K(C,δ,μ,γ), then it is easy to prove that
νT(K(C,δ,γ,μ))=1T∫T0Qu(i)0(u(i)(t,⋅+R1(t))∈K(C,δ,γ,μ))ds≥1T∫T0Qu(i)0((u(i)(t,⋅+R1(t−1))∈K(Ce−μd,δ,γ,μ))×|R1(t)−R1(t−1)|≤d)ds≥1T∫T1Qu(i)0(QZ1(t−1)(u(i)(1)∈K(Ce−μd,δ,γ,μ)))dt−1T∫T1Qu(i)0(|R1(t)−R1(t−1)|≥d)dt=:I−II. |
With Lemma 2.8, II→0 as d→∞. Via the Kolmogorov tightness and Lemma 2.7, for given d,μ>0, one can choose C,δ,γ to make I as close to T−1T as desired. In addition, we have
νT{u(i)0:∫Ru(i)0(x)e−|x|dx≤∫Ru(i)0(x)exdx=1}=1. |
The definition of tightness implies that for given μ>0, one can choose C,δ,γ such that νT(K(C,δ,μ,γ)∩{u(i)0:∫Ru(i)0(x)e−|x|dx}) as close to 1 as desired for T and d sufficient large, which implies that the sequence {νT:T∈N} is tight.
Theorem 2.10. For any Heaviside functions u(i)0, and for a.e. ω∈Ω, there is a travelling wave solution to Eq (1.3), and Qν is the law of travelling wave solution.
Proof. By the comparison method, we have
Zi(t,x)≤et−ϵ22t+∫t0ϵdWs×1√2πt∫−x√2−∞e−|y|22tdya.s., |
under the law Qu(i)0 for t>0. Taking u(1)(t,x) together with Doob's inequality and (2.3), we have
u(1)(1,x)≤et−ϵ22+∫10ϵdWs×e−ϵ22(t−1)+∫t−10ϵdWs×12π√t−1∫+∞−∞∫−x√2−z−∞e−|y|22(t−1)dye−|y|22dz≤et−ϵ22+∫10ϵdWs×e−ϵ22(t−1)+∫t−10ϵdWs−x24ta.s., | (2.22) |
for all t>1. Integrate (2.22) in [d,∞) and take the expectation, we have
limd→∞Qu0(QZ1(t−1)(∫∞du(1)(1,x)dx))≤limd→∞√tet−d24t=0. | (2.23) |
Furthermore, it follows that
limd→∞Qu(1)0(QZ1(t−1)(∫∞du(1)(1,x)dx))=1, | (2.24) |
and
νT(u(1)0:limd→∞∫∞2du(1)0(x)dx=0)=1T∫T0Qu(1)0(∀δ>0,∃d0,∫∞2dZ1(t,x)dx)<δ∀d>d0)dt,|R1(t)−R1(t−1)|≤d,∀d>d0)dt≥1T∫T1Qu(1)0(QZ1(t−1)(limd→∞∫∞du(1)(1,x)dx=0))dt−limd→∞QνT(|R1(1)|≥d). | (2.25) |
Thus by Lemma 2.8, combining (2.24) with (2.25) gives
limT→∞limd→∞νT(u(1)0:∫∞du(1)0(x)dx=0)=1. | (2.26) |
To prove the boundness of R0(t), it follows from νTn(u(1)0:∫Ru(1)0(x)exdx=p1)=1 that ν(u(1)0:∫Ru(1)0(x)exdx≤p1)=1. Taking ed1(x)=ed−|x−d|, we have
ν(u(1)0:(u(1)0,ex)≥p1)≥ν(u(1)0:∫Ru(1)0(x)ed1(x)dx≥p1)≥limsupn→∞νTn(u(1)0:∫Ru(1)0(x)ed1(x)dx=p1)=limsupn→∞νTn(u(1)0:∫Ru(1)0(x)I(d,∞)dx)=0)→1,asd→∞. |
As ν(u(1)0:∫Ru(1)0(x)exdx=p1)=1, we obtain ν(u(1)0:R0(u(1)0)>−∞)=1. Now, we complete the half of the proof of the boundness of the wavefront marker R0(t). Take ψd∈Φ with (ψd>0)=(d,∞), then
ν(u(1)0:R0(u(1)0)≤d)=ν(u(1)0:∫Ru(1)0(x)ψd(x)dx=0)≥limsupn→∞νTn(u(1)0:∫Ru(1)0(x)ψd(x)dx=0)=limsupn→∞νTn(u(1)0:∫Ru(1)0(x)I(d,∞)dx=0)→1,asd→∞, |
so we have ν(Y0:−∞<R0(Y0)<∞)=1 and complete the proof of the boundedness of the wavefront marker R0(t). To verify that the solution Y(t) is nontrivial, let Rd1(t)=ln∫||Y(t)||∞ed1(x)dx, we have
Qν(∃s≤t,|Y(s)|=0)≤Qν(Rd1(t)<−d)≤limsupn→∞QνTn(Rd1(t)<−d)≤limsupn→∞(QνTn(R1(t)<−d)+QνTn(∫Ru(i)(t,x)I(d,∞)dx>0))≤C(t)d→0,asd→∞. |
We now show that Z(t) is a stationary process and Qν is the law of a travelling wave solution to (1.3). Let F:C+tem→R be bounded and continuous, and take u(i)(t,x) for example, for any fixed t>0
|QνTn(F(Zi(t)))−Qν(F(Zi(t)))|≤|QνTn(F(u(i)(t,⋅+Rd1(t))))−Qν(F(u(i)(t,⋅+Rd1(t))))|+||F(u(i)0)||∞(QνTn(R1(t)≠Rd1(t))+Qν(R1(t)≠Rd1(t))), |
since νTn(u(i)0:∫Ru(i)0exdx=pi)=1, we have
QνTn(R1(t)≠Rd1(t))≤QνTn(∫Ru(i)(t,x)I(d,∞)dx>0)≤C(k0,t)/d, | (2.27) |
and with ν(u(i)0:∫Ru(i)0exdx=pi)=1, we have
Qν(R1(t)≠Rd1(t))≤Qν(∫Ru(t,x)I(d,∞)dx>0)≤C(k0,t)/d. | (2.28) |
By the continuity of u(i)0→Qu(i)0, one have QνTn→Qν. Since F is bounded and continuous, we obtain that
|QνTn(F(u(i)(t,⋅+Rd1(t))))−Qν(F(u(i)(t,⋅+Rd1(t))))|→0,asn→∞. |
Therefore, we have
Qν(F(Zi(t)))=limn→∞QνTn(F(Zi(t)))=limn→∞1Tn∫Tn0Qu0(F(Zi(s)))ds=ν(F). |
It is straightforward to check that {Z(t):t≥0} is Markov, hence {Z(t):t≥0} is stationary. Since the map Y0→Y0(⋅−R0(Y0)) is measurable on C+tem, the process {Z0(t):t≥0} is also stationary, which implies that Qν is the law of the travelling wave solution to Eq (1.3).
In this section, we investigate the asymptotic property of the travelling wave solutions. By constructing the sup-solution and the sub-solution, we obtain the asymptotic wave speed for the two travelling wave solutions respectively. Then we have the estimation of the wave speed of travelling wave solutions to (1.3). Since the asymptotic wave speed c of the travelling wave solution defined as
c=limt→∞R0(t)ta.s., |
we denote by R0(u(i)(t))=sup{x∈R:u(i)(t,x)>0} for the sub-systems of the cooperative system. Since the wavefront marker R0(t) of the cooperative system is R0(t)=maxi{R0(u(i)(t))}, and the asymptotic wave speed is the maximum value among limt→∞R0(u(i)(t))t, we can define the wave speed c⋆ as
c⋆=limt→∞R0(Y(t))ta.s. |
We now construct a sup-solution. Let ˉY(t,x)=(ˉu(1)(t,x),⋯,ˉu(n)(t,x))T satisfying
{dˉu(i)=[ˉu(i)xx+ˉu(p−biiˉu)]dt+ϵˉudWt,ˉu(i)0=u(i)0,i=1,2,⋯,n, | (3.1) |
where Fi(Y)≤u(i)(p−biiu(i)), p=maxi≠j{bij}×maxi{√∑ni=1|u(i)0|2+K,C(ϵ,t)(n∑i=1u(i)0+αk−ϵ22k),pi}+1. Then we construct a sub-solution, denote by a=min{ai} and let Y_(t,x)=(u_(1)(t,x),⋯,u_(n)(t,x))T satisfy
{du_(i)=[u_(i)xx+u_(i)(a−biiu_)]dt+ϵu_dWt,u_(i)0=u(i)0,i=1,2,⋯,n. | (3.2) |
Obviously, Fi(Y)≥u(i)(a−biiu(i)). With Eq (3.1) and (3.2), we have such following conclusion:
Theorem 3.1. For any Heaviside functions u(i)0, let c⋆ be the asymptotic wave speed of Eq (1.3), then
√4a−2ϵ2≤c⋆≤√4p−2ϵ2a.s. | (3.3) |
In order to prove Theorem 3.1, we need the following lemmas. We first introduce the comparison method for the asymptotic wave speed.
Lemma 3.2. Let Y_(t,x) and ˉY(t,x) be the solutions to (3.2) and (3.1) respectively, if c_ is the asymptotic wave speed of Y_(t,⋅+R0(Y_(t))) and ˉc is the asymptotic wave speed of ˉY(t,⋅+R0(ˉY(t))), then
c_≤c⋆≤ˉca.s. |
Proof. The comparison method for the stochastic diffusion equation gives that Y_(t,x)≤Y(t,x)≤ˉY(t,x), which implies u_(i)(t,x)≤u(i)(t,x)≤ˉu(i)(t,x) a.s. and v_(i)(t,x)≤v(i)(t,x)≤ˉv(i)(t,x) a.s.. Denote the wavefront markers by R1(Y_(t)), R1(Y(t)) and R1(ˉY(t)), with the definition of asymptotic wave speed
c=limt→∞R1(t)ta.s., |
and the definition of the wavefront marker
R1(Y(t))=maxi{ln∫Ru(i)(t,x)exdx}, |
it gives
limt→∞R1(Y_(t))t≤limt→∞R1(Y(t))t≤limt→∞R1(ˉY(t))ta.s., | (3.4) |
which implies c_≤c⋆≤ˉca.s.. Thus, the proof of Lemma 3.1 is complete.
Now we show the asymptotic property of the wavefront marker of the sub-solution. Consider Eq (3.2), for i=1,2,⋯,n,
{du_(i)=[u_(i)xx+u_(i)(a−biiu_(i))]dt+ϵu_(i)dWt,u_(i)0=u0. |
Obviously u_(i) are independent from each other, thus we can divide (3.2) into n equations to study. For each equation one can have the asymptotic wave speed c(u_(i)) respectively, so the asymptotic wave speed of (3.2) is c(Y_)=maxi{c(u_(i))}.
Theorem 3.3. For any Heaviside functions u(i)0, Y_(t,x) is solution to (3.2), then the asymptotic wave speed c(Y_) satisfies
c(Y_)=√4a−2ϵ2a.s., | (3.5) |
where a=mini{ai}.
Proof. For any h>0, take κ∈(0,h24+√1−ϵ22h) and define
ηt(ω)=e∫t0ϵdWs−12∫t0ϵ2ds,0≤t≤∞, |
construct new probability space (˜Ω,˜F,˜P), ˜W=(˜W(t):t≥0) is a Brownian motion. Then there exists T1>0, such that for t≥T1 and a.e. ω∈Ω
e−ϵ22t−κt≤ηt(ω)≤e−ϵ22t+κt. |
Thus the stochastic Feynman-Kac formula gives
u_(i)(t,x)≤eat−12ϵ2t+κt˜P(˜W(t)≤−x√2)≤eat−12ϵ2t+κt−x24ta.s., |
for t≥T1. For a constant k, set x≥(k+h)t. Multiple ex with both sides and integrate in [(k+h)t,∞), we have
∫∞(k+h)tu_(i)(t,x)exdx≤∫∞(k+h)texp(at−12ϵ2t+κt−x24t+x)dx≤2√teat−12ϵ2t+κt+t∫∞(k+h)t−2t√4te−x2dx≤√tea+κ−k24−kh2−h24−k−h−ϵ22ta.s., |
for t≥T1. Let k=√4a−2ϵ2+4−2, then we obtain
limt→∞∫∞(k+h)tu_(i)(t,x)exdx=0a.s. | (3.6) |
Integrating u_(i)(t,x)ex in [(√4a−2ϵ2+h)t,(k−h)t) yields
∫(k−h)t(√4a−2ϵ2+h)tu_(i)(t,x)exdx≤∫(k−h)t(√4a−2ϵ2+h)texp(at−12ϵ2t+κt−x24t+x)dx≤2√teat−12ϵ2t+κt+t∫(k−h)t−2t2√2(√4a−2ϵ2+h)t−2t2√te−x2dx≤√texp(at−ϵ22t+κt−4a−2ϵ24t−(√4a−2ϵ2)h2t−h24t+√4a−2ϵ2t+ht)−√texp(at−ϵ22t+κt−k24t+kh2t−h24t+kt−ht)≤√teκt+√4a−2ϵ2t−(√4a−2ϵ2)h2t−h24t+ht−√teκt−k24t+kh2t−h24t−hta.s., |
for t≥T1. Thus, we have
∫(√4a−2ϵ2+h)t(√4a−2ϵ2−h)tu_(i)(t,x)exdx≤√teκt+√4a−2ϵ2t+√4a−2ϵ2h2t−h24t−ht−√teκt+√4a−2ϵ2t−√4a−2ϵ2h2t−h24t+hta.s., |
and
∫(k+h)t(k−h)tu_(i)(t,x)exdx≤√teκt+kh2t−h24t−ht−√teκt−kh2t−h24t+hta.s., |
for t≥T1. Referring to [7], there exists T2>0, such that for all t≥T2 and x<(√4a−2ϵ2−h)t, there exist ρ1,ρ2>0 satisfying
e−ρ1√2tlnlnt≤u_(i)(t,x)≤eρ2√2tlnlnta.s., | (3.7) |
which goes into
∫(√4a−2ϵ2−h)t−∞u_(i)(t,x)exdx≤eρ2√2tlnlnt+(√4a−2ϵ2−h)ta.s. | (3.8) |
Since ∫∞(k+h)tu_(i)(t,x)exdx≤1, then we have
∫Ru_(i)(t,x)exdx≤eρ2√2tlnlnt+(√4a−2ϵ2−h)t(2+H(t)+G(t))a.s., | (3.9) |
where
H(t)=√te12ϵ2−ϵ22t+κt+kh2t−h24t−ρ2√2tlnlnt−√4a−2ϵ2t≤1, |
and
G(t)=√te12ϵ2−ϵ22t+κt−√4a−2ϵ2h2t−ρ2√2tlnlnt−h24t+2ht. |
Since h and κ are arbitrary, we derive that H(t)≤1 a.s. for large t. Direct calculation implies that almost surely
1tlnG(t)=12tln4t−1t(ln2−ϵ22+ϵ22t)+κ−4a−2ϵ24h−h24+2h−1tρ2√2tlnlnt, |
and
limt→∞1tlnG(t)=0. | (3.10) |
Hence, we obtain the upper bound of the asymptotic wave speed of the travelling wave solution to (3.2)
R1(t)t≤1tρ2√2tlnlnt+√4a−2ϵ2−h+1tln2+1tlnG(t)a.s. | (3.11) |
Moreover, it follows that
limsupt→∞R1(t)t≤√4a−2ϵ2a.s. | (3.12) |
and
R1(t)t≥−1tρ1√2lnlnt+√4a−2ϵ2−ha.s. | (3.13) |
Thus, we deduce that the lower bound followed as
liminft→∞R1(t)t≥√4a−2ϵ2a.s. | (3.14) |
Combining (3.12) and (3.14), we can get
limt→∞R1(t)t=√4a−2ϵ2a.s. | (3.15) |
The proof of Theorem 3.3 is complete.
By the method used in Theorem 3.3, we consider the sup-solution ˉY(t,x) satisfying the following equation, for i=1,2,⋯,n
{dˉu(i)=[ˉu(i)xx+ˉu(i)(p−a1ˉu(i))]dt+ϵˉudWt,ˉu(i)0=u(i)0. |
Similar to the proof of Theorem 3.3, we obtain the following result:
Theorem 3.4. For any Heaviside functions u(i)0, ˉY(t,x) is a solution to (3.1), then the asymptotic wave speed c(ˉY) satisfies
c(ˉY)=√4p−2ϵ2a.s. | (3.16) |
Based on discussion above, and combaining Theorem 3.3 and Theorem 3.4, with Lemma 3.2 we can achieve the conclusion:
√4a−2ϵ2≤c⋆≤√4p−2ϵ2a.s. | (3.17) |
which ends of the proof of Theorem 3.1.
Recently, Zhao and Shao [26] studied the asymptotic stability and stability of stochastic 3-species cooperative system without diffusion. Shao et al. [27] studied the stochastic permanence, stability and optimal harvesting policy of a 3-three species cooperative system with delays and Lévy jumps. In this section, we apply the above conclusions to the following 3-species stochastic cooperative system and give some results about stochastic travelling waves
{du=[uxx+u(a1−b1u+c1v)]dt+ϵudWt,dv=[vxx+v(a2−b2v+c2u+d1w)]dt+ϵvdWt,dw=[wxx+w(a3−b3w+c3v)]dt+ϵwdWt,u(0,x)=u0,v(0,x)=v0,w(0,x)=w0. | (4.1) |
If min{bi}>max{ci,d1} and b2≥b1+b3, it is easy to know that (0,0,0) is unstable, and (a1b1+c1b1×a2b1b3+a1b3c2+a3b1d1b1b2b3−b1c3d1−b3c1c2,a2b1b3+a1b3c2+a3b1d1b1b2b3−b1c3d1−b3c1c2,a3b3+c3b3×a2b1b3+a1b3c2+a3b1d1b1b2b3−b1c3d1−b3c1c2):=(p1,p2,p3) is the only stable point, which implies that 3-species coexist. Repeating the above argument on the stochastic cooperative systems (4.1), we have the following results:
Theorem 4.1. For any Heaviside functions u0,v0,w0, and ai,bi,ci,d1 are positive constants satisfying min{bi}>max{ci,d1}, b2≥b1+b3, then for a.e. ω∈Ω, there exists a travelling wave solution to Eq (4.1). Moreover, the asymptotic wave speed can be obtained
√4a−2ϵ2≤c≤√4p−2ϵ2a.s., | (4.2) |
where
p=2max{ci,d1}×max{E[esup0≤r≤t∫trϵdWs](u0+v0+w0+αk−ϵ22k),√|u0|2+|v0|2+|w0|2+ϵ6+(2α+1)318k2,p1,p2,p3}+α, |
and α=max{ai}, a=min{ai}, k=min{bi}−max{ci,d1}3.
This paper introduces the travelling wave solution of stochastic N-species cooperative systems with noise, and we obtain the existence of travelling wave solution in law and estimate its corresponding wave speed. The upper bound of asymptotic wave speed depends on all the coefficients and the strength and noise, while the lower bound only relies on the environment capacity and strength of the noise. In fact, the minimal propagation speed of travelling wave depends on the supporting capacity of the natural environment, and the maximum propagation speed relies on the interspecific interaction intensity and intrinsic growth rate.
The authors have not used Artificial Intelligence (AI) tools in the creation of this article.
This paper has been funded by National Natural Science Foundation of China (11771449, 12031020, 61841302), and Natural Science Foundation of Hunan Province, China (2020JJ4102). In addition, we thank the anonymous referees for their valuable comments and suggestions.
The authors declare that there are no conflicts of interest.
[1] |
Mathee K, Cickovski T, Deoraj A, et al. (2020) The gut microbiome and neuropsychiatric disorders: implications for attention deficit hyperactivity disorder (ADHD). J Med Microbiol 69: 14-24. doi: 10.1099/jmm.0.001112
![]() |
[2] |
Vigo D, Thornicroft G, Atun R (2016) Estimating the true global burden of mental illness. Lancet Psychiatry 3: 171-178. doi: 10.1016/S2215-0366(15)00505-2
![]() |
[3] |
Os J, Kenis G, Rutten BP (2010) The environment and schizophrenia. Nature 468: 203-212. doi: 10.1038/nature09563
![]() |
[4] |
Köhler-Forsberg O, Petersen L, Gasse C, et al. (2019) A nationwide study in denmark of the association between treated infections and the subsequent risk of treated mental disorders in children and adolescents. JAMA Psychiatry 76: 271-279. doi: 10.1001/jamapsychiatry.2018.3428
![]() |
[5] |
Goldsmith DR, Rapaport MH, Miller BJ (2016) A meta-analysis of blood cytokine network alterations in psychiatric patients: comparisons between schizophrenia, bipolar disorder and depression. Mol Psychiatry 21: 1696-1709. doi: 10.1038/mp.2016.3
![]() |
[6] |
Krefft M, Frydecka D, Zalsman G, et al. (2021) A pro-inflammatory phenotype is associated with behavioural traits in children with Prader-Willi syndrome. Eur Child Adolesc Psychiatry 30: 899-908. doi: 10.1007/s00787-020-01568-7
![]() |
[7] |
Shahbazi R, Yasavoli-Sharahi H, Alsadi N, et al. (2020) Matar, C. Probiotics in treatment of viral respiratory infections and neuroinflammatory disorders. Molecules 25: 4891. doi: 10.3390/molecules25214891
![]() |
[8] |
Barona M, Brown M, Clark C, et al. (2019) White matter alterations in anorexia nervosa: Evidence from a voxel-based meta-analysis. Neurosci Biobehav Rev 100: 285-295. doi: 10.1016/j.neubiorev.2019.03.002
![]() |
[9] |
Bastiaanssen TFS, Cryan JF (2021) The microbiota-gut-brain axis in mental health and medication response: parsing directionality and causality. Int J Neuropsychopharmacol 24: 216-220. doi: 10.1093/ijnp/pyaa088
![]() |
[10] |
Martins LB, Braga Tibães JR, Sanches M, et al. (2021) Nutrition-based interventions for mood disorders. Expert Rev Neurother 21: 303-315. doi: 10.1080/14737175.2021.1881482
![]() |
[11] |
Cerdó T, Diéguez E, Campoy C (2020) Impact of gut microbiota on neurogenesis and neurological diseases during infancy. Curr Opin Pharmacol 50: 33-37. doi: 10.1016/j.coph.2019.11.006
![]() |
[12] |
Gubert C, Kong G, Renoir T, et al. (2020) Exercise, diet and stress as modulators of gut microbiota: Implications for neurodegenerative diseases. Neurobiol Dis 134: 104621. doi: 10.1016/j.nbd.2019.104621
![]() |
[13] |
Berding K, Vlckova K, Marx W, et al. Diet and the microbiota-gut-brain axis: sowing the seeds of good mental health (2021) . doi: 10.1093/advances/nmaa181
![]() |
[14] |
Rea K, Dinan TG, Cryan JF (2020) Gut microbiota: a perspective for psychiatrists. Neuropsychobiology 79: 50-62. doi: 10.1159/000504495
![]() |
[15] |
Zinchenko E, Navolokin N, Shirokov A, et al. (2019) Pilot study of transcranial photobiomodulation of lymphatic clearance of beta-amyloid from the mouse brain: breakthrough strategies for non-pharmacologic therapy of Alzheimer's disease. Biomed Opt Express 10: 4003-4017. doi: 10.1364/BOE.10.004003
![]() |
[16] |
Mishra SP, Shukla SK, Pandey BL (2014) A preliminary evaluation of comparative effectiveness of riluzole in therapeutic regimen for irritable bowel syndrome. Asian Pac J Trop Biomed 4: S335-S340. doi: 10.12980/APJTB.4.2014C205
![]() |
[17] |
Barberio B, Zamani M, Black CJ, et al. (2021) Prevalence of symptoms of anxiety and depression in patients with inflammatory bowel disease: a systematic review and meta-analysis. Lancet Gastroenterol Hepatol 6: 359-370. doi: 10.1016/S2468-1253(21)00014-5
![]() |
[18] |
Dinan TG, Cryan JF (2017) Gut instincts: microbiota as a key regulator of brain development, ageing and neurodegeneration. J Physiol 595: 489-503. doi: 10.1113/JP273106
![]() |
[19] |
Wang J, Gu X, Yang J, et al. (2019) Gut microbiota dysbiosis and increased plasma LPS and TMAO levels in patients with preeclampsia. Front Cell Infect Microbiol 9: 409. doi: 10.3389/fcimb.2019.00409
![]() |
[20] |
Stasi C, Caserta A, Nisita C, et al. (2019) The complex interplay between gastrointestinal and psychiatric symptoms in irritable bowel syndrome: A longitudinal assessment. J Gastroenterol Hepatol 34: 713-719. doi: 10.1111/jgh.14375
![]() |
[21] |
Kelly JR, Clarke G, Cryan JF, et al. (2016) Brain-gut-microbiota axis: challenges for translation in psychiatry. Ann Epidemiol 26: 366-372. doi: 10.1016/j.annepidem.2016.02.008
![]() |
[22] |
Winter G, Hart RA, Charlesworth RPG, et al. (2018) Gut microbiome and depression: what we know and what we need to know. Rev Neurosci 29: 629-643. doi: 10.1515/revneuro-2017-0072
![]() |
[23] |
Zheng P, Zeng B, Zhou C, et al. (2016) Gut microbiome remodeling induces depressive-like behaviors through a pathway mediated by the host's metabolism. Mol Psychiatry 21: 786-796. doi: 10.1038/mp.2016.44
![]() |
[24] |
Yang C, Qu Y, Fujita Y, et al. (2017) Possible role of the gut microbiota-brain axis in the antidepressant effects of (R)-ketamine1 in a social defeat stress model. Transl Psychiatry 7: 1294. doi: 10.1038/s41398-017-0031-4
![]() |
[25] |
Lyte M, Daniels KM, Schmitz-Esser S (2019) Fluoxetine-induced alteration of murine gut microbial community structure: evidence for a microbial endocrinology-based mechanism of action responsible for fluoxetine-induced side effects. Peer J 7: e6199. doi: 10.7717/peerj.6199
![]() |
[26] |
Saini A, Ardine M, Berruti A (2008) Major depressive disorder. N Engl J Med 358: 1868-1869. doi: 10.1056/NEJMc080186
![]() |
[27] |
Arneth BM (2018) Gut-brain axis biochemical signalling from the gastrointestinal tract to the central nervous system: gut dysbiosis and altered brain function. Postgrad Med J 94: 446-452. doi: 10.1136/postgradmedj-2017-135424
![]() |
[28] |
Borre YE, O'Keeffe GW, Clarke G, et al. (2014) Microbiota and neurodevelopmental windows: implications for brain disorders. Trends Mol Med 20: 509-518. doi: 10.1016/j.molmed.2014.05.002
![]() |
[29] |
Barbara G, Stanghellini V, Brandi G, et al. (2005) Interactions between commensal bacteria and gut sensorimotor function in health and disease. Am J Gastroenterol 100: 2560-2568. doi: 10.1111/j.1572-0241.2005.00230.x
![]() |
[30] |
Strandwitz P (2018) Neurotransmitter modulation by the gut microbiota. Brain Res 1693: 128-133. doi: 10.1016/j.brainres.2018.03.015
![]() |
[31] |
Sivamaruthi BS, Suganthy N, Kesika P, et al. (2020) The role of microbiome, dietary supplements, and probiotics in autism spectrum disorder. Int J Environ Res Public Health 17: 2647. doi: 10.3390/ijerph17082647
![]() |
[32] |
Song Q, Wang Y, Huang L, et al. (2021) Review of the relationships among polysaccharides, gut microbiota, and human health. Food Res Int 140: 109858. doi: 10.1016/j.foodres.2020.109858
![]() |
[33] |
Salami M (2021) Interplay of good bacteria and central nervous system: cognitive aspects and mechanistic considerations. Front Neurosci 15: 613120. doi: 10.3389/fnins.2021.613120
![]() |
[34] |
Niederseer D, Wernly B, Aigner E, et al. (2021) NAFLD and cardiovascular diseases: epidemiological, mechanistic and therapeutic considerations. J Clin Med 10: 467. doi: 10.3390/jcm10030467
![]() |
[35] |
Burgueño JF, Fritsch J, Santander AM, et al. (2019) Intestinal epithelial cells respond to chronic inflammation and dysbiosis by synthesizing H2O2. Front Physiol 10: 1484. doi: 10.3389/fphys.2019.01484
![]() |
[36] |
Belizário JE, Faintuch J, Garay-Malpartida M (2018) Gut microbiome dysbiosis and immunometabolism: New frontiers for treatment of metabolic diseases. Mediators Inflamm 2018: 2037838. doi: 10.1155/2018/2037838
![]() |
[37] | Andreyev AY, Kushnareva YE, Starkova NN, et al. (2020) Metabolic ROS signaling: to immunity and beyond. Biochemistry 85: 1650-1667. |
[38] | Saint-Georges-Chaumet Y, Attaf D, Pelletier E, et al. (2015) Targeting microbiota-mitochondria inter-talk: Microbiota control mitochondria metabolism. Cell Mol Biol 61: 121-124. |
[39] |
Li M, Gu MM, Lang Y, et al. (2019) The vanillin derivative VND3207 protects intestine against radiation injury by modulating p53/NOXA signaling pathway and restoring the balance of gut microbiota. Free Radi Biol Med 145: 223-236. doi: 10.1016/j.freeradbiomed.2019.09.035
![]() |
[40] |
Wang W, Im J, Kim S, et al. (2020) ROS-induced SIRT2 upregulation contributes to cisplatin sensitivity in ovarian cancer. Antioxidants 9: 1137. doi: 10.3390/antiox9111137
![]() |
[41] |
Muralitharan RR, Marques FZ (2021) Diet-related gut microbial metabolites and sensing in hypertension. J Hum Hypertens 35: 162-169. doi: 10.1038/s41371-020-0388-3
![]() |
[42] |
Zhou Y, Jiang Q, Zhao S, et al. (2019) Impact of buckwheat fermented milk combined with high-fat diet on rats' gut microbiota and short-chain fatty acids. J Food Sci 84: 3833-3842. doi: 10.1111/1750-3841.14958
![]() |
[43] |
Skonieczna-Żydecka K, Grochans E, Maciejewska D, et al. (2018) Short chain fatty acids profile is changed in Polish depressive women. Nutrients 10: 1939. doi: 10.3390/nu10121939
![]() |
[44] |
Hu L, Zhu S, Peng X, et al. (2020) High salt elicits brain inflammation and cognitive dysfunction, accompanied by alternations in the gut microbiota and decreased SCFA production. J Alzheimers Dis 77: 629-640. doi: 10.3233/JAD-200035
![]() |
[45] |
Luceri C, Femia AP, Fazi M, et al. (2016) Effect of butyrate enemas on gene expression profiles and endoscopic/histopathological scores of diverted colorectal mucosa: A randomized trial. Dig Liver Dis 48: 27-33. doi: 10.1016/j.dld.2015.09.005
![]() |
[46] | Häselbarth L, Ouwens DM, Teichweyde N, et al. (2016) The small chain fatty acid butyrate antagonizes the TCR-stimulation-induced metabolic shift in murine epidermal gamma delta T cells. EXCLI J 19: 334-350. |
[47] |
Haase S, Haghikia A, Wilck N, et al. (2018) Impacts of microbiome metabolites on immune regulation and autoimmunity. Immunology 154: 230-238. doi: 10.1111/imm.12933
![]() |
[48] |
Macfarlane GT, Macfarlane S (2012) Bacteria, colonic fermentation, and gastrointestinal health. J AOAC Int 95: 50-60. doi: 10.5740/jaoacint.SGE_Macfarlane
![]() |
[49] |
Ray S, Das S, Panda PK, et al. (2018) Identification of a new alanine racemase in Salmonella Enteritidis and its contribution to pathogenesis. Gut Pathog 10: 30. doi: 10.1186/s13099-018-0257-6
![]() |
[50] |
Gilmore MS, Skaugen M, Nes I (1996) Enterococcus faecalis cytolysin and lactocin S of Lactobacillus sake. Antonie Van Leeuwenhoek 69: 129-138. doi: 10.1007/BF00399418
![]() |
[51] |
Pidgeon SE, Fura JM, Leon W, et al. (2015) Metabolic profiling of bacteria by unnatural C-terminated d-Amino Acids. Angew Chem 127: 6256-6260. doi: 10.1002/ange.201409927
![]() |
[52] |
Sasabe J, Miyoshi Y, Rakoff-Nahoum S, et al. (2016) Interplay between microbial d-amino acids and host d-amino acid oxidase modifies murine mucosal defence and gut microbiota. Nat Microbiol 1: 16125. doi: 10.1038/nmicrobiol.2016.125
![]() |
[53] |
Nagano T, Yamao S, Terachi A, et al. (2019) d-amino acid oxidase promotes cellular senescence via the production of reactive oxygen species. Life Sci Alliance 2: e201800045. doi: 10.26508/lsa.201800045
![]() |
[54] |
Zhong C, Zhu N, Zhu Y, et al. (2020) Antimicrobial peptides conjugated with fatty acids on the side chain of D-amino acid promises antimicrobial potency against multidrug-resistant bacteria. Eur J Pharm Sci 141: 105123. doi: 10.1016/j.ejps.2019.105123
![]() |
[55] |
Arai T, Ashraful Hoque M, Nishino N, et al. (2013) Cyclic tetrapeptides with -SS- bridging between amino acid side chains for potent histone deacetylases' inhibition. Amino Acids 45: 835-843. doi: 10.1007/s00726-013-1527-8
![]() |
[56] |
Hergueta T, Weiller E (2013) Evaluating depressive symptoms in hypomanic and manic episodes using a structured diagnostic tool: validation of a new Mini International Neuropsychiatric Interview (M.I.N.I.) module for the DSM-5 ‘With Mixed Features’ specifier. Int J Bipolar Disord 1: 21. doi: 10.1186/2194-7511-1-21
![]() |
[57] |
Ryu JC, Zimmer ER, Rosa-Neto P, et al. (2019) Consequences of metabolic disruption in Alzheimer's disease pathology. Neurotherapeutics 16: 600-610. doi: 10.1007/s13311-019-00755-y
![]() |
[58] |
Laversenne V, Nazeeruddin S, Källstig EC, et al. (2020) Anti-Aβ antibodies bound to neuritic plaques enhance microglia activity and mitigate tau pathology. Acta Neuropathol Commun 8: 198. doi: 10.1186/s40478-020-01069-3
![]() |
[59] |
Guo LX, Tong Y, Wang J, et al. (2020) Determination and comparison of short-chain fatty acids in serum and colon content samples: Alzheimer's disease rat as a case study. Molecules 25: 5739. doi: 10.3390/molecules25235739
![]() |
[60] |
Liu H, Zhang JJ, Li X, et al. (2015) Post-occlusion administration of sodium butyrate attenuates cognitive impairment in a rat model of chronic cerebral hypoperfusion. Pharmacol Biochem Behav 135: 53-59. doi: 10.1016/j.pbb.2015.05.012
![]() |
[61] |
Infante R, Scaglione C, Incensi A, et al. (2020) Longitudinal skin biopsy study of phosphorylated alpha-synuclein in a patient with Parkinson disease and orthostatic hypotension. J Neuropathol Exp Neurol 79: 813-816. doi: 10.1093/jnen/nlaa048
![]() |
[62] |
Mannal N, Kleiner K, Fauler M, et al. (2021) Multi-electrode array analysis identifies complex dopamine responses and glucose sensing properties of substantia nigra neurons in mouse brain slices. Front Synaptic Neurosci 13: 635050. doi: 10.3389/fnsyn.2021.635050
![]() |
[63] |
Unger MM, Spiegel J, Dillmann KU, et al. (2016) Short chain fatty acids and gut microbiota differ between patients with Parkinson's disease and age-matched controls. Parkinsonism Relat Disord 32: 66-72. doi: 10.1016/j.parkreldis.2016.08.019
![]() |
[64] |
Ostendorf F, Metzdorf J, Gold R, et al. (2020) Propionic acid and fasudil as treatment against rotenone toxicity in an in vitro model of Parkinson's disease. Molecules 25: 2502. doi: 10.3390/molecules25112502
![]() |
[65] |
Ostendorf F, Metzdorf J, Gold R, et al. (2020) Differential effects of Δ9-tetrahydrocannabinol dosing on correlates of schizophrenia in the sub-chronic PCP rat model. PLoS One 15: e0230238. doi: 10.1371/journal.pone.0230238
![]() |
[66] |
Gubert C, Kong G, Uzungil V, et al. (2020) Microbiome profiling reveals gut dysbiosis in the metabotropic glutamate receptor 5 knockout mouse model of schizophrenia. Front Cell Dev Biol 8: 582320. doi: 10.3389/fcell.2020.582320
![]() |
[67] |
Hu M, Zheng P, Xie Y, et al. (2018) Propionate protects haloperidol-induced neurite lesions mediated by neuropeptide Y. Front Neurosci 12: 743. doi: 10.3389/fnins.2018.00743
![]() |
[68] |
Girardi Paskulin LM, Kottwitz Bierhals CCB, Oliveira Dos Santos N, et al. (2017) Depressive symptoms of the elderly people and caregiver's burden in home care. Invest Educ Enferm 35: 210-220. doi: 10.17533/udea.iee.v35n2a10
![]() |
[69] |
Wu M, Tian T, Mao Q, et al. (2020) Associations between disordered gut microbiota and changes of neurotransmitters and short-chain fatty acids in depressed mice. Transl Psychiatry 10: 350. doi: 10.1038/s41398-020-01038-3
![]() |
[70] |
Mendonça IP, Duarte-Silva E, Chaves-Filho AJM, et al. (2020) Neurobiological findings underlying depressive behavior in Parkinson's disease: A review. Int Immunopharmacol 83: 106434. doi: 10.1016/j.intimp.2020.106434
![]() |
[71] |
Maigoro AY, Lee S (2021) Gut microbiome-based analysis of lipid a biosynthesis in individuals with autism spectrum disorder: an in ailico valuation. Nutrients 13: 688. doi: 10.3390/nu13020688
![]() |
[72] |
Rose DR, Yang H, Serena G, et al. (2018) Differential immune responses and microbiota profiles in children with autism spectrum disorders and co-morbid gastrointestinal symptoms. Brain Behav Immun 70: 354-368. doi: 10.1016/j.bbi.2018.03.025
![]() |
[73] |
Huo W, Qi P, Cui L, et al. (2020) Polysaccharide from wild morels alters the spatial structure of gut microbiota and the production of short-chain fatty acids in mice. Biosci Microbiota Food Health 39: 219-226. doi: 10.12938/bmfh.2020-018
![]() |
[74] |
Dickerson FB, Stallings C, Origoni A, et al. Effect of probiotic supplementation on schizophrenia symptoms and association with gastrointestinal functioning: a randomized, placebo-controlled trial (2014) . doi: 10.4088/PCC.13m01579
![]() |
[75] |
Varela RB, Valvassori SS, Lopes-Borges J, et al. (2015) Sodium butyrate and mood stabilizers block ouabain-induced hyperlocomotion and increase BDNF, NGF and GDNF levels in brain of Wistar rats. J Psychiatr Res 61: 114-121. doi: 10.1016/j.jpsychires.2014.11.003
![]() |
[76] |
Yamawaki Y, Yoshioka N, Nozaki K, et al. (2018) Sodium butyrate abolishes lipopolysaccharide-induced depression-like behaviors and hippocampal microglial activation in mice. Brain Res 1680: 13-38. doi: 10.1016/j.brainres.2017.12.004
![]() |
[77] |
Lee J, Venna VR, Durgan DJ, et al. (2020) Young versus aged microbiota transplants to germ-free mice: increased short-chain fatty acids and improved cognitive performance. Gut Microbes 12: 1814107. doi: 10.1080/19490976.2020.1814107
![]() |
[78] |
D'Mello SR (2019) Regulation of central nervous system development by class I histone deacetylases. Dev Neurosci 41: 149-165. doi: 10.1159/000505535
![]() |
[79] |
Sinn DI, Kim SJ, Chu K, et al. (2007) Valproic acid-mediated neuroprotection in intracerebral hemorrhage via histone deacetylase inhibition and transcriptional activation. Neurobiol Dis 26: 464-472. doi: 10.1016/j.nbd.2007.02.006
![]() |
[80] |
Nestler EJ, Peña CJ, Kundakovic M, et al. (2016) Epigenetic basis of mental illness. Neuroscientist 22: 447-463. doi: 10.1177/1073858415608147
![]() |
[81] |
Kwon B, Houpt TA (2010) Phospho-acetylation of histone H3 in the amygdala after acute lithium chloride. Brain Res 1333: 36-47. doi: 10.1016/j.brainres.2010.03.068
![]() |
[82] |
Xiang B, Liu K, Yu M, et al. (2018) Systematic genetic analyses of genome-wide association study data reveal an association between the key nucleosome remodeling and deacetylase complex and bipolar disorder development. Bipolar Disord 20: 370-380. doi: 10.1111/bdi.12580
![]() |
[83] |
Arent CO, Valvassori SS, Fries GR, et al. (2011) Neuroanatomical profile of antimaniac effects of histone deacetylases inhibitors. Mol Neurobiol 43: 207-214. doi: 10.1007/s12035-011-8178-0
![]() |
[84] |
Guidotti A, Auta J, Chen Y, et al. (2011) Epigenetic GABAergic targets in schizophrenia and bipolar disorder. Neuropharmacology 60: 1007-1016. doi: 10.1016/j.neuropharm.2010.10.021
![]() |
[85] |
Kramer JM (2013) Epigenetic regulation of memory: implications in human cognitive disorders. Biomol Concepts 4: 1-12. doi: 10.1515/bmc-2012-0026
![]() |
[86] |
Martínez-Pacheco H, Picazo O, López-Torres A, et al. (2020) Biochemical and Behavioral Characterization of IN14, a New Inhibitor of HDACs with Antidepressant-Like Properties. Biomolecules 10: 299. doi: 10.3390/biom10020299
![]() |
[87] |
Cuadrado-Tejedor M, Pérez-González M, García-Muñoz C, et al. (2019) Taking advantage of the selectivity of histone deacetylases and phosphodiesterase inhibitors to design better therapeutic strategies to treat Alzheimer's disease. Front Aging Neurosci 11: 149. doi: 10.3389/fnagi.2019.00149
![]() |
[88] |
Mazzocchi M, Collins LM, Sullivan AM, et al. (2020) The class II histone deacetylases as therapeutic targets for Parkinson's disease. Neuronal Signal 4: NS20200001. doi: 10.1042/NS20200001
![]() |
[89] |
Marsh JL, Lukacsovich T, Thompson LM (2009) Animal models of polyglutamine diseases and therapeutic approaches. J Biol Chem 284: 7431-7435. doi: 10.1074/jbc.R800065200
![]() |
[90] |
Frost G, Sleeth ML, Sahuri-Arisoylu M, et al. (2014) The short-chain fatty acid acetate reduces appetite via a central homeostatic mechanism. Nat Commun 5: 3611. doi: 10.1038/ncomms4611
![]() |
[91] |
Braniste V, Al-Asmakh M, Kowal C, et al. (2014) The gut microbiota influences blood-brain barrier permeability in mice. Sci Transl Med 6: 263ra158. doi: 10.1126/scitranslmed.3009759
![]() |
[92] |
Zhou Z, Xu N, Matei N, et al. (2021) Sodium butyrate attenuated neuronal apoptosis via GPR41/Gbetagamma/PI3K/Akt pathway after MCAO in rats. J Cereb Blood Flow Metab 41: 267-281. doi: 10.1177/0271678X20910533
![]() |
[93] |
Simonini MV, Camargo LM, Dong E, et al. (2006) The benzamide MS-275 is a potent, long-lasting brain region-selective inhibitor of histone deacetylases. Proc Natl Acad Sci USA 103: 1587-1592. doi: 10.1073/pnas.0510341103
![]() |
[94] |
Tseng CJ, Gilbert TM, Catanese MC, et al. (2020) In vivo human brain expression of histone deacetylases in bipolar disorder. Transl Psychiatry 10: 224. doi: 10.1038/s41398-020-00911-5
![]() |
[95] |
Kennedy H, Montreuil TC (2021) The late positive potential as a reliable neural marker of cognitive reappraisal in children and youth: a brief review of the research literature. Front Psychol 11: 608522. doi: 10.3389/fpsyg.2020.608522
![]() |
[96] |
Gilbert TM, Zürcher NR, Wu CJ, et al. (2019) PET neuroimaging reveals histone deacetylase dysregulation in schizophrenia. J Clin Invest 129: 364-372. doi: 10.1172/JCI123743
![]() |
[97] |
Wang C, Schroeder FA, Hooker JM (2014) Visualizing epigenetics: current advances and advantages in HDAC PET imaging techniques. Neuroscience 264: 186-197. doi: 10.1016/j.neuroscience.2013.09.018
![]() |
[98] |
Seo YJ, Muench L, Reid A, et al. (2013) Radionuclide labeling and evaluation of candidate radioligands for PET imaging of histone deacetylase in the brain. Bioorg Med Chem Lett 23: 6700-6705. doi: 10.1016/j.bmcl.2013.10.038
![]() |
[99] |
Gilbert TM, Zürcher NR, Catanese MC, et al. (2019) Neuroepigenetic signatures of age and sex in the living human brain. Nat Commun 10: 2945. doi: 10.1038/s41467-019-11031-0
![]() |
[100] |
Omori K, Miyakawa H, Watanabe A, et al. (2021) The combined effects of magnesium oxide and inulin on intestinal microbiota and cecal short-chain fatty acids. Nutrients 13: 152. doi: 10.3390/nu13010152
![]() |
[101] |
Minami NS, Sousa RS, Oliveira FLC, et al. (2020) Subacute ruminal acidosis in zebu cattle: clinical and behavioral aspects. Animals 11: 21. doi: 10.3390/ani11010021
![]() |
[102] |
Takewaki D, Suda W, Sato W, et al. (2020) Alterations of the gut ecological and functional microenvironment in different stages of multiple sclerosis. Proc Natl Acad Sci USA 117: 22402-22412. doi: 10.1073/pnas.2011703117
![]() |
[103] |
Borgo F, Riva A, Benetti A, et al. (2017) Microbiota in anorexia nervosa: The triangle between bacterial species, metabolites and psychological tests. PLoS One 12: e0179739. doi: 10.1371/journal.pone.0179739
![]() |
[104] |
Geirnaert A, Calatayud M, Grootaert C, et al. (2017) Butyrate-producing bacteria supplemented in vitro to Crohn's disease patient microbiota increased butyrate production and enhanced intestinal epithelial barrier integrity. Sci Rep 7: 11450. doi: 10.1038/s41598-017-11734-8
![]() |
[105] | Kilinçarslan S, Evrensel A (2020) The effect of fecal microbiota transplantation on psychiatric symptoms among patients with inflammatory bowel disease: an experimental study. Actas Esp Psiquiatr 48: 1-7. |
[106] | Tjellström B, Högberg L, Stenhammar L, et al. (2013) Faecal short-chain fatty acid pattern in childhood coeliac disease is normalised after more than one year's gluten-free diet. Microb Ecol Health Dis 24: 20905. |
[107] | Lerner A, Freire de Carvalho J, Kotrova A, et al. (2021) Gluten-free diet can ameliorate the symptoms of non-celiac autoimmune diseases . |
[108] |
Mohan M, Okeoma CM, Sestak K (2020) Dietary gluten and neurodegeneration: a case for preclinical studies. Int J Mol Sci 21: 5407. doi: 10.3390/ijms21155407
![]() |
[109] |
Bruce-Keller AJ, Salbaum JM, Luo M, et al. (2015) Obese-type gut microbiota induce neurobehavioral changes in the absence of obesity. Biol Psychiatry 77: 607-615. doi: 10.1016/j.biopsych.2014.07.012
![]() |
[110] |
Simeonova D, Ivanovska M, Murdjeva M, et al. (2018) Recognizing the leaky gut as a trans-diagnostic target for neuroimmune disorders using clinical chemistry and molecular immunology assays. Curr Top Med Chem 18: 1641-1655. doi: 10.2174/1568026618666181115100610
![]() |
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