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Research article

Octonion-valued b-metric spaces and results on its application

  • This study introduces octonion-valued b-metric spaces as a natural extension of the octonion-valued metric spaces developed by establishing a partial ordering relation on octonions. Octonion-valued b-metric spaces are constructed by modifying the triangle inequality of a semi-metric space, where one side of the inequality is multiplied by a positive scalar b1. On the other hand, octonion-valued metric spaces generalize the concept of classical metric spaces by employing octonions, which provide a higher-dimensional and non-associative algebraic framework. Two key reasons make this novel generalization of metric spaces very interesting: First, octonions are not even a ring since they do not have the associative feature in multiplication; second, the spaces do not meet the standard triangle inequality. In addition to explanations on sequences, convergence, Cauchy characteristics, boundedness, theorems, and associated conclusions, examples are given to help visualize this recently formed metric space. Lastly, the building of a fixed point finds extensive applications in a variety of mathematical analytic subjects as well as applied mathematics domains like differential equations and dynamical systems. Because of this, octonion-valued b-metric spaces have been used to study the Banach fixed-point theorem and a few additional fixed-point theorems.

    Citation: Xiu-Liang Qiu, Selim Çetin, Ömer Kişi, Mehmet Gürdal, Qing-Bo Cai. Octonion-valued b-metric spaces and results on its application[J]. AIMS Mathematics, 2025, 10(5): 10504-10527. doi: 10.3934/math.2025478

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  • This study introduces octonion-valued b-metric spaces as a natural extension of the octonion-valued metric spaces developed by establishing a partial ordering relation on octonions. Octonion-valued b-metric spaces are constructed by modifying the triangle inequality of a semi-metric space, where one side of the inequality is multiplied by a positive scalar b1. On the other hand, octonion-valued metric spaces generalize the concept of classical metric spaces by employing octonions, which provide a higher-dimensional and non-associative algebraic framework. Two key reasons make this novel generalization of metric spaces very interesting: First, octonions are not even a ring since they do not have the associative feature in multiplication; second, the spaces do not meet the standard triangle inequality. In addition to explanations on sequences, convergence, Cauchy characteristics, boundedness, theorems, and associated conclusions, examples are given to help visualize this recently formed metric space. Lastly, the building of a fixed point finds extensive applications in a variety of mathematical analytic subjects as well as applied mathematics domains like differential equations and dynamical systems. Because of this, octonion-valued b-metric spaces have been used to study the Banach fixed-point theorem and a few additional fixed-point theorems.



    Infectious diseases remain a significant contributor to overall human mortality. According to data reported by the WHO, a large number of people die from infectious diseases every year. In 2019, new measles cases worldwide increased to 869 770, and since 2016, the death rate from measles has increased by almost 50%. In 2019 alone, the number of measles deaths was about 207 500 [1]. In 2022, there were major outbreaks of monkeypox in the Americas and Western Pacific, with 87 929 confirmed cases and 146 deaths in 111 countries by June 2023 [2]. COVID-19 also remains a significant risk to people's lives, with at least 767 million cases confirmed and over 6.9 million fatalities worldwide by June 4, 2023 [3]. These data show that infectious diseases pose a severe threat to human lives.

    Vaccination is one of the most important means of reducing both mortality and the number of infected persons. For most infectious diseases, vaccination could reduce the number of infected people, thus decreasing the mortality rate. New antibodies are produced when an unfamiliar etiologic agent or disease enters the body. Many vaccines are or contain a weakened or inactivated part of a specific pathogen that, when injected into the body, forms an antigen and induces an immune response [4]. For example, from 2000 to 2017, measles immunization has averted an estimated 21.1 million deaths, and vaccination efforts contributed to an 80% decline in measles deaths worldwide, making the measles vaccine one of the most effective products in public health [5]. After years of research, three vaccines (MVA-BN, LC16, and OrthopoxVac) have been approved for the prevention of monkeypox [6]. Coronavirus vaccination has been shown to increase immunity to COVID-19 and reduce the incidence of the disease. As of today, at least 70.3% of the global population has received at least a single dose of coronavirus vaccine [7].

    Many scholars have explored epidemic dynamical models of infectious diseases. In 1927, Kermack and McKendrick first studied the deterministic compartment model and proposed the susceptible-infectious-recovered (SIR) model [8]. Other scholars have since developed improved epidemic dynamical models on this foundation, including the susceptible-infectious-susceptible (SIS) and susceptible-exposed-infectious-recovered (SEIR) models [9]. Considering the susceptible-vaccinated-infectious-recovered (SVIR) model with vaccination age, Duan et al. showed the influence of vaccine effectiveness and vaccination age on disease transmission [10]. By establishing a SVIR model with two different vaccination strategies, Liu et al. demonstrated that diseases can be eliminated under appropriate vaccination strategies [11].

    Guzzi et al. investigated some graph-based epidemiological models, and their results showed that these models significantly improved disease transmission control [12]. Petrizzelli et al. considered a network-based model to assess the impact of different vaccination strategies and showed that topological awareness and age-based vaccination strategies were able to mitigate the spread of virus [13]. Han et al. formulated the vaccinated-susceptible-exposed-infectious-recovered (VSEIR) model with vaccination and immunity decline, and investigate the impact of vaccination on the transmission of COVID-19 [14]. Further, they considered the effects of the Omicron variant, and the susceptible-exposed-asymptomatic infected-infected-recovered (SEIAIR) model was developed to explore prevention and control strategies to contain COVID-19 [15]. Song et al. applied an susceptible-exposed-asymptomatic infected-symptomatic infectious-isolated-recovered (SEAIQR) model with vaccination and isolation delays, and their results showed that decreasing the isolation delays and increasing the vaccination rate were effective in preventing the spread of COVID-19 [16]. Zhang et al. established a multi-patch model of heterosexual transmission and investigated the impact of population migration on HIV /AIDS spreading [17]. Considering different age groups, Chen et al. investigated the transmission dynamics model and optimal control strategy of COVID-19 in Hong Kong [18]. To study the monkeypox outbreak in Nigeria, Li et al. developed a new mathematical model to study the optimal control measures to contain the epidemic [19].

    There is always some level of discrepancy between the actual data and the parameter values. However, sensitivity analysis can be used to measure the robustness of the predicted values with respect to the parameter values provided [20]. By analyzing the sensitivity of the basic reproduction number, Ndaïrou et al. found the two parameters with the largest impact on R0 to be the contact rate and the mortality rate from disease [21]. To identify the vital parameters in the mechanism of the Zika virus, Biswas et al. performed a sensitivity analysis of important threshold numbers, and their results produced a scheme to control the transmission of Zika virus [22]. Optimal control can help decision-makers develop the most cost-effective solutions to minimize losses to people and society. Li et al. used optimal control theory to develop an optimal solution to this problem and to realize the aim of the lowest possible number of infections and the lowest possible vaccination rate for a given vaccination period [23]. Wang et al. studied the time-varying optimal control model, considering seasonal factors, and they addressed the issue numerically using the symplectic pseudospectral method, showing that seasonality changes may cause optimal vaccination strategies to also shift [24].

    Our model takes into account the vaccination rate, vaccine effectiveness and the vaccine-induced decline in the immune rate, thus analyzing the stability of equilibria. We also performed a sensitivity analysis on these threshold parameters. We found solutions to the optimal vaccination control problem using the Pontryagin maximum principle, and we chose the proper parameters to prove that the theoretical results hold.

    This paper is organized as follows. The formulation of the model and the basic reproduction number are presented in Section 2. The stability of equilibria is analyzed in Section 3. The bifurcation analysis of the model is presented in Section 4. The sensitivity analysis of the threshold parameters is described in Section 5. The optimal vaccination model is shown in Section 6. Numerical simulation is presented in Section 7. The conclusion is presented in Section 8.

    Developing an epidemic dynamical model of vaccination, the total population is N(t), which consists of vaccinated V(t), susceptible S(t), infected I(t), and recovered individuals R(t), where

    N(t)=V(t)+S(t)+I(t)+R(t). (2.1)

    Suppose all the population is homogeneously mixed. After vaccination, susceptible people will carry antibodies to the vaccine and develop immunity. With the increase of time, the immunity of the vaccine will weaken and eventually disappear, and the vaccinated people become susceptible. Susceptible people become infected by coming into contact with infected people, and because immunity disappears over time, a subset of individuals in the vaccinated population become infected again. As the treatment progresses, some of the infected individuals may recover, while others may succumb to the disease. Assuming that the natural mortality rate is equal in each compartment, the schematic diagram of this model is in Figure 1, and the epidemic dynamical model is given by the following four equations:

    Figure 1.  A schematic diagram SVIR for the transmission of diseases.
    {dV(t)dt=γS(1θ)βVI(δ+d)V,dS(t)dt=Λ+δVβSI(γ+d)S,dI(t)dt=βSI+(1θ)βVI(d+α+b)I,dR(t)dt=bIdR, (2.2)

    where Λ represents the susceptible individuals recruited by immigration or birth. β represents the effective contact rate which results from contact between susceptible individuals and infected individuals, d represents the natural death rate of each compartment. θ represents vaccine effectiveness rate, which is between 0 and 1. When θ=0, the vaccines are invalid, and when θ=1, it shows that the vaccines are completely active. γ represents the vaccination rate of susceptible individuals. b represents the cure rate of infected individuals. α represents the disease-induced mortality, since the immunity of the vaccine weakens over time. δ represents the loss rate of immunity. All parameters are non-negative.

    Theorem 2.1. The solutions of the system remain non-negative, when S(0)>0, I(0)0, V(0)0, R(0)0, for all t>0.

    Proof. According to the expression of the system (2.2), we have

    dI(t)dt=(βS+(1θ)βV(d+α+b))I.

    Simultaneously integrating from 0 to t for the above equation, then getting the analytic expression for I(t),

    I(t)=I(0)expt0(βS+(1θ)βV(d+α+b))ds.

    Similarly,

    V(t)=V(0)expt0(γSV(1θ)βI(δ+d))ds,
    S(t)=S(0)expt0(Λ+δVSβI(γ+d))ds,
    R(t)=R(0)expt0(bIRd)ds.

    Since S(0)>0, I(0)0, V(0)0, R(0)0, that is, S(t)>0, I(t)0, V(t)0, R(t)0.

    Theorem 2.2. The closed set

    Γ={(V,S,I,R)R|V,I,R0,S>0,V+S+I+RΛd} (2.3)

    is a bounded set.

    Proof. According to [25], we have

    dN(t)dt=ΛdN(t)0,

    by the comparison theorem [26],

    limsuptN(t)Λd.

    In summary, the close set Γ is a positively invariant set.

    The basic reproduction number R0 is an essential threshold parameter which can show the prevalence of the disease in the epidemic dynamical model. If R0<1, it will die out, and if R0>1, it will become prevalent in the population. In our paper, R0 is determined via the next-generation matrix method [27].

    When θ=γ=δ=0, the system (2.2) reduced to the SIR model without the vaccine,

    {dS(t)dt=ΛβSIdS,dI(t)dt=βSI(d+α+b)I,dR(t)dt=bIdR,

    computing the regeneration matrix and transfer matrix for the SIR model,

    F0=(βSI00),V0=((d+α+b)IbI+dRΛ+βSI+dS)

    differentiating F0 and V0, calculate the value of E00=(S00,0,0)=(Λd,0,0) which is the disease-free equilibrium point of SIR model

    F0=(βS0000000000),V0=(d+α+b00bd0βS00d)

    Then, R0=ρ(F0V01)=βS00d+b+α=βΛd(d+b+α), and 1d+b+α is the number of the secondary infections developed by an infected person throughout his or her infectious period [28].

    To compute the system's disease-free equilibrium, let the left of system (2.2) equal to be zero, that is,

    E0=(V0,S0,0,0)=(Λγd(δ+d+γ),Λ(δ+d)d(δ+d+γ),0,0). (2.4)

    Let x=(I,R,V,S)T, and the system (2.2) can be written as ˙x=FV, where the regeneration matrix F and the transfer matrix V is as follows:

    F=(βSI+(1θ)βVI000),V=((d+α+b)IbI+dRγS+(1θ)βVI+(δ+d)VΛδV+βSI+(γ+d)S),

    differentiating F and V, calculate the value of E0,

    DF(E0)=[F000],DV(E0)=[V0J3J4],

    where

    F=[βS0+(1θ)βV0000],V=[d+α+b0bd],
    J3=[(1θ)βV00βS00],J4=[δ+dγδγ+d],

    since the basic reproduction number is the spectral radius of FV1, thus

    ρ(FV1)=βd+α+b(S0+(1θ)V0). (2.5)

    So, the basic reproduction number of the system (2.2) is

    Rvac=βd+α+b(S0+(1θ)V0) (2.6)
    =R0(1dθγd(δ+d+γ)).

    The interpretation of Eq (2.6) is as follows: β(d+α+b)θΛγd(δ+d+γ) is the proportion of secondary infections attributed to the average vaccinated people with a vaccination rate γ, β(d+α+b)Λd is the number of secondary infections attributed to the susceptible individuals [29].

    In the above, we defined the basic reproduction number of the system (2.2). In the following text, the local asymptotic stability (LAS) and globally asymptotically stable (GAS) of the equilibria is analyzed using the relationship between the magnitude of Rvac and unity.

    Since the equation for variable R(t) is decoupled from the first three equations of system (2.2), it is just considering the following system (3.1).

    {dV(t)dt=γS(1θ)βVI(δ+d)V,dS(t)dt=Λ+δVβSI(γ+d)S,dI(t)dt=βSI+(1θ)βVI(d+α+b)I. (3.1)

    Theorem 3.1. When Rvac<1, E0 is LAS, and when Rvac>1, it is unstable.

    Proof. The disease-free equilibrium of the system (3.1) is as follows:

    E0=(V0,S0,0)=(Λγd(δ+d+γ),Λ(δ+d)d(δ+d+γ),0). (3.2)

    Calculating the Jacobian matrix at E0,

    J(E0)=[(δ+d)γ(1θ)βV0δ(γ+d)βS000βS0+(1θ)βV0(d+α+b)],

    where βS0+(1θ)βV0(d+α+b)=(Rvac1)(d+α+b).

    The characteristic equation is

    (λ+d)[λ+(d+δ+γ)][λ(Rvac1)(d+α+b)]=0, (3.3)

    then solve Eq (3.3), and the eigenvalues are as follows:

    λ1=d,λ2=(d+δ+γ),λ3=(Rvac1)(d+α+b),

    that is, when Rvac<1, all eigenvalues are negative, which shows that E0 is LAS, and otherwise, it is unstable.

    In this context, we analyze the global stability of E0. [30] proposed a method to prove the global asymptotically stable of the disease-free equilibrium, by dividing system (3.1) into two subsystems, that is,

    dXdt=F(X,Z),
    dZdt=G(X,Z),G(X,0)=0,

    where X denotes uninfected individuals, and Z denotes infected individuals. If system (3.1) satisfies (H1) and (H2), the disease free equilibrium is globally asymptotically stable.

    (H1) If dXdt=F(X,0), X is the disease free equilibrium;

    (H2) G(X,Z)=FZˆG(X,Z), where ˆG(X,Z)0 for G(X,Z)Ω, and F=DZG(X0,0) is a M-matrix (i.e., the M-matrix is the non-diagonal element is non-negative), Ω is positive invariant set. In this paper, it can obtain the following Theorem 3.2.

    Theorem 3.2. If Rvac<1, E0 is GAS.

    Proof. Let X denotes the uninfected individuals, Z denotes the infected individuals. So, we can get X = (V,S)T, and Z=I.

    dXdt=F(X,Z)=(γS(1θ)βVI(δ+d)VΛ+δVβSI(γ+d)S),
    dZdt=G(X,Z)=βSI+(1θ)βVI(d+α+b)I.

    From the Eq (3.2), we have computed E0. Here, it is noted as U0=(X0,0), where

    X0=(Λγd(δ+d+γ),Λ(δ+d)d(δ+d+γ)).

    For dXdt=F(X,0), assumption (H1) is satisfied, and when t+, XX0, i.e., X0 is GAS.

    Computing matrix F at X0,

    F=DZG(X0,0)=(βS+(1θ)βV(d+α+b))|X0=(Rvac1)(d+α+b),

    where F is a M-matrix.

    FZ=(βS0+(1θ)βV0(d+α+b))I=(βΛ(δ+d)d(δ+d+γ)+(1θ)βΛγd(δ+d+γ)(d+α+b))I,

    from assumption (H2),

    ˆG(X,Y)=βI(βΛ(δ+d)d(δ+d+γ)S)+(1θ)βI((1θ)βΛγd(δ+d+γ)V),

    thus

    G(X,Y)=FZˆG(X,Y)=(Rvac1)(d+α+b)IˆG(X,Y).

    Since Γ is a positive invariant set, i.e., SΛ(δ+d)d(δ+d+γ), VΛγd(δ+d+γ), then ˆG(X,Y)0. That is, when t+, then I(t)I0.

    Consequently, if Rvac<1, E0 is GAS.

    From the system (3.1), the expressions for calculating the endemic equilibrium are as follows. I0, so by the third expression of the system (3.1), where S=(d+b+α)(1θ)βVβ, bringing S into the first equation

    V=γ(d+α+b)β[(1θ)γ+(1θ)βI+(δ+d)],

    so

    S=(d+α+b)[(1θ)βI+(δ+d)]β[(1θ)γ+(1θ)βI+(δ+d)],

    bringing S and V into the second equation, set I as the positive root of Eq (3.4).

    AI2+BI+C=0, (3.4)

    where

    A=(1θ)(d+α+b)β2,
    B=β{Λβ(1θ)(d+α+b)[(δ+d)+(γ+d)(1θ)]},C=Λβγ(1θ)+Λβ(δ+d)d(d+α+b)(δ+d+γ),
    =d(d+α+b)(δ+d+γ)(Rvac1),

    obviously, A<0. Clearly, it shows that Rvac>1C>0; Rvac=1C=0; Rvac<1C<0.

    Since A<0 combined with the above equivalence relationship, the results show that: when Rvac=1, i.e., C=0, Eq (3.4) has one positive root provided B>0, otherwise Eq (3.4) has no positive root; when Rvac>1 i.e., C>0, Eq (3.4) has a unique positive root I1=BB24AC2A. Next, we will consider the case of the roots of the equation, when Rvac<1, i.e., C<0.

    Let Δ=B24AC=0, that is,

    β2{Λβ(1θ)(d+α+b)[(δ+d)+(γ+d)(1θ)]}2+4d(d+α+b)2(δ+d+γ)(Rvac1)(1θ)β2=0.

    Set

    R=1{Λβ(1θ)(d+α+b)[(δ+d)+(γ+d)(1θ)]}24d(d+α+b)2(δ+d+γ)(1θ), (3.5)

    And then get the following equivalence:

    Rvac<RΔ<0;Rvac=RΔ=0;Rvac>RΔ>0.

    Thus, when it satisfies Rvac<1 and B0, Eq (3.4) does not exist positive root, and when it satisfies Rvac<1 and B>0, the following equivalence relationship is established:

    (1) if R<Rvac<1, there are two positive roots I2=BB24AC2A and I3=B+B24AC2A;

    (2) if Rvac=R<1, there is a unique positive root I4=B2A;

    (3) if Rvac<R, there is no positive root.

    In summary, the following theorem can be derived.

    Theorem 3.3. In the system (3.1), when Rvac>1, there exists a unique endemic equilibrium E1=(I1,S1,V1); when Rvac=1, there is an endemic equilibrium with B>0; when Rvac<1 and B0, there exists no endemic equilibrium; when Rvac<1 and B>0, there are two endemic equilibria E2=(I2,S2,V2) and E3=(I3,S3,V3) for R<Rvac, the unique endemic equilibrium E4=(I4,S4,V4) for R=Rvac, no endemic equilibrium for Rvac<R.

    Lemma 1. [31] Suppose A is 3×3, a real matrix, if tr(A)<0, det(A)<0, det(A[2])<0. Then, all eigenvalues of A have negative real parts.

    In [32], for n×n matrix A=(aij), when n=2, the second additive compound matrix of A is A[2]=a11+a22, when n=3, A[2]=[a11+a22a23a13a32a11+a33a12a31a21a22+a33].

    Theorem 3.4. When Rvac>1 and {δ(1θ)[(1θ)βI1+(δ+d)]}<0, E1 is LAS.

    Proof. Calculating the Jacobian matrix of the system (3.1),

    J=[(1θ)βI(δ+d)γ(1θ)βVδβI(γ+d)βS(1θ)βIβIβS+(1θ)βV(d+α+b)], (3.6)

    we can compute βS+(1θ)βV(d+α+b) = 0, then

    tr(J)=(1θ)βI(δ+d)βI(γ+d)<0, (3.7)
    det(J)=δ(1θ)β2IV(1θ)β2γIS
    (1θ)2β2(βI+γ+d)IVβ2((1θ)βI+δ+d)SI<0. (3.8)

    Computing J[2]

    J[2]=[((1θ)βI+βI+δ+γ+2d)βS(1θ)βVβI((1θ)βI+δ+d)γ(1θ)βIδ(βI+γ+d)], (3.9)

    then, calculate the value of the determinant of J[2]

    detJ[2]=[((2θ)βI+(γ+δ+2d))((1θ)βI+δ+d)(βI+γ+d)]+(1θ)β2δIV+(1θ)β2γSI((1θ)βI+δ+d)(1θ)2β2IV(βI+γ+d)β2SI+[(2θ)βI+(γ+δ+2d)]δγ,=[((2θ)βI+(γ+δ+2d))((1θ)β2I2+δ+d)+(γ+d)(1θ)βI+d(d+δ+γ)]
    (θγ+βI+d)β2SI+{δ(1θ)[(1θ)βI+δ+d]}(1θ)β2IV. (3.10)

    When Rvac>1, bringing E1 into matrices (3.8) and (3.10), it can be calculated as tr(J1)<0, det(J1)<0, if {δ(1θ)[(1θ)βI1+(δ+d)]}<0 is satisfied, then det(J[2]1)<0. According to Lemma 1, every eigenvalue of J1 has a negative real part, it shows that E1 is LAS.

    In this context, the geometric method is used to demonstrate GAS of endemic equilibriums. In Li and Muldowney [33], it shows the theoretical knowledge about how to prove GAS of endemic equilibriums, which considering the following differential system,

    ˙x=f(x),

    where f(x):DRn be C1 continuous, DRn be an open set, x(t,x0) is uniquely determined by the initial value condition x(0)=x0. Suppose system ˙x=f(x) satisfies the following three hypotheses:

    (1) The open set D is a simply connected,

    (2) There exists a compact absorbing set KD,

    (3) There exists a unique endemic equilibrium ˉx in open set D.

    Suppose |·| represents the vector norm induced by the n×n order matrix. The Lozinskii measure of matrix W with respect to the induced matrix norm is defined by

    μ1(W)=limx0+|I+xW|1x.

    Lemma 2. [34] The Lozinskii measure of a real n×n matrix M for the matrix norm induced by the l1 vector norm is given by

    μ1(M)=maxi(mii+|mji|ji). (3.11)

    Theorem 3.5. If ˉq0, ˉx is GAS.

    In the system (2.2), we have the following lemma:

    Lemma 3. [35,36] The system (2.2) is uniformly persistent, i.e., there exists constant φ>0 such that

    lim inft{V(t),S(t),I(t),R(t)}φ. (3.12)

    Proof. In the above section, E0 exists on the boundary of region Γ, and Theorem 3.1 provides the stability condition for E0, i.e., E0 is stable when Rvac<1, and otherwise E0, is unstable, which leads to the instability of E0. Since the instability of E0 is equivalent to the uniform persistence of the system (2.2), it can be proved that the system (2.2) uniformly persists in the interior of Γ, that is, there exists a constant φ>0 such that

    liminftV(t)>φ,liminftS(t)>φ,liminftI(t)>φ,liminftR(t)>φ,

    with original values (V(0),S(0),I(0),R(0))D, which shows the hypothesis (2) holds.

    In the system (2.2), when Rvac>1, there exists E1 which is a unique equilibrium in the region of Γ, and then hypotheses (1) and (3) are satisfied.

    Theorem 3.6. When Rvac>1, E1 is GAS.

    Proof. Consider the following subsystem (3.13):

    {dI(t)dt=βSI+(1θ)βVI(d+α+b)I,dV(t)dt=γS(1θ)βVI(δ+d)V, (3.13)

    the Jacobian matrix is as follows:

    J1=[(1θ)βI(δ+d)(1θ)βV(1θ)βIβS+(1θ)βV(d+α+b)],

    then, the second compound matrix is

    J1[2]=βS+(1θ)βV(d+α+b)(1θ)βI(δ+d)Q. (3.14)

    Set matrix-value functions

    P=P(V,I)=[VI00VI],

    thus Pf=[VIIVI200VIIVI2], P1=[IV00IV], PfP1=[VVII00VVII],

    then, PJ1[2]P1=[Q00Q].

    Clearly, we can obtain

    W=PfP1+PJ1[2]P1=[W11W12W21W22], (3.15)

    where

    W11=W22=VVII+Q,W12=W21=0.

    The Lozinskii measure is determined as follows:

    μ1(W)max{g1,g2}, (3.16)

    where g1=μ1(W11)+|W12|, g2=|W21|+μ1(W22), obviously

    |W12|=|W21|=0,g1=μ1(W11),g2=μ1(W22).

    Thus, we have

    μ1(W)VVII+Q. (3.17)

    According to the system (2.2), computing that,

    II=βS+(1θ)βV(d+α+b), (3.18)

    substitute the above equation into μ1(W), that is

    max{g1,g2}=VV(1θ)βI(δ+d)VV(δ+d), (3.19)

    then the measure ˉq is as follows

    ˉq=limsuptsup1tt0μ1(W)dslimsuptsup1tt0(VV(δ+d))ds,
    =1tlnV(t)V(0)(δ+d).

    The above inequality indicates ˉq0, so II1, VV1 with t+.

    Under expression of the system (2.2), we have

    dS(t)dt=Λ+δVβSI(γ+d)S, (3.20)

    when t+, we have

    dS(t)dt=Λ+δV1βSI1(γ+d)S, (3.21)

    that is dS(t)dt+(βI1+(γ+d))S=Λ+δV1, apparently a linear differential equation about S, thus SΛ+δV1βI1+(γ+d)=S1, RbI1d=R1 as t+ [37].

    Comprehensively stated, when t+, we have (V,S,I,R)(V1,S1,I1,R1), thus E1 is GAS.

    Bifurcation analysis plays a vital role in controlling and eradicating epidemic diseases. In modeling epidemic diseases, when the basic reproduction number is less than unity, the disease will be eradicated. However, when bifurcation occurs, and the basic reproduction number exceeds unity, the endemic equilibrium will persist, i.e., susceptible individuals and infected individuals coexist. Thus, it is significant to analyze the bifurcation of the model in epidemiology.

    Theorem 4.1. If Rvac=1, the system (2.2) will undergo forward bifurcation at β=β.

    Proof. Compute the Jacobian matrix at E0,

    J(E0)=[(δ+d)γ(1θ)βV0δ(γ+d)βS000(Rvac1)(d+b+α)],

    when Rvac=1, calculate the characteristic polynomial as follows:

    |λIJ(E0)|=[λ+(δ+d)γ(1θ)βV0δλ+(γ+d)βS000λ]=0,

    that is

    λ(λ2+(2d+δ+γ)λ+d(d+δ+γ))=0. (4.1)

    The three eigenvalues that can be calculated for this characteristic equation are

    λ1=0,λ2=(d+δ+γ),λ3=d.

    There is a zero eigenvalue and the rest of the roots are negative, in the light of the center manifold theorem [38], the system (3.1) exists the forward bifurcation.

    When Rvac=1, let bifurcation parameter

    β:=β=d(d+δ+γ)(d+α+b)Λ[(1θ)γ+(δ+d)]. (4.2)

    Then compute the eigenvector whose eigenvalue is zero, set the right eigenvector w=(w1,w2,w3)T, and then we can obtain

    (δ+dγ(1θ)βV0δγ+dβS0000)(w1w2w3)=(000),

    getting the following relation:

    w1=(1θ)(γ+d)βV0+βS0(δ+d)d(d+δ+γ)w3,w2=(1θ)βδV0+(δ+d)βS0d(d+δ+γ)w3.

    Similarly, set the left eigenvector v=(v1,v2,v3), and then we can obtain

    (v1,v2,v3)(δ+dγ(1ϑ)βV0δγ+dβS0000)=(000),

    it also satisfies vw=1, that is, v1w1+v2w2+v3w3=1. So we can get the left eigenvector as follows,

    v1=0,v2=0,v3w3=1.

    To determine the type of bifurcation, set V=x1, S=x2, I=x3, dVdt=f1(x), dSdt=f2(x), dIdt=f3(x), according to the system (3.1), it can obtain

    {f1(x)=γx2(1θ)βx1x3(δ+d)x1,f2(x)=Λ+δx1βx2x3(γ+d)x2,f3(x)=βx2x3+(1θ)βx1x3(d+α+b)x3. (4.3)

    According to v and w computing e1 and e2, where

    e1=3k,i,j=1vkwiwj2fkxixj(E0,β),
    =v1w122f1(x1)2(E0,β)+v1w222f1(x2)2(E0,β)+v1w322f1(x3)2(E0,β)+2v1w1w22f1x1x2(E0,β)
    +2v1w1w32f1x1x3(E0,β)+2v1w2w32f1x2x3(E0,β)+v2w122f2(x1)2(E0,β)+v2w222f2(x2)2(E0,β)
    +v2w322f2(x3)2(E0,β)+2v2w1w22f2x1x2(E0,β)+2v2w1w32f2x1x3(E0,β)+2v2w2w32f2x2x3(E0,β)+v3w122f3(x1)2(E0,β)+v3w222f3(x2)2(E0,β)+v3w322f3(x3)2(E0,β)+2v3w1w22f3x1x2(E0,β)
    +2v3w1w32f3x1x3(E0,β)+2v3w2w32f3x2x3(E0,β),
    e2=3k,i=1vkwi2fkxiβ(E0,β),
    =v1w12f1x1β(E0,β)+v1w22f1x2β(E0,β)+v1w32f1x3β(E0,β)
    +v2w12f2x1β(E0,β)+v2w22f2x2β(E0,β)+v2w32f2x3β(E0,β)
    +v3w12f3x1β(E0,β)+v3w22f3x2β(E0,β)+v3w32f3x3β(E0,β). (4.4)

    Then, calculate the partial derivative at (E0,β),

    2f1x1x3=(1θ)β,2f3x1x3=(1θ)β,2f3x2x3=β,2f2x2x3=β,
    2f3x3β=S0+(1θ)V0,2f1x3β=(1θ)V0,2f2x3β=S0,

    and others are zero. Then e1 and e2 are computed,

    e1=3k,i,j=1vkwiwj2fkxixj(E0,β)=2d(d+δ+γ)[w1w3(1θ)β+w2w3β]<0,
    e2=3k,i=1vkwi2fkxiβ(E0,β)=v3w32f3x3β>0.

    According to [39], the system (3.1) will undergo forward bifurcation. Since the fourth equation of system (2.2) is decoupled from the previous three, system (3.1) has the same stability as system (2.2), and there also exists a forward bifurcation for the system (2.2).

    Theorem 4.2. [40] Suppose Rvac>1. When vaccination rate γ exceeds thresholds γ, there will be a Hopf bifurcation around E1.

    Proof. When Rvac>1, calculate the Jacobian matrix of E1, and then matrix (3.8) is as follows:

    J(E1)=[(1θ)βI1(δ+d)γ(1θ)βV1δβI1(γ+d)βS1(1θ)βI1βI1βS1+(1θ)βV1(d+α+b)]. (4.5)

    Calculate its characteristic equation,

    λ3+a1λ2+a2λ+a3=0, (4.6)

    where

    a1=(2θ)βI1+γ+δ+2d,
    a2=(βI1+γ+d)((1θ)βI1+δ+d)+(1θ)2β2I1V1+β2I1S1δγ,
    a3=(1θ)δβ2I1V1+(1θ)γβ2S1I1+(βI1+γ+d)(1θ)2β2I1V1+β2I1S1((1θ)βI1+δ+d).

    Let γ=γ, and a1(γ)a2(γ)a3(γ)=0, and the roots of characteristic Eq (4.6) are

    λ1=a2(γ)i,λ2=a2(γ)i,λ3=a1(γ),

    λ1 and λ2 are a pair of purely imaginary roots.

    In general, the form of characteristic roots λ is

    λ1=κ1+κ2i,λ2=κ1κ2i,λ3=a1,

    thus, when λ1=κ1+κ2i, characteristic Eq (4.6) is replaced by the following equation:

    (κ133κ1κ22+a1κ12a1κ22+κ1a2+a3)+(2a1κ1κ2+a2κ23κ12κ2κ23)i=0,

    separate the real and imaginary parts, let R(κ1,γ)=κ133κ1κ22+a1κ12a1κ22+κ1a2+a3, then, compute the transversality conditions, by the implicit function theorem,

    dκ1dγ=RγRκ1, (4.7)

    and κ1=0, κ2=a2, then

    dκ1dγ|γ=γ=a3a1a2a2a12a2,=(βI1+γ+d)((1θ)βI1+δ+d)(1(1θ)2)β2I1V1δγ((1θ)βI1+d)((2θ)βI1+γ+δ+2d)2((βI1+γ+d)((1θ)βI1+δ+d)+(1θ)2β2I1V1+β2I1S1δγ)

    since sgn(dκ1dγ)=1, and thus it generates Hopf bifurcation at γ=γ.

    In determining how vaccines contribute to the reduction of mortality from disease in populations and control disease transmission of disease, we must explore the importance of vaccines in relation to different factors involved in disease transmission and epidemiology. Sensitivity analysis of Rvac shows how each parameter contributes to the propagation of the disease. In Section 2.2, we calculate Rvac, which is correlated with the transmission and prevalence. In this paper, the normalized forward sensitivity index analysis is used to analyze the parametric variable's effect on Rvac.

    Definition 1. [41] The normalized forward sensitivity index of Rvac that depends differentiably on a parameter ω, which is defined as

    Oω=ωRvacRvacω, (5.1)

    shows that Rvac rises with ω increasing when Oω>0, but Rvac declines with increasing ω when Oω<0.

    The normalized forward sensitivity index of Rvac with regard to β,Λ,b,α,γ,θ as follows:

    Oβ=OΛ=1,Oγ=γθ(d+δ)d+δ+(1θ)γ,Oθ=γθd+δ+(1θ)γ,
    Oα=αdd+α+b,Ob=bdd+α+b,Oδ=θγδd+δ+(1θ)γ,Od=(δ+(1θ)γ)[(d+α+b)(d+δ+γ)+d(2d+b+δ+γ)]Λβ(d+δ+(1θ)γ),

    these equations show that β, Λ, δ has a negative effect on Rvac, and when β and Λ increase, Rvac also increases. Conversely b,d,α,γ,θ have a positive effect on Rvac, which shows that the number of individuals with secondary infections is lower, when b,d,α,γ,θ increase, which shows that vaccines are very successful in halting the propagation of diseases.

    Optimal control theory is employed to identify method of to achieve the maximum performance at the minimum cost under different assumptions. In Section 5, we analyzed the sensitivity of Rvac. Therefore, in conjunction with the actual situation of infectious diseases transmission, we formulate the optimal vaccination control strategy [23].

    In this section, to get as many people vaccinated as possible, the vaccination rate γ is selected as the control variable u(t). Since the vaccines produce are limited, thus the vaccinated people also are limited, it is possible to get uSΩ, where Ω is the maximum vaccination number.

    Thus, the optimal vaccination control problem with inequality constraints is described as follows,

    Problem(P){minY=tf0(P1I2+u2)dt,s.t.V=uS(1θ)βVI(δ+d)V,S=Λ+δVβSI(u+d)S,I=βSI+(1θ)βVI(d+b+α)I,R=bIdR,V(0)=V0,S(0)=S0,I(0)=I0,R(0)=R0,0uumax,0SSmax,uSΩ, (6.1)

    where tf represents the final time and tfR+, P1 represents the weight coefficient, and P1R+.

    In Problem (P), there exists the inequality constraint (0uumax,0SSmax,uSΩ), and it is translated into equality constraints by non-negative parameters ηi(i=1,2,3,4), that is,

    {u+η1=0,uumax+η2=0,SSmax+η3=0,uSΩ+η4=0. (6.2)

    Thus, the Hamiltonian function of Problem(P) is expressed as follows [42,43]:

    H=P1I2+u2+λV[uS(1θ)βVI(δ+d)V]+λS[Λ+δVβSI(u+d)S]+λI[βSI+(1θ)βVI(d+b+α)I]
    +λR[bIdR]+μ1(u+η1)+μ2(uumax+η2)+μ3(SSmax+η3)+μ4(uSΩ+η4),

    where λ=[λV,λS,λI,λR]T is the cost variable, and μ=[μ1,μ2,μ3,μ4]T is non-negative.

    In order to prove the existence of the optimal vaccination strategy u, we apply Theorem 2.2 in [44] and Theorem 5.1 in [45]. We need to check the following assumptions:

    (1) The set of controls and corresponding state variables is nonempty.

    (2) The admissible set is convex and closed.

    (3) The right hand side of (6.1) is bounded by a linear function in the state and control variables.

    (4) The integrand of the objective functional is convex.

    (5) There exist constants C1>0, C2>0, and τ>1 such that the integrand of the objective functional satisfies YC1|u|τC2.

    It is obvious that assumption 1 holds. Note that the solutions are bounded, so assumption 2 holds. To simplify the notation, we define L(t,ϕ,u):

    ϕt=[VSIR]=L(t,ϕ,u)=[uS(1θ)βVI(δ+d)VΛ+δVβSI(u+d)SβSI+(1θ)βVI(d+b+α)IbIdR],

    For assumption 3, there exist ϕ1(t), ϕ2(t), it follows that

    |L(t,ϕ1,u)L(t,ϕ2,u)|=|[uS1(1θ)βV1I1(δ+d)V1(uS2(1θ)βV2I2(δ+d)V2)Λ+δV1βS1I1(u+d)S1(Λ+δV2βS2I2(u+d)S2)βS1I1+(1θ)βV1I1(d+b+α)I1(βS2I2+(1θ)βV2I2(d+b+α)I2)bI1dR1(bI2dR2)]|,
    =|[u(S1S2)+(1θ)βV1(I1I2)+(1θ)βI2(V1V2)+(δ+d)(V2V1)δ(V2V1)+βS1(I1I2)+βI2(S1S2)+(u+d)(S2S1)βS1(I1I2)+βI2(S1S2)+(1θ)βV1(I1I2)+(1θ)βI2(V1V2)+(d+b+α)(I2I1)b(I1I2)+d(R2R1)]|
    u|S1S2|+(1θ)βV1|I1I2|+(1θ)βI2|V1V2|+(δ+d)|V1V2|+δ|V1V2|
    +βS1|I1I2|+βI2|S1S2|+(u+d)|S1S2|+βS1|I1I2|+βI2|S1S2|
    +(1θ)βV1|I1I2|+(1θ)βI2|V1V2|+(d+b+α)|I1I2|+b|I1I2|+d|R1R2|,
    =M1|S1S2|+M2|I1I2|+M3|V1V2|+M4|R1R2|,
    M(|S1S2|+|I1I2|+|V1V2|+|R1R2|),

    where M1=2u+d+2βI2, M2=2(1θ)βV1+βS1+(2θ)βI2+2b+d+α, M4=d, M3=2(1θ)βI2+2δ+d, M=max{M1,M2,M3,M4}. The assumption 3 holds.

    For assumption 4, there exists the constant k(0,1) and u1, u2, then it obtains

    Y((1k)u1+ku2)(1k)Y(u1)kY(u2)
    =((1k)u1+ku2)2(1k)u21ku22=k(k1)(u1u2)2<0.

    Hence, Y((1k)u1+ku2)<(1k)Y(u1)+kY(u2), it proves that assumption 4 holds.

    For assumption 5, it is obviously that

    P1I2+u2u2C1uτC2,

    and C1=1, τ=2, C2>0. The assumption 5 is satisfied. The existence of u is proved. In the next context, denote the optimal control of Problem(P) as u and the trajectory of the corresponding optimal control state as x=[V,S,I,R]. In [44], it shows that base on a set of necessary conditions that the optimal control and state must satisfy, which is the optimality conditions, the adjoint equations and the transversality conditions, solving the optimal control problems. Here is the specific solution step to find the necessary conditions.

    The first-order necessary conditions can derive by utilizing the Pontryagin maximum principle [44]. Based on the conditions of optimality, co-state, and parametric variables, the two-point boundary value problems and nonlinear complementarity problems can formulated as follows [24]:

    ˙x=Hλ, (6.3)
    ˙λ=Hx(the adjoint equation),  (6.4)

    where η0, μ0, ηTμ=0.

    The optimal conditions for the control variables u(t) are given by:

    Hu=0. (6.5)

    Combining Eqs (6.3) and (6.4), bringing the optimal solution, and ˙λV,˙λS,˙λI,˙λR are as follows:

    {˙λV=λV[(1θ)βI+(δ+d)]λSδλI(1θ)βI˙λS=λS[βI+(u+d)]λVuλIβIμ3uμ4,˙λI=λV(1θ)βV+λSβS+λI(d+α+b)λI(1θ)βVλIβSλRb2AI,˙λR=λRd, (6.6)

    where the transversality conditions are determined as

    λV(tf)=λS(tf)=λI(tf)=λR(tf)=0. (6.7)

    For a particular optimal control problem, Eqs (6.4), (6.5) and (6.7) form a set of necessary conditions that an optimal control and state must satisfy.

    By the Section 3.1 in [44], if our goals depend on the state at the terminal time, the objective function is

    ϕ(x(t1))+maxut1t0f(t,x(t),u(t))dt, 

    where ϕ(x(t1)) represents the payoff term, which is a goal with respect to the final position or population level, x(t1). Then, compute the necessary conditions, where the transversality conditions have changed. The transversality conditions are as

    λ(t1)=ϕ(x(t1)).

    In the optimal vaccination control problem of this paper, the objective functional did not explicitly depend on the state at the terminal time. Thus, let the transversality conditions be stated as: λV(tf)=λS(tf)=λI(tf)=λR(tf)=0.

    Let the control variable u meet 0uumax and uΩS, and then 0umin{umax,ΩS} is received. Set umax is equal to unity and Ω<Smax, and thus, it can be obtained that ΩS<umax.

    By solving Eq (6.5), the optimal vaccination control u can be solved

    u=λSS+μ1λVSμ2μ4S2. (6.8)

    In the following discussion, consider ΩS>umax, under the case with u<ΩS, where μ40. In order to determine the explicit expression without μ1, μ2, consider the following three cases:

    (1) when 0<u<umax, μ1=μ2=0, hence u=(λSλV)S2;

    (2) when u=0, μ2=0, hence 0=u=(λSλV)S+μ12, and when μ10, there is (λSλV)S0;

    (3) when u=umax, μ1=0, hence umax=u=(λSλV)Sμ22, and when μ20, there is (λSλV)Sumax.

    Summarize the three conclusions when ΩS>umax, the optimal vaccination control solution u is as follows,

    u=max{0,min{(λSλV)S2,umax}}. (6.9)

    When ΩSumax, the optimal vaccination control solution u is as follows

    u=max{0,min{(λSλV)S2,ΩS}}. (6.10)

    Thus, the analytical formula for optimal control is:

    u=max{0,min{(λSλV)S2,ΩS,umax}}. (6.11)

    In this section, numerical simulations will be performed to demonstrate the results of the above theory using MATLAB.

    For the parameter values: b=0.008, d=0.0518, θ=0.8125, β=0.0563, δ=0.111, Λ=1, α=0.35, γ=0.99, and Rvac=0.8016 < 1 which satisfied the condition of the Theorem 3.2. It can be seen from Figure 2, which proved the validity of the Theorem 3.2.

    Figure 2.  Global stability of E0.

    The parameter values are as follows:b=0.0085, d=0.005, θ=0.6, β=0.29, δ=0.005, Λ=10, α=0.0099, γ=0.2, we can obtain Rvac = 2.4716×104, in Figure 3, it can observe that for any given different initial values, these initial points can eventually tend to be endemic equilibrium, that is, which proves the Theorem 3.6 numerically.

    Figure 3.  Global stability of the endemic equilibrium.

    The bifurcation diagram is shown in Figure 4, with bifurcation parameter β(0.15,0.85), and other parameter values are α = 0.11, γ = 0.85, δ = 0.005, θ = 0.95, b=0.943, d=0.0718, Λ=2. In Figure 4, it can be seen that the system generates a forward bifurcation at Rvac=1. When Rvac<1, E0 is stability, when Rvac>1, there exists a stable E1 and an unstable E0.

    Figure 4.  Forward bifurcation.

    In Section 4, we have shown that the system generates Hopf bifurcation when the parameter γ crosses the threshold γ. By choosing the appropriate parameters, the result of the Theorem 4.1 is proved numerically. In Figure 5(a), (b) we show the stability of the system (2). In Figure 5(a) b=0.85, d=0.001, θ=0.3, β=0.0006, δ=0.009, Λ=100, α=0.95, γ=0.065, and R0=23.4129, which shows there exists the unique endemic equilibrium. In Figure 5(b) γ=0.45 and all other parameters are the same.

    Figure 5.  Phase diagram: (a) the limit cycle and (b) the system (2.2) is stable.

    With given parameter values, the normalized forward sensitivity index is obtained as shown in Table 1.

    Table 1.  Normalized forward sensitivity index.
    Parameter β Λ b d α δ γ θ
    Sensitivity Index 1 1 -0.0602 -0.0036 -0.0070 0.0338 -0.5198 -6.7687

     | Show Table
    DownLoad: CSV

    In Table 1, we choose the proper parameters, obtain the value of the sensitivity index. The index of β, Λ, δ is positive, where when β, Λ increase 10%, Rvac will increase 10%. Similarly, when δ increases 10%, Rvac will increase 0.338%. Inversely, the index of b,d,α,γ,θ is negative, which means that b,d,α,γ,θ are all negative effect on the basic regeneration number, that is, Rvac decreases with the increase of b,d,α,γ,θ. For example, if γ increases 10%, Rvac will decrease 5.198%. These results show that when changing the vaccination rate, vaccine effective rate values and the rate of vaccine-induced immunity, Rvac also changes dramatically. Thus, to control the transmission of disease, people are encouraged to be active in vaccinations, and biologists should increase the vaccine effectiveness rate.

    In Section 6, the vaccination rate γ was selected as the control parameter, and the expression for the optimal solution was obtained. Set the parameter values as A=0.002, umax=1, Rmax=1100, and the final time is tf=100. From Figure 6, it can be identified that the infected is apparently lower after adding control measures (red curve) than when no control measures were added, which indicates that the addition of control measures is beneficial to restrain the transmission of the disease, and the prevention and control strategy is effective.

    Figure 6.  Changes in the vaccinated and infectious population over time before and after controlling.

    In this paper, an epidemic dynamical model of vaccination is developed. It includes vaccine effectiveness, vaccination rate, and the vaccine-induced immune decline rate. The qualitative theoretical analysis of the model leads us to the following conclusions.

    Through the next-generation method, we calculated Rvac and confirm the stability of E0. When Rvac<1, E0 is GAS. A high vaccine effectiveness and vaccination rate and a low vaccine-induced immune decline were found to drive the elimination of the disease. When Rvac>1, E1 is GAS, that is, when certain threshold conditions for Rvac are achieved, the propagation of the disease can be contained by employing vaccination, increased vaccine effectiveness, and similar factors.

    Using the center manifold theory, we showed that the system will generate the forward bifurcation at Rvac=1. As the bifurcation parameter β increases, the system will undergo the forward bifurcation, and with it, reflecting that the disease will not become extinct. Therefore, when controlling the transmission of the disease, it is possible to reduce the patient's contact with the external community by taking preventive measures such as wearing masks, lengthening social distance, and isolation. We chose the vaccination rate γ as the bifurcation parameter, providing theoretical demonstrations of the existence of the Hopf bifurcation under certain parameter conditions.

    Next, sensitivity analysis of Rvac shows that the vaccination rates and vaccine effectiveness are fundamental to Rvac.Vaccine-induced immune decline rate also plays an essential role in disease containment. Thus, we can show that vaccinations are a vital component in containing the transmission of disease. Community policymakers use the outcomes of sensitivity analyses to develop strategies to limit the transmission of diseases, which encourages people to be vaccinated while investing more in vaccine research to improve vaccine effectiveness rate.

    To find the most cost-effective strategy for controlling infectious diseases, we selected the vaccination rate γ as the control parameter, and the optimal control function with respect to vaccination is obtained, which was solved using the Pontryagin maximum principle. Results showed that vaccination is effective in decreasing the number of infected individuals, and vaccination is an essential way to slow down the number of infected people.

    The authors declare they have not used Artificial Intelligence (AI) tools in the creation of this article.

    This work was supported by the Gansu Science and Technology Fund (20JR5RA512), the Research Fund for Humanities and Social Sciences of the Ministry of Education (20XJAZH006), the Fundamental Research Funds for the Central Universities (31920220041), the Leading Talents Project of State Ethnic Affairs Commission of China, the Gansu Provincial Education Department's Outstanding Graduate Student "Innovation Star" Project (2023CXZX-197).

    The authors declare that they have no conflict of interest.



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