Loading [MathJax]/jax/output/SVG/jax.js
Research article Special Issues

Abnormal dynamics of functional brain network in Apolipoprotein E ε4 carriers with mild cognitive impairment

  • As is well known, the Apolipoprotein E (APOE) ε4 allele is the most pertinent genetic hazardous element for Alzheimer's disease (AD). Mild cognitive impairment (MCI) is considered a prodromal stage of AD. How the APOE ε4 allele modulates functional connectivity of brain network in MCI group is a question worth exploring. At present, some studies have evaluated the relationship between APOE ε4 allele and static functional network connectivity (sFNC) for MCI individuals, while the relationship of dynamic FNC (dFNC) with APOE ε4 allele still remained puzzled. Thus, we aim to detect aberrant dFNC for APOE ε4 carriers in the MCI group. On the basis of the resting-state functional magnetic resonance imaging (rs-fMRI) data, seven intrinsic brain functional networks were first recognized by the group independent component analysis. Then, the technique of sliding window was employed to determine the dFNC, and two dFNC states were detected by the k-means clustering algorithm. Finally, three temporal properties of fraction time, mean dwell time as well as transition numbers in the dFNC states were investigated. The results found that the dFNC and temporal properties in APOE ε4 carriers were abnormal compared with those in APOE ε4 noncarriers. In detail, in the MCI group, compared with APOE ε4 noncarriers, carriers had 9 pairs of abnormal dFNC and had significant differences in all the three temporal properties of the two dFNC states. In addition, two pairs of dFNC were found significantly correlated with clinical measure. This detected abnormal dynamics of temporal properties and dFNC in APOE ε4 carriers were similar with that reported for AD patients in previous studies. These results may suggest that in the MCI group, APOE carriers are more at risk for AD compared to noncarriers. Our findings may offer novel insights into the mechanisms of abnormal brain reconfiguration for individuals at genetic risk for AD, which could also be regarded as biomarkers for the early identification of AD.

    Citation: Xiaoli Yang, Yan Liu. Abnormal dynamics of functional brain network in Apolipoprotein E ε4 carriers with mild cognitive impairment[J]. Electronic Research Archive, 2024, 32(1): 1-16. doi: 10.3934/era.2024001

    Related Papers:

    [1] Weijie Ding, Xiaochen Mao, Lei Qiao, Mingjie Guan, Minqiang Shao . Delay-induced instability and oscillations in a multiplex neural system with Fitzhugh-Nagumo networks. Electronic Research Archive, 2022, 30(3): 1075-1086. doi: 10.3934/era.2022057
    [2] Xiaochun Gu, Fang Han, Zhijie Wang, Kaleem Kashif, Wenlian Lu . Enhancement of gamma oscillations in E/I neural networks by increase of difference between external inputs. Electronic Research Archive, 2021, 29(5): 3227-3241. doi: 10.3934/era.2021035
    [3] Yuchen Zhu . Blow-up of solutions for a time fractional biharmonic equation with exponentional nonlinear memory. Electronic Research Archive, 2024, 32(11): 5988-6007. doi: 10.3934/era.2024278
    [4] Songbai Guo, Xin Yang, Zuohuan Zheng . Global dynamics of a time-delayed malaria model with asymptomatic infections and standard incidence rate. Electronic Research Archive, 2023, 31(6): 3534-3551. doi: 10.3934/era.2023179
    [5] Tianyi Li, Xiaofeng Xu, Ming Liu . Fixed-time synchronization of mixed-delay fuzzy cellular neural networks with $ L\acute{e}vy $ noise. Electronic Research Archive, 2025, 33(4): 2032-2060. doi: 10.3934/era.2025090
    [6] Ariel Leslie, Jianzhong Su . Modeling and simulation of a network of neurons regarding Glucose Transporter Deficiency induced epileptic seizures. Electronic Research Archive, 2022, 30(5): 1813-1835. doi: 10.3934/era.2022092
    [7] Peng Gao, Pengyu Chen . Blowup and MLUH stability of time-space fractional reaction-diffusion equations. Electronic Research Archive, 2022, 30(9): 3351-3361. doi: 10.3934/era.2022170
    [8] Hongyu Zhang, Yiwei Wu, Lu Zhen, Yong Jin, Shuaian Wang . Optimization problems in liquefied natural gas transport and storage for multimodal transport companies. Electronic Research Archive, 2024, 32(8): 4828-4844. doi: 10.3934/era.2024221
    [9] Jorge Rebaza . On a model of COVID-19 dynamics. Electronic Research Archive, 2021, 29(2): 2129-2140. doi: 10.3934/era.2020108
    [10] Ke Yin, Kewei Zhang . Some computable quasiconvex multiwell models in linear subspaces without rank-one matrices. Electronic Research Archive, 2022, 30(5): 1632-1652. doi: 10.3934/era.2022082
  • As is well known, the Apolipoprotein E (APOE) ε4 allele is the most pertinent genetic hazardous element for Alzheimer's disease (AD). Mild cognitive impairment (MCI) is considered a prodromal stage of AD. How the APOE ε4 allele modulates functional connectivity of brain network in MCI group is a question worth exploring. At present, some studies have evaluated the relationship between APOE ε4 allele and static functional network connectivity (sFNC) for MCI individuals, while the relationship of dynamic FNC (dFNC) with APOE ε4 allele still remained puzzled. Thus, we aim to detect aberrant dFNC for APOE ε4 carriers in the MCI group. On the basis of the resting-state functional magnetic resonance imaging (rs-fMRI) data, seven intrinsic brain functional networks were first recognized by the group independent component analysis. Then, the technique of sliding window was employed to determine the dFNC, and two dFNC states were detected by the k-means clustering algorithm. Finally, three temporal properties of fraction time, mean dwell time as well as transition numbers in the dFNC states were investigated. The results found that the dFNC and temporal properties in APOE ε4 carriers were abnormal compared with those in APOE ε4 noncarriers. In detail, in the MCI group, compared with APOE ε4 noncarriers, carriers had 9 pairs of abnormal dFNC and had significant differences in all the three temporal properties of the two dFNC states. In addition, two pairs of dFNC were found significantly correlated with clinical measure. This detected abnormal dynamics of temporal properties and dFNC in APOE ε4 carriers were similar with that reported for AD patients in previous studies. These results may suggest that in the MCI group, APOE carriers are more at risk for AD compared to noncarriers. Our findings may offer novel insights into the mechanisms of abnormal brain reconfiguration for individuals at genetic risk for AD, which could also be regarded as biomarkers for the early identification of AD.



    This study investigates a specific variational inequality problem described by

    {min{Lu,uu0}=0,(x,t)ΩT,u(x,0)=u0(x),xΩ,u(x,t)=uν=0,(x,t)Ω×(0,T) (1)

    with a non-divergence parabolic operator

    Lu=utudiv(|u|p2u)γu|u|p. (2)

    Here, Ω denotes a bounded and open subset of Rn. We consider the case where p2, γ(0,1) and T>0 are positive constants, ΩT=Ω×(0,T), and u0 satisfies

    u0C(ˉΩ)W1,p0(Ω).

    From (1), we can infer that u>u0 and Lu0 in ΩT. It is easily observed that when u>u0, then Lu=0 in ΩT; conversely, when u=u0, it follows that Lu0. Therefore, in some literature [1,2,3], the variational inequality (1) is often stated in the following manner:

    {Lu0,(x,t)ΩT,uu0,(x,t)ΩT,Lu×(uu0)=0,(x,t)ΩT,u(0,x)=u0(x),xΩ,u(t,x)=uν=0,(x,t)Ω×(0,T).

    It is evident that the above formulation is not as concise as the model presented in (1). This paper adopts the statement of the model in (1) for clarity and simplicity.

    The study of variational inequality problems of the form (1) originated from the pricing problems of American contingent claims with the inclusion of early exercise provisions [1]. The inclusion of early exercise provisions results in a variational inequality model that is characterized by Eq (1). Further studies on this aspect can be found in [2,3], and necessary explanations are provided in Section 2. Therefore, we will not repeat them here.

    In recent years, there has been an increasing amount of theoretical research on variational inequalities under the framework of linear and quasilinear parabolic operators. In [4], the solvability and regularity of quasilinear parabolic obstacle problems were studied using a symmetric dual-wind discontinuous Galerkin (DG) method. Reference [5] investigated a new class of constrained abstract evolutionary variational inequalities in three-dimensional space. By utilizing mathematical analysis of the unsteady Oseen model for generalized Newtonian incompressible fluids, sufficient conditions for the existence of weak solutions were obtained. Reference [6] focused on studying the existence and stability of weak solutions to variational inequalities under fuzzy parameters. By introducing two parameters into the mappings and constraint sets involved, [6] established the existence results for weak solutions of parameter fuzzy fractional differential variational inequalities (PFFDVI) and further analyzed the compactness and continuous dependence on the initial values of PFFDVI. For more results on the existence of solutions, please refer to [7,8,9].

    There have been some novel results in theoretical research on variational inequalities as well. Reference [10] established the local upper bounds, Harnack inequalities, and Hölder continuity up to the boundary for solutions of variational equations defined by degenerate elliptic operators. Studies on the Hölder continuity of solutions to variational inequalities under parabolic operator structures and other regularity results can be found in [11,12]. Reference [13] applied regularization and penalization operator methods to prove the existence of solutions to nonlinear degenerate pseudo-parabolic variational inequalities defined in regions with microstructures, and derived a priori estimates for solutions to the microscale problem.

    Inspired by [10,11,12], this study investigates the inverse Hölder estimate for solutions of the variational inequality (1), which has not yet been addressed in the literature. First, we define the integral mean operator I(t) on a spherical region and analyze its uniform continuity with respect to the time variable. Second, using the integral mean operator I(t) and other inequality amplification techniques, we obtain a Sobolev estimate for the variational inequality (1). Then, by combining the Caccioppoli inequality for the variational inequality (1), we derive the inverse Hölder estimate for the gradient of solutions, which allows us to estimate the higher-order norms of the gradient of solutions using lower-order Lp norms. Such results play a key role in many regularity studies.

    The valuation of American options ultimately boils down to a well-posed problem of variational inequality similar to Eq (1). An American call option gives the investor the right to purchase an underlying asset at a predetermined price K at any time within the investment horizon [0,T]. It is known that the value of an American option on the maturity date T is given by

    C(S,T)=max{SK,0}.

    American options only grant the investor the right to exercise their option within the investment horizon [0,T] without imposing any obligations. Thus, we have

    C(S,t)max{SK,0},t[0,T].

    If the value of the option C(S,t) at time t exceeds max{SK,0}, the investor may consider exercising the option, thereby forfeiting the opportunity for higher past returns. In this case, it follows that

    L1CΔ=tC+12σ2S2SSC+rSSCrC=0 (3)

    as stated in [1]. Here, σ represents the volatility of the underlying asset linked to the American option, and r denotes the risk-free rate of return in the financial market. On the other hand, if the value C(S,t) of the option at time t is max{SK,0}, the investor can retain the option to capture higher returns, leading to

    L1C0 (4)

    as indicated in [1].

    This is a backward differential inequality. Let us define τ=Tt and x=lnS. By combining Eqs (3) and (4), we have

    {min{L2C,Cmax{exK,0}}=0,(x,t)(0,B)×(0,T),C(x,0)=max{exK,0},x(0,B),C(0,t)=u(B,t)=0,t(0,T), (5)

    where

    L2C=τC+12σ2xxC+(r12σ2)xCrC.

    It is worth noting for the reader that x is a one-dimensional variable here, as in this financial example, the American option is linked to only one risky asset. Model (5) represents a specific financial case of the main problem studied in model (1), and thus, in model (1), we set x as an n-dimensional variable. Additionally, the variational inequality suitable for American options shows a high degree of structural similarity with Eq (1).

    On the other hand, transaction costs are often associated with the exercise of options, which necessitates a modification of the volatility σ. For instance, Pars and Avellaneda provided a transaction cost model where the volatility σ satisfies [13]

    σ2=σ02(1+ψsign(x(|xC|p2xC))).

    Here, σ02 represents the long-term volatility level, and the constant ψ is determined by the trading frequency and cost ratio. This adjustment is also consistent with the parabolic operator structure of model (1).

    Lastly, the spatial gradient of solutions to the variational inequality (5) applicable to American options not only measures the change in option value with respect to the underlying asset, but it also allows Black and Scholes to construct a risk-free portfolio to hedge against risk.

    Based on this, we examine more general cases than variational inequality (5). This article mainly analyzes the Sobolev estimation of the solution to variational inequality (1) and the inverse Hölder estimation of the spatial gradient. Before that, let us give a few useful symbols.

    Expanding upon this framework, we broaden our analysis to encompass wider scenarios than those addressed in variational inequality (5). The main objective of this paper is to conduct a thorough investigation into the Sobolev estimation for solving variational inequality (1), along with exploring the inverse Hölder estimation of the spatial gradient. Before delving into these aspects, we introduce a set of relevant mathematical symbols. For a given non-negative constant ρ, and any (x0,t0)ΩT, we define

    Dρ=Dρ(x0)={yRn:|yx0|<ρ}

    to denote the ball in space Rn that is also contained within the bounded region Ω. Similarly, we use

    Qρ,s=Qρ,s(x0,t0)=Dρ(x0)×(t0s,t0+s)

    to denote the cylinder in space Rn+1 that is also contained within ΩT. Lastly, let |Dρ| represent the Lebesgue measure of the set Dρ in space Rn, then the averaging operator of u on Dρ is defined as Iρ(t), given by

    Iρ(t)=Dρudx=1|Dρ|Dρudx.

    With the help of the maximal monotone operator,

    ξ(x)={0,x>0,M0,x=0,

    References [8,11,12] analyzed the existence of generalized solutions, whose definition is as follows:

    Definition 2.1 A pair (u,ξ) is defined as a generalized solution of the variational inequality (1) if it satisfies the following conditions:

    (a) uL(0,T,W1,p(Ω)) and tuL(0,T,L2(Ω)),

    (b) u(x,t)u0(x),u(x,0)=u0(x)forany(x,t)ΩT,

    (c) For every test function φC1(ˉΩT) and for each t[0,T], the following equality holds:

    Ωttuφ+u|u|p2uφdxdt+(1γ)Ωt|u|pφdxdt=Ωtξφdxdt.

    In order to ensure the solvability of the problem, we still impose the restriction γ(0,1) in this study.

    Lemma 2.2 The solution u of variational inequality (1) is uniformly bounded in ΩT. That is, for any (x,t)ΩT, there exists a constant ϑ0, independent of (x,t), such that

    |u|ϑ0.

    Proof Note that from (1), we obtain Lu0 for any (x,t)ΩT. By multiplying both sides of Lu0 by ϕ=(uϑ0)+, we have

    Ωt(uϑ0)(uϑ0)+dx+Ωu|(uϑ0)|p2(uϑ0)(uϑ0)+dx+(1γ)Ωu|(uϑ0)|p(uϑ0)+dx0. (6)

    Note that when uϑ0, t(uϑ0)+=0 and (uϑ0)+=0; when uϑ0, t(uϑ0)+=tu and (uϑ0)+=u, thus

    Ωu|(uϑ0)|p2(uϑ0)(uϑ0)+dx=Ωu|(uϑ0)|pdx0. (7)

    By further removing the non-negative terms Ωu|(uϑ0)|pdx and Ωu|(uϑ0)|p(uϑ0)+dx from (6), we obtain

    Ωt(uϑ0)2+dx0.

    Clearly, when ϑ0 is sufficiently large, Ω(u0ϑ0)2+dx=0 holds. Therefore, for any t(0,T),

    12Ω(uϑ0)2+dx0.

    This demonstrates uϑ0a.e.inΩT □.

    Note that from (1), it is easy to see that Lu0 in Q2ρ,2s. By choosing the test function ϕ=ψ2(uλ)+, and then integrating ϕLu0 over Q2ρ,2s,

    Q2ρ,2stuudxdt+Q2ρ,2s|u|p2uudxdt+(1γ)Q2ρ,2su|u|pdxdt0.

    From Eq (13) in [11] or Theorem 2.1 in [12], it is easy to see that when γ(0,1), for any t(0,T),

    uLp(Ω). (8)

    This section examines the Sobolev estimates for the solution u. A Sobolev estimate on a local spherical region Qρ,s(x,t) is constructed using the lower-order Wp1 norm of the solution u. Initially, we investigate the time continuity results of an operator Iρ(t).

    Lemma 3.1 For any Q4ρ,sΩT, there exists a constant C, which depends solely on p and ϑ0, such that

    |Iρ(t1)Iρ(t2)|CsρQ2ρ,s|u|p1dxdt.

    Proof Assume t1<t2, choose η sufficiently small, and suppose the function ψ1C0(t1η,t2+η) satisfies

    ψ1=1in(t1,t2)and0ψ11in(t1η,t2+η).

    By applying integration by parts, it is easy to obtain

    Ωudiv(|u|p2u)dx=Ωu|u|p2udxΩ|u|pdx.

    Furthermore, due to |Dˉρ|×(Iˉρ(t1)Iˉρ(t2))=Dˉρ×(t1,t2)tudxdt, we have

    |Dˉρ|×(Iˉρ(t1)Iˉρ(t2))Dˉρ×(t1,t2)u|u|p2udxdt(1γ)Dˉρ×(t1,t2)|u|pdxdt. (9)

    Considering (1γ)Dˉρ×(t1,t2)|u|pdxdt is non-negative, by Lemma 2.2, we obtain

    |Dˉρ|×(Iˉρ(t1)Iˉρ(t2))ϑ0Dˉρ×(t1,t2)|u|p2udxdt. (10)

    Here, we choose ˉρ to satisfy ρ<ˉρ<2ρ. On the other hand, according to [14, p. 5, line 3] and Lemma 4.4 of [14], there exists a constant C that depends only on n and p such that

    Dˉρ×(t1,t2)|u|p1dxdtCρD2ρ×(t1,t2)|u|p1dxdt. (11)

    By combining (10) and (11) and substituting the result into (9), the proposition is established. □

    Theorem 3.1 Assume u is a solution to the variational inequality (1). If uLα(τ2s,τ+2s; W1,p(D2ρ(z))), then for any α(1,), we have

    Qρ,s|u(x,t)Iρ(t)|α(1+2/n)dxdtC(Qρ,s|u|αdxdt)(esssupt(τ2s,τ+2s)D2ρ|uIˆρ(t)|2dx)αn.

    Proof By selecting τ2s<t<τ+2s and 1<α<, we analyze the Sobolev-type estimates for the solution to the variational inequality problem (1) under the condition

    uLα(τ2s,τ+2s;W1,p(D2ρ(z))).

    Define

    v(x,t)=|u(x,t)Iρ(t)|ψ(x,t), (12)

    where ψ(x,t) is a cut-off function on Q2ρ,2s,

    ψ(x,t)=1inQρ,s,0ψ(x,t)1inQ2ρ,2s,|ψ(x,t)|C1ρ. (13)

    Evidently, when t(τs,τs), for any xD2ρ(z), we have ψ(x,τ)=0. When t(τs,τs), for any xD2ρ(z), we have

    ψ(x,t)0and|tψ(x,t)|Cs (14)

    For convenience, let ˆρ=2ρ, and define

    J=Dˆρvα(1+2/n)dx=Dˆρv2/nvα(1+2/n)2/ndx. (15)

    Thus, by the Hölder inequality,

    J(Dˆρv2dx)1/n(Dˆρv[α+(2/n)(α1)]n/(n1)dx)(n1)/n. (16)

    Further applying the Sobolev inequality to (Dˆρv[α+(2/n)(α1)]n/(n1)dx)(n1)/n, we get

    (Dˆρv[α+(2/n)(α1)]n/(n1)dx)(n1)/nC(n)Dˆρ|vα+(2/n)(α1)|dxC(n)Dˆρv(α1)(1+2/n)vdx. (17)

    The final inequality sign in the above expression holds because (α1)(1+2n)=α+2(α1)n1. Using the Hölder inequality again,

    Dˆρv(α1)(1+2/n)|v|dx(Dˆρ|v|αdx)1α(Dˆρvα(1+2/n)|v|dx)α1α. (18)

    Therefore, by combining inequalities (16)–(18), we obtain

    JC(n)Jα1α(Dˆρv2dx)1/n(Dˆρ|v|αdx)1α. (19)

    Thus, to estimate J, it suffices to analyze (Dˆρ|v|αdx)1α and (Dˆρv2dx)1/n and obtain their upper bounds with respect to u. Notice that the cut-off function ψ(x,t) satisfies 0ψ(x,t)1inQ2ρ,2s and |ψ(x,t)|C1ρ, thus

    (Dˆρ|v|αdx)1αCˆρ(Dˆρ|uIρ(t)|αdx)1α+(Dˆρ|u|αdx)1α. (20)

    Applying the Minkowski inequality again, we get

    (Dˆρ|uIρ(t)|αdx)1α(Dˆρ|uIˆρ(t)|αdx)1α+(Dˆρ|Iˆρ(t)Iρ(t)|αdx)1α(Dˆρ|uIˆρ(t)|αdx)1α+|Iˆρ(t)Iρ(t)|×|Dˆρ|1α. (21)

    Further analyzing |Iˆρ(t)Iρ(t)|×|Dˆρ|1α in (21), by Iρ(t), we have

    |Iˆρ(t)Iρ(t)|×|Dˆρ|1α|Dˆρ|1α|Dρ|1×Dρ|uIˆρ(t)|dx|Dˆρ|1α|Dρ|1×Dˆρ|uIˆρ(t)|dx. (22)

    Note that we previously assumed uLα(τ2s,τ+2s;W1,p(D2ρ(z))). Thus, combining inequalities (21) and (22), and using the Sobolev inequality, we obtain

    (Dˆρ|uIρ(t)|αdx)1αC(1+ρn/αˆρn)(Dˆρ|uIˆρ(t)|αdx)1αCˆρ(Dˆρ|u|αdx)1α. (23)

    Here, we have used the conditions α>1 and ˆρ>ρ>0. Substituting (23) into (20), we obtain an estimate for (Dˆρ|v|αdx)1α as

    (Dˆρ|v|αdx)1αC(Dˆρ|u|αdx)1α. (24)

    First, we analyze (Dˆρv2dx)1n. By estimating (Dˆρ|uIρ(t)|2dx)1n and applying Minkowski's inequality, we can derive

    (Dˆρ|uIρ(t)|2dx)1n((Dˆρ|uIˆρ(t)|2dx)2+(Dˆρ|Iρ(t)Iˆρ(t)|2dx)2)12n. (25)

    By utilizing the inequality (a+b)12n(2n)2n(a12n+b12n), the estimate for (Dˆρ|uIρ(t)|2dx)1n can be reformulated as

    (Dˆρ|uIρ(t)|2dx)1n(2n)2n((Dˆρ|uIˆρ(t)|2dx)1n+(Dˆρ|Iρ(t)Iˆρ(t)|2dx)1n). (26)

    Furthermore, by the definition of Iρ(t), we obtain

    (Dˆρ|Iρ(t)Iˆρ(t)|2dx)1n=|Iˆρ(t)Iρ(t)|2n×|Dˆρ|1nCρn/2ˆρn(Dˆρ|uIˆρ(t)|2dx)1n. (27)

    Thus, by combining inequalities (17) and (18), we derive

    (Dˆρ|uIρ(t)|2dx)1nCρn/2ˆρn(Dˆρ|uIˆρ(t)|2dx)1n. (28)

    The truncation function ψ(x,t) fulfills 0ψ(x,t)1inQ2ρ,2s, thereby yielding an estimate for (Dˆρv2dx)1n denoted as

    (Dˆρv2dx)1n(Dˆρ|uIρ(t)|2dx)1nCρn/2ˆρn(Dˆρ|uIˆρ(t)|2dx)1n. (29)

    In summary, by substituting the results from (24) and (29) into Eq (19), we obtain

    JC(n)Jα1αCρn/2ˆρn(Dˆρ|uIˆρ(t)|2dx)1nC(Dˆρ|u|αdx)1α.

    It is readily seen that Dρ|u(x,t)Iρ(t)|α(1+2/n)dxJ, and thus we obtain the result of Theorem 3.1. □

    This section presents an inverse Hölder inequality result. Before that, we introduce a Caccioppoli inequality, which is utilized in the proof.

    Lemma 4.1 (Caccioppoli's Inequality) Suppose u is a solution to the variational inequality (1). Then, for any non-negative constant λ, we have

    suptIρDρ(uλ)2dx+Qρ,su|u|pdxdtCsQ2ρ,2s(uλ)2dxdt+CρpQ2ρ,2s(uλ)pdxdt.

    Proof Note that from (1), it can be easily deduced that Lu0 in Q2ρ,2s. Let us choose a test function ϕ=ψ2×(uλ)+, and then integrate ϕ×Lu0 over Q2ρ,2s, resulting in

    Q2ρ,2stuψ2(uλ)dxdt+Q2ρ,2s|u|p2u[ψ2(uλ)]dxdt+(1γ)Q2ρ,2sψ2(uλ)+|u|pdxdt=0. (30)

    First, let us analyze Q2ρ,2stu×ψ2(uλ)+dxdt by employing the method of integration by parts, yielding

    Q2ρ,2st[ψ2(uλ)+2]dxdt=Q2ρ,2stuψ2(uλ)+dxdt+2Q2ρ,2sψψ(uλ)+2dxdt, (31)

    and

    Q2ρ,2su|u|p2u[ψ2(uλ)+]dxdt=Q2ρ,2sψ2u|u|pdxdt+2Q2ρ,2sψψ×u|u|p2u×(uλ)+dxdt. (32)

    Substituting Eqs (31) and (32) into Eq (30), we obtain

    QsRt[ψ2(uλ)+2]dxdt2QsRψψ(uλ)+2dxdt+QsRψ2|u|pdxdt+2QsRψψ×|u|p2u×(uλ)+dxdt=0,

    that is

    BRψ2(uλ)+2dx|t=s+QsRψ2|u|pdxdt=2QsRψψ(uλ)+2dxdt2QsRψψ×|u|p2u×(uλ)+dxdt. (33)

    Based on [11,12], by applying the Hölder's inequality and Young's inequality to Eq (4), we have

    suptIρDρ(uλ)+2dx+Qρ,su|u|pdxdtCsQ2ρ,2s(uλ)2dxdt+CρpQ2ρ,2s(uλ)pdxdt. (34)

    Moreover, by selecting ϕ=ψ2(uλ) and repeating the proof process of Eqs (30)–(34), we can easily obtain

    suptIρDρ(uλ)+2dx+Qρ,su|u|pdxdtCsQ2ρ,2s(uλ)2dxdt+CρpQ2ρ,2s(uλ)pdxdt. (35)

    By combining Eqs (34) and (35), the theorem is proven.□

    Theorem 4.1 Define q=max{p1,pn/(n+2)} and let u be a solution to the variational inequality (1). Then, we have

    Qρ,su|u|pdxdt(Q2ρ,2s|u|qdxdt)qp.

    Proof It is important to note that I2ρ(t) is not a constant over Q2ρ,2s, and thus, we choose

    λ=a(Q2ρ,2s)=1|Q2ρ,2s|Q2ρ,2sudxdt

    in the Caccioppoli inequality, resulting in

    Qρ,su|u|pdxdtCsQ2ρ,2s|ua(Q2ρ,2s)|2dxdt+CρpQ2ρ,2s|ua(Q2ρ,2s)|pdxdt. (36)

    By utilizing the Hölder and Young inequalities, we can obtain

    CsQ2ρ,2s|ua(Q2ρ,2s)|2dxdtCs|Q2ρ,2s|p2p(Q2ρ,2s|ua(Q2ρ,2s)|pdxdt)2pC(p)|QsR|(ρ2s)pp2+1ρpQ2ρ,2s|ua(Q2ρ,2s)|pdxdt. (37)

    Combining Eqs (36) and (37), we can estimate Qρ,su|u|pdxdt by analyzing only Q2ρ,2s|ua(Q2ρ,2s)|pdxdt. Using the Minkowski inequality, we have

    CpρpQ2ρ,2s|ua(Q2ρ,2s)|pdxdtCρpQ2ρ,2s|uI2ρ(t)|pdxdt+Cρp|Q2ρ|esssupt(τs,τ+s)|I2ρ(t)a(Q2ρ,2s)|p. (38)

    Next, we analyze the Q2ρ,2s|uI2ρ(t)|pdxdt and |I2ρ(t)a(Q2ρ,2s)|p in Eq (38). By the definition of Iρ(t) and Lemma 3.1, we have

    |I2ρ(t)a(Q2ρ,2s)|p(4s)p(τ+2sτ2s|I2ρ(t)I2ρ(ξ)|dξ)pCρp(Q2ρ,2s|u|p1dxdt)p. (39)

    Therefore, by utilizing the Hölder and Young inequalities, we can estimate the second term on the right-hand side of Eq (38) as follows:

    |I2ρ(t)a(Q2ρ,2s)|pCρp|Q2ρ,2s|1p(Q2ρ,2s|u|pdxdt)p1p. (40)

    Now, let us estimate the first term on the right-hand side of Eq (38). By considering Theorem 3.1, we have

    Q2ρ,2s|u(x,t)I2ρ(t)|pdxdtC(Q2ρ,2s|u|qdxdt)(esssupt(τ4s,τ+4s)D4ρ|uI4ρ(t)|2dx)qn. (41)

    Furthermore, by utilizing the Sobolev inequality on D4ρ, we obtain

    D4ρ|uI4ρ(t)|2dxCρ2D4ρ|u|2dxCρ2(D4ρ|u|pdx)2/p|D4ρ|(p2)/p=Cρ2(D4ρ|u|pdx)2/p|D4ρ|. (42)

    By substituting (42) into (41) and combining it with (40), we obtain

    Qρ,su|u|pdxdtC(p)|QsR|(ρ2s)pp2+Cρp(cρ2|D4ρ|)qn(Q2ρ,2s|u|qdxdt)+Cρ2p|Q2ρ,2s|1p(Q2ρ,2s|u|p1dxdt)p.

    Here, we make use of the fundamental result uLp(Ω), which is detailed in (8). With this, the proof of Theorem 4.1 is complete. □

    This study considers a type of variational inequality problem involving a non-divergence parabolic operator, as shown in (1) and (2). In other words, the Sobolev estimates and inverse Hölder estimates are examined for the solutions of variational inequality (1). First, we define the averaging operator of the variational inequality (1) on the local spatial region Dρ as Iρ(t) and prove the uniform continuity of the mean inequality Iρ(t) with respect to time t. Second, we establish a Sobolev inequality for the averaging operator Iρ(t), which serves as the cornerstone for proving the inverse Hölder estimates, as stated in Theorem 3.1. Finally, we examine the inverse Hölder estimate problem in local cylindrical regions. The proof relies on Lemma 4.1 and Theorem 3.1, as well as commonly used amplification techniques such as Minkowski inequality, Young's inequality, and Hölder's inequality.

    There are still some areas for improvement in the proofs presented in this paper. It is important to note that we make use of the condition γ(0,1), as when γ>1 holds, Eqs (6), (9), and (30) cannot be used as they are in this paper. In such cases, 1γ<0, and we cannot eliminate the non-negative terms containing 1γ. Furthermore, in [8], the existence of weak solutions to similar problems is discussed under the condition γ(0,1), which we also continue to adopt here. On the other hand, in order to employ Young's inequality and Hölder's inequality, we also restrict p2. It is worth noting that in the study of regularity theory for parabolic equations, the literature has considered the case p(1,2), and we also aim to explore this limitation in our future research.

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

    The authors are very grateful to the anonymous referees for their insightful comments and constructive suggestions, which considerably improve our manuscript. This work is supported by Growth Project of Young Scientific and Technological Talents in Colleges and Universities of Guizhou Province (NO. KY[2022]191).

    The author declares there is no conflict of interest.



    [1] X. Liu, Q. Zeng, X. Luo, K. Li, H. Hong, S. Wang, et al., Effects of APOE ε2 on the fractional amplitude of low-frequency fluctuation in mild cognitive impairment: a study based on the resting-state functional MRI, Front. Aging Neurosci., 13 (2021), 1–11. https://doi.org/10.3389/fnagi.2021.591347 doi: 10.3389/fnagi.2021.591347
    [2] P. Liang, Z. Wang, Y. Yang, X. Jia, K. Li, Functional disconnection and compensation in mild cognitive impairment: evidence from DLPFC connectivity using resting-state fMRI, PLoS One, 6 (2011), e22153. https://doi.org/10.1371/journal.pone.0022153 doi: 10.1371/journal.pone.0022153
    [3] A. Chandra, P. E. Valkimadi, G. Pagano, O. Cousins, G. Dervenoulas, M. Politis, Applications of amyloid, tau, and neuroinflammation PET imaging to Alzheimer's disease and mild cognitive impairment, Hum. Brain Mapp., 40 (2019), 5424–5442. https://doi.org/10.1002/hbm.24782 doi: 10.1002/hbm.24782
    [4] C. Reitz, R. Mayeux, Alzheimer disease: epidemiology, diagnostic criteria, risk factors and biomarkers, Biochem. Pharmacol., 88 (2014), 640–651. https://doi.org/10.1016/j.bcp.2013.12.024 doi: 10.1016/j.bcp.2013.12.024
    [5] P. T. Nelson, I. Alafuzoff, E. H. Bigio, C. Bouras, H. Braak, N. J. Cairns, et al., Correlation of Alzheimer disease neuropathologic changes with cognitive status: a review of the literature, J. Neuropathol. Exp. Neurol., 71 (2012), 362–381. https://doi.org/10.1097/NEN.0b013e31825018f7 doi: 10.1097/NEN.0b013e31825018f7
    [6] J. Sheffler, J. Moxley, N. Sachs-Ericsson, Stress, race, and APOE: understanding the interplay of risk factors for changes in cognitive functioning, Aging Mental Health, 18 (2014), 784–791. https://doi.org/10.1080/13607863.2014.880403 doi: 10.1080/13607863.2014.880403
    [7] J. Raber, Y. Huang, J. W. Ashford, ApoE genotype accounts for the vast majority of AD risk and AD pathology, Neurobiol. Aging, 25 (2004), 641–650. https://doi.org/10.1016/j.neurobiolaging.2003.12.023 doi: 10.1016/j.neurobiolaging.2003.12.023
    [8] C. C. Liu, T. Kanekiyo, H. Xu, G. Bu, Apolipoprotein E and Alzheimer disease: risk, mechanisms and therapy, Nat. Rev. Neurol., 9 (2013), 184. https://doi.org/10.1038/nrneurol.2013.32 doi: 10.1038/nrneurol.2013.32
    [9] T. Li, B. Wang, Y. Gao, X. Wang, T. Yan, J. Xiang, et al., APOE ε4 and cognitive reserve effects on the functional network in the Alzheimer's disease spectrum, Brain Imaging Behav., 15 (2021), 758–771. https://doi.org/10.1007/s11682-020-00283-w doi: 10.1007/s11682-020-00283-w
    [10] B. C. Dickerson, R. A. Sperling, Large-scale functional brain network abnormalities in Alzheimer's disease: insights from functional neuroimaging, Behav. Neurol., 21 (2009), 63–75. https://doi.org/10.3233/BEN-2009-0227 doi: 10.3233/BEN-2009-0227
    [11] P. Wang, B. Zhou, H. Yao, Y. Zhan, Z. Zhang, Y. Cui, et al., Aberrant intra- and inter-network connectivity architectures in Alzheimer's disease and mild cognitive impairment, Sci. Rep., 5 (2015), 14824. https://doi.org/10.1038/srep14824 doi: 10.1038/srep14824
    [12] M. A. Binnewijzend, M. M. Schoonheim, E. Sanz-Arigita, A. M. Wink, W. M. van der Flier, N. Tolboom, et al., Resting-state fMRI changes in Alzheimer's disease and mild cognitive impairment, Neurobiol. Aging, 33 (2012), 2018–2028. https://doi.org/10.1016/j.neurobiolaging.2011.07.003 doi: 10.1016/j.neurobiolaging.2011.07.003
    [13] M. Sendi, E. Zendehrouh, Z. Fu, J. Liu, Y. Du, E. Mormino, et al., Disrupted dynamic functional network connectivity among cognitive control networks in the progression of Alzheimer's disease, Brain Connect., 13 (2023), 334–343. https://doi.org/10.1089/brain.2020.0847 doi: 10.1089/brain.2020.0847
    [14] M. Sendi, E. Zendehrouh, R. L. Miller, Z. Fu, Y. Du, J. Liu, et al., Alzheimer's disease projection from normal to mild dementia reflected in functional network connectivity: a longitudinal study, Front. Neural Circuits, 14 (2020). https://doi.org/10.3389/fncir.2020.593263 doi: 10.3389/fncir.2020.593263
    [15] J. Huang, P. Beach, A. Bozoki, D. C. Zhu, Alzheimer's disease progressively reduces visual functional network connectivity, J. Alzheimers Dis. Rep., 5 (2021), 549–562. https://doi.org/10.3233/ADR-210017 doi: 10.3233/ADR-210017
    [16] F. Tang, D. Zhu, W. Ma, Q. Yao, Q. Li, J. Shi, Differences changes in cerebellar functional connectivity between mild cognitive impairment and Alzheimer's disease: a seed-based approach, Front. Neurol., 12 (2021). https://doi.org/10.3389/fneur.2021.645171 doi: 10.3389/fneur.2021.645171
    [17] Q. Wang, C. He, Z. Wang, Z. Zhang, C. Xie, Dynamic connectivity alteration facilitates cognitive decline in Alzheimer's disease spectrum, Brain Connect., 11 (2021), 213–224. https://doi.org/10.1089/brain.2020.0823 doi: 10.1089/brain.2020.0823
    [18] G. Sanabria-Diaz, L. Melie-Garcia, B. Draganski, J. F. Demonet, F. Kherif, Apolipoprotein E4 effects on topological brain network organization in mild cognitive impairment, Sci. Rep., 11 (2021), 845. https://doi.org/10.1038/s41598-020-80909-7 doi: 10.1038/s41598-020-80909-7
    [19] H. Song, H. Long, X. Zuo, C. Yu, B. Liu, Z. Wang, et al., APOE effects on default mode network in Chinese cognitive normal elderly: relationship with clinical cognitive performance, PLoS One, 10 (2015), e0133179. https://doi.org/10.1371/journal.pone.0133179 doi: 10.1371/journal.pone.0133179
    [20] Y. Zhu, L. Gong, C. He, Q. Wang, Q. Ren, C. Xie, Default mode network connectivity moderates the relationship between the APOE genotype and cognition and individualizes identification across the Alzheimer's disease spectrum, J. Alzheimer's Dis., 70 (2019), 843–860. https://doi.org/10.3233/JAD-190254 doi: 10.3233/JAD-190254
    [21] P. A. Chiesa, E. Cavedo, A. Vergallo, S. Lista, M. C. Potier, M. O. Habert, et al., Differential default mode network trajectories in asymptomatic individuals at risk for Alzheimer's disease, Alzheimer's Dementia, 15 (2019), 940–950. https://doi.org/10.1016/j.jalz.2019.03.006 doi: 10.1016/j.jalz.2019.03.006
    [22] H. Lu, S. L. Ma, S. W. Wong, C. W. Tam, S. T. Cheng, S. S. Chan, et al., Aberrant interhemispheric functional connectivity within default mode network and its relationships with neurocognitivefeatures in cognitively normal APOE ε4 elderly carriers, Int. Psychogeriatrics, 29 (2017), 805–814. https://doi.org/10.1017/S1041610216002477 doi: 10.1017/S1041610216002477
    [23] M. M. Machulda, D. T. Jones, P. Vemuri, E. McDade, R. Avula, S. Przybelski, et al., Effect of APOE ε4 status on intrinsic network connectivity in cognitively normal elderly subjects, Arch. Neurol., 68 (2011), 1131–1136. https://doi.org/10.1001/archneurol.2011.108 doi: 10.1001/archneurol.2011.108
    [24] M. S. E. Sendi, E. Zendehrouh, C. A. Ellis, Z. Fu, J. Chen, R. L. Miller, et al., The link between static and dynamic brain functional network connectivity and genetic risk of Alzheimer's disease, Neuroimage: Clin., 37 (2023), 103363. https://doi.org/10.1016/j.nicl.2023.103363 doi: 10.1016/j.nicl.2023.103363
    [25] S. G. Mueller, M. W. Weiner, L. J. Thal, R. C. Petersen, C. R. Jack, W. Jagust, et al., Ways toward an early diagnosis in Alzheimer's disease: the Alzheimer's Disease Neuroimaging Initiative (ADNI), Alzheimer's Dementia, 1 (2005), 55–66. https://doi.org/10.1016/j.jalz.2005.06.003 doi: 10.1016/j.jalz.2005.06.003
    [26] C. G. Yan, Y. F. Zang, DPARSF: a MATLAB toolbox for "pipeline" data analysis of resting-state fMRI, Front. Syst. Neurosci., 4 (2010). https://doi.org/10.3389/fnsys.2010.00013 doi: 10.3389/fnsys.2010.00013
    [27] H. Chen, Z. Zou, X. Zhang, J. Shi, N. Huang, Y. Lin, Dynamic changes in functional network connectivity involving amyotrophic lateral sclerosis and its correlation with disease severity, J. Magn. Reson. Imaging, 54 (2021), 239–248. https://doi.org/10.1002/jmri.27521 doi: 10.1002/jmri.27521
    [28] Y. Gu, Y. Lin, L. Huang, J. Ma, J. Zhang, Y. Xiao, et al., Abnormal dynamic functional connectivity in Alzheimer's disease, CNS Neurosci. Ther., 26 (2020), 962–971. https://doi.org/10.1111/cns.13387 doi: 10.1111/cns.13387
    [29] J. Kim, M. Criaud, S. S. Cho, M. Díez-Cirarda, A. Mihaescu, S. Coakeley, et al., Abnormal intrinsic brain functional network dynamics in Parkinson's disease, Brain, 140 (2017), 2955–2967. https://doi.org/10.1093/brain/awx233 doi: 10.1093/brain/awx233
    [30] E. A. Allen, E. Damaraju, S. M. Plis, E. B. Erhardt, T. Eichele, V. D. Calhoun, Tracking whole-brain connectivity dynamics in the resting state, Cereb. Cortex, 24 (2014), 663–676. https://doi.org/10.1093/cercor/bhs352 doi: 10.1093/cercor/bhs352
    [31] G. Li, L. Zhou, Z. Chen, N. Luo, M. Niu, Y. Li, et al., Dynamic functional connectivity impairments in idiopathic rapid eye movement sleep behavior disorder, Parkinsonism Relat. Disord., 79 (2020), 11–17. https://doi.org/10.1016/j.parkreldis.2020.08.003 doi: 10.1016/j.parkreldis.2020.08.003
    [32] S. Roweis, EM algorithms for PCA and SPCA, in Advances in Neural Information Processing Systems, 10 (1997), 626–632. Available from: https://proceedings.neurips.cc/paper_files/paper/1997/file/d9731321ef4e063ebbee79298fa36f56-Paper.pdf.
    [33] A. J. Bell, T. J. Sejnowski, An information-maximization approach to blind separation and blind deconvolution, Neural Comput., 7 (1995), 1129–1159. https://doi.org/10.1162/neco.1995.7.6.1129 doi: 10.1162/neco.1995.7.6.1129
    [34] T. Yin, Z. He, P. Ma, R. Sun, K. Xie, T. Liu, et al., Aberrant functional brain network dynamics in patients with functional constipation, Hum. Brain Mapp., 42 (2021), 5985–5999. https://doi.org/10.1002/hbm.25663 doi: 10.1002/hbm.25663
    [35] Z. Yao, J. Shi, Z. Zhang, W Zheng, T. Hu, Y. Li, et al., Altered dynamic functional connectivity in weakly-connected state in major depressive disorder, Clin. Neurophysiol., 130 (2019), 2096–2104. https://doi.org/10.1016/j.clinph.2019.08.009 doi: 10.1016/j.clinph.2019.08.009
    [36] E. Agoalikum, B. Klugah-Brown, H. Yang, P. Wang, S. Varshney, B. Niu, et al., Differences in disrupted dynamic functional network connectivity among children, adolescents, and adults with attention deficit/hyperactivity disorder: a resting-state fMRI study, Front. Hum. Neurosci., 15 (2021). https://doi.org/10.3389/fnhum.2021.697696 doi: 10.3389/fnhum.2021.697696
    [37] X. Ma, X. Wu, Y. Shi, Changes of dynamic functional connectivity associated with maturity in late preterm infants, Front. Pediatr., 8 (2020). https://doi.org/10.3389/fped.2020.00412 doi: 10.3389/fped.2020.00412
    [38] J. Friedman, T. Hastie, R. Tibshirani, Sparse inverse covariance estimation with the graphical lasso, Biostatistics, 9 (2008), 432–441. https://doi.org/10.1093/biostatistics/kxm045 doi: 10.1093/biostatistics/kxm045
    [39] Q. Chen, J. Lu, X. Zhang, Y. Sun, W. Chen, X. Li, et al., Alterations in dynamic functional connectivity in individuals with subjective cognitive decline, Front. Aging Neurosci., 13 (2021). https://doi.org/10.3389/fnagi.2021.646017 doi: 10.3389/fnagi.2021.646017
    [40] R. P. Viviano, N. Raz, P. Yuan, J. S. Damoiseaux, Associations between dynamic functional connectivity and age, metabolic risk, and cognitive performance, Neurobiol. Aging, 59 (2017), 135–143. https://doi.org/10.1016/j.neurobiolaging.2017.08.003 doi: 10.1016/j.neurobiolaging.2017.08.003
    [41] L. Tian, Q. Li, C. Wang, J. Yu, Changes in dynamic functional connections with aging, Neuroimage, 172 (2018), 31–39. https://doi.org/10.1016/j.neuroimage.2018.01.040 doi: 10.1016/j.neuroimage.2018.01.040
    [42] K. Mevel, G. Chételat, F. Eustache, B. Desgranges, The default mode network in healthy aging and Alzheimer's disease, Int. J. Alzheimer's Dis., 2011 (2011), 535816. https://doi.org/10.4061/2011/535816 doi: 10.4061/2011/535816
    [43] Y. Zhan, J. Ma, A. F. Alexander-Bloch, K. Xu, Y. Cui, Q. Feng, et al., Longitudinal study of impaired intra- and inter-network brain connectivity in subjects at high risk for Alzheimer's disease, J. Alzheimer's Dis., 52 (2016), 913–927. https://doi.org/10.3233/JAD-160008 doi: 10.3233/JAD-160008
    [44] Y. I. Sheline, J. C. Morris, A. Z. Snyder, J. L. Price, Z. Yan, G. D'Angelo, et al., APOE4 allele disrupts resting state fMRI connectivity in the absence of amyloid plaques or decreased CSF Aβ42, J. Neurosci., 30 (2010), 17035–17040. https://doi.org/10.1523/JNEUROSCI.3987-10.2010 doi: 10.1523/JNEUROSCI.3987-10.2010
    [45] Z. Yao, B. Hu, J. Zheng, W. Zheng, X. Chen, X. Gao, et al., A FDG-PET study of metabolic networks in apolipoprotein E ε4 allele carriers, PLoS One, 10 (2015), e0132300. https://doi.org/10.1371/journal.pone.0132300 doi: 10.1371/journal.pone.0132300
    [46] C. Y. Lin, C. H. Chen, S. E. Tom, S. H. Kuo, Cerebellar volume is associated withcognitive decline in mild cognitive impairment: results from ADNI, Cerebellum, 19 (2020), 217–225. https://doi.org/10.1007/s12311-019-01099-1 doi: 10.1007/s12311-019-01099-1
    [47] M. Zhang, Z. Guan, Y. Zhang, W. Sun, W. Li, J. Hu, et al., Disrupted coupling between salience network segregation and glucose metabolism is associated with cognitive decline in Alzheimer's disease–a simultaneous resting-state FDG-PET/fMRI study, Neuroimage: Clin., 34 (2022), 102977. https://doi.org/10.1016/j.nicl.2022.102977 doi: 10.1016/j.nicl.2022.102977
    [48] G. Aghakhanyan, A. Vergallo, M. Gennaro, S. Mazzarri, F. Guidoccio, C. Radicchi, et al., The Precuneus–a witness for excessive Aβ gathering in Alzheimer's disease pathology, Neurodegener. Dis., 18 (2019), 302–309. https://doi.org/10.1159/000492945 doi: 10.1159/000492945
    [49] X. Tang, D. Holland, A. M. Dale, L. Younes, M. I. Miller, Shape abnormalities of subcortical and ventricular structures in mild cognitive impairment and Alzheimer's disease: detecting, quantifying, and predicting, Hum. Brain Mapp., 35 (2014), 3701–3725. https://doi.org/10.1002/hbm.22431 doi: 10.1002/hbm.22431
    [50] E. Lella, N. Amoroso, D. Diacono, A. Lombardi, T. Maggipinto, A. Monaco, et al., Communicability characterization of structural DWI subcortical networks in Alzheimer's disease, Entropy, 21 (2019), 475. https://doi.org/10.3390/e21050475 doi: 10.3390/e21050475
    [51] P. Mattila, T. Togo, D. W. Dickson, The subthalamic nucleus has neurofibrillary tangles in argyrophilic grain disease and advanced Alzheimer's disease, Neurosci. Lett., 320 (2002), 81–85. https://doi.org/10.1016/s0304-3940(02)00006-x doi: 10.1016/s0304-3940(02)00006-x
  • This article has been cited by:

    1. Mingtao Cui, Wennan Cui, Wang Li, Xiaobo Wang, A polygonal topology optimization method based on the alternating active-phase algorithm, 2024, 32, 2688-1594, 1191, 10.3934/era.2024057
  • Reader Comments
  • © 2024 the Author(s), licensee AIMS Press. This is an open access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0)
通讯作者: 陈斌, bchen63@163.com
  • 1. 

    沈阳化工大学材料科学与工程学院 沈阳 110142

  1. 本站搜索
  2. 百度学术搜索
  3. 万方数据库搜索
  4. CNKI搜索

Metrics

Article views(1414) PDF downloads(122) Cited by(0)

Other Articles By Authors

/

DownLoad:  Full-Size Img  PowerPoint
Return
Return

Catalog