Processing math: 100%
Review Special Issues

Convolutional neural networks for computer-aided detection or diagnosis in medical image analysis: An overview

  • Received: 03 March 2019 Accepted: 11 June 2019 Published: 15 July 2019
  • Computer-aided detection or diagnosis (CAD) has been a promising area of research over the last two decades. Medical image analysis aims to provide a more efficient diagnostic and treatment process for the radiologists and clinicians. However, with the development of science and technology, data interpretation manually in the conventional CAD systems has gradually become a challenging task. Deep learning methods, especially convolutional neural networks (CNNs), are successfully used as tools to solve this problem. This includes applications such as breast cancer diagnosis, lung nodule detection and prostate cancer localization. In this overview, the current state-of-the-art medical image analysis techniques in CAD research are presented, which focus on the convolutional neural network (CNN) based methods. The commonly used medical image databases in literature are also listed. It is anticipated that this paper can provide researchers in radiomics, precision medicine, and imaging grouping with a systematic picture of the CNN-based methods used in CAD research.

    Citation: Jun Gao, Qian Jiang, Bo Zhou, Daozheng Chen. Convolutional neural networks for computer-aided detection or diagnosis in medical image analysis: An overview[J]. Mathematical Biosciences and Engineering, 2019, 16(6): 6536-6561. doi: 10.3934/mbe.2019326

    Related Papers:

    [1] Zhizhou Ma, Yujun Qi, Weiqing Liu . A comparative study of pull-out performance of bolted joints in pultruded FRP with drilled holes or punched holes. Mathematical Biosciences and Engineering, 2019, 16(5): 4213-4228. doi: 10.3934/mbe.2019210
    [2] Peng Jing, Weichao Wang, Chengxi Jiang, Ye Zha, Baixu Ming . Determinants of switching behavior to wear helmets when riding e-bikes, a two-step SEM-ANFIS approach. Mathematical Biosciences and Engineering, 2023, 20(5): 9135-9158. doi: 10.3934/mbe.2023401
    [3] Linxuan Zhou, Jingwei Gao, Qiao Li, Cheng Hu . Simulation study on tractive performance of off-road tire based on discrete element method. Mathematical Biosciences and Engineering, 2020, 17(4): 3869-3893. doi: 10.3934/mbe.2020215
    [4] Yuriy Stoyan, Georgiy Yaskov, Tatiana Romanova, Igor Litvinchev, Sergey Yakovlev, José Manuel Velarde Cantú . Optimized packing multidimensional hyperspheres: a unified approach. Mathematical Biosciences and Engineering, 2020, 17(6): 6601-6630. doi: 10.3934/mbe.2020344
    [5] Guirong Jiang, Qishao Lu, Linping Peng . Impulsive Ecological Control Of A Stage-Structured Pest Management System. Mathematical Biosciences and Engineering, 2005, 2(2): 329-344. doi: 10.3934/mbe.2005.2.329
    [6] Jiaxin Nan, Wanbiao Ma . Stability and persistence analysis of a microorganism flocculation model with infinite delay. Mathematical Biosciences and Engineering, 2023, 20(6): 10815-10827. doi: 10.3934/mbe.2023480
    [7] Dongmei Zhang . Unveiling dynamics of urbanization, rural logistics, and carbon emissions: A study based on China's empirical data. Mathematical Biosciences and Engineering, 2024, 21(2): 2731-2752. doi: 10.3934/mbe.2024121
    [8] Hongying Shu, Wanxiao Xu, Zenghui Hao . Global dynamics of an immunosuppressive infection model with stage structure. Mathematical Biosciences and Engineering, 2020, 17(3): 2082-2102. doi: 10.3934/mbe.2020111
    [9] Hui Li, Mengyao Zhang, Chenbo Zeng . Circular Jaccard distance based multi-solution optimization for traveling salesman problems. Mathematical Biosciences and Engineering, 2022, 19(5): 4458-4480. doi: 10.3934/mbe.2022206
    [10] Guangxun Sun, Binxiang Dai . Stability and bifurcation of a delayed diffusive predator-prey system with food-limited and nonlinear harvesting. Mathematical Biosciences and Engineering, 2020, 17(4): 3520-3552. doi: 10.3934/mbe.2020199
  • Computer-aided detection or diagnosis (CAD) has been a promising area of research over the last two decades. Medical image analysis aims to provide a more efficient diagnostic and treatment process for the radiologists and clinicians. However, with the development of science and technology, data interpretation manually in the conventional CAD systems has gradually become a challenging task. Deep learning methods, especially convolutional neural networks (CNNs), are successfully used as tools to solve this problem. This includes applications such as breast cancer diagnosis, lung nodule detection and prostate cancer localization. In this overview, the current state-of-the-art medical image analysis techniques in CAD research are presented, which focus on the convolutional neural network (CNN) based methods. The commonly used medical image databases in literature are also listed. It is anticipated that this paper can provide researchers in radiomics, precision medicine, and imaging grouping with a systematic picture of the CNN-based methods used in CAD research.


    The spread of infectious diseases threatens people's health and social stability. To control the spread of the epidemic, governments usually take some measures, such as developing vaccines and isolating patients carrying the virus. Before the successful promotion of the vaccine, the government's non-pharmaceutical control measures, which reduce people's contact rate through lockdown and isolation, play a leading role in controlling the epidemic. However, it cannot relieve people's fear of the virus and may deteriorate the national or regional economy [1,2].

    Mathematical models are useful tools to analyze the formation of social and economic phenomena under various backgrounds. In recent years, the Boltzmann-type equation, which uses the collision theory to study the statistical distribution of rarefied gas molecules [3], is adopted to investigate the socio-economic phenomena of multi-agent systems, such as opinion formation and wealth distribution (see [4,5,6,7,8]). To discover the socio-economic impact of epidemics, researchers extend the classical Susceptible-Infectious-Recovered (SIR) epidemic model [9,10,11,12], in which agents are separated into three categories: susceptible (S), infected (I) and recovered (R), and integrate the SIR model with the socio-economic phenomena of multi-agent systems, such as people's social contact and wealth exchange behavior [13,14].

    The description of socio-economic features involves knowledge of mathematics, sociology, economics, psychology and other fields [15,16,17,18]. In the physical-economic dynamic models, the wealth distribution is determined by the continuous trading features of a large number of agents according to a wealth exchange mechanism, which is characterized by the saving (exchange) propensity of agents and uncertain elements. The uncertainty includes market risks and speculative risks [5]. Saving means that agents are risk-conscious and only use part of their wealth for trading. The saving (exchange) propensity reflects agents' trading decision-making. Decision-making problems are common in life, such as commodity selection, product evaluation, company management, etc. (see [19,20,21]). Persons' decision-making behaviors are affected by psychological preferences, health status, wealth and other factors (see [5,13,22,23,24,25,26]).

    Dimarco et al. [13] introduce a kinetic system consisting of three Boltzmann-type equations to describe how a wealth distribution might evolve under the course of an epidemic. In the kinetic system, the transport parts reflect the movement of individuals in different infection statuses and the Boltzmann collision operators depict the change in wealth distributions caused by the wealth exchange behaviors. The wealth exchange mechanism is depicted by the Cordier-Pareschi-Toscani (CPT) model

    w=(1PL)w+PJw+ηLJw, (1.1a)
    w=(1PJ)w+PLw+˜ηLJw. (1.1b)

    In (1.1), the pre-trade wealth (w,w) of two agents with infection status L,J{S,I,R} becomes (w,w) after the transaction, and the constant PJ[0,1] is exchange propensity for the class of agents with the infectious state J. The random variables ηLJ and ˜ηLJ stand for the uncertain impact of market risks. Dimarco et al. [13] find that epidemics affect wealth distribution.

    In [13], agents in the same infection state have the same exchange propensity (see (1.1)) without considering the psychological differences of people when trading. In addition, the impact of government policies and measures on wealth distribution is not considered. Based on the work in [13], the motivation in our work includes two points. Firstly, we explore wealth distribution when the agent's trading decision is influenced by psychology. Secondly, we discuss the impact of contact control measures and vaccination on wealth distribution.

    In a speculative market with one stock and two populations of chartists and fundamentalists, Maldarella and Pareschi [27] consider the influence of agents' behavioral and psychological factors on their investment. The psychological impact is represented by an appropriate value function corresponding to the prospect theory in Kahneman and Tversky [28]. The prospect theory is applied to dynamic models of social and biological phenomena, such as social contacts, alcohol consumption, the age of first marriage, the size of cities, tumor growth, etc. (see [14,29,30,31]). In these studies, the micro modification of the social trait x is expressed as a single interaction model

    x=xΦϵδ(xˉx)x+ηx, (1.2)

    where x denotes the value of the trait after the interaction, and η is a random variable with mean zero and bounded variance. For the variable s=x/ˉx, the general function Φϵδ(s) is given by

    Φϵδ(s)=μeϵ(sδ1)/δ1eϵ(sδ1)/δ+1. (1.3)

    The constant parameters ˉx, μ(0,1), δ[1,1] and ϵ>0 are related to the phenomenon in society.

    The parameter δ plays a key role in determining the properties of the value function (1.3) and the trait's macroscopic features under the updating rule (1.2). Provided that δ0, the value function (1.3) is concave, and the stationary solution of the Boltzmann-type kinetic model is a lognormal density describing situations of call center service time and human behaviors (see [30,32,33]). When δ0, (1.3) possesses properties of the prospect theory in [28,34]. For example, the value function (1.3) is concave above ˉx and convex below it. In the case of δ>0, the stationary distribution of the trait x is a generalized gamma distribution depicting the alcohol consumption in [29]. δ<0 leads to an Amoroso-type distribution, which depicts the formation of social elites caused by social climbing activities [35].

    In this paper, to study the influence of epidemics and the psychology of agents on wealth distribution, we will generalize the CPT model (1.1) in [13]. Assuming that agents' trading behavior is affected by their characteristics (such as health state and wealth level) and the prevalence of infectious diseases, we extend the constant exchange propensity of (1.1) as a function of the infected fraction and wealth. Firstly, as a response to the severity of the epidemic, we multiply the constant exchange propensity PJ by a function of the infected fraction at time t to describe a possible way for agents to reduce the exchange propensity PJ. Secondly, considering that the rich have better anti-risk abilities than the poor, unlike the assumption that agents in the same infection state have the same trading propensity in [13], in this paper, we assume that the rich tend to use more wealth for trading to obtain better life enjoyment or investment return, while the poor tend to save wealth to ensure future life needs. We adopt a function Φ() (see (2.4)), which is a generalized form of (1.3) with δ=1, as a component of the exchange propensity to represent the disturbance of these psychological factors when making trading decisions. We introduce an additional parameter on the denominator of (1.3) to avoid the extreme situation that the increased investment proportion is too large (small) when the wealth level is high (low).

    The stationary solution of the conservative socio-economic dynamic model, whose form is determined by the micro-interaction rules, plays a significant role in describing the large-time behavior of the trait under investigation. In this work, we utilize the Boltzmann system [13] to describe the evolutions of wealth distributions, and generalize the constant contact rate in [13] to a time-dependent function. Under the modified binary wealth exchange mechanism proposed in this paper, the Boltzmann system is transformed into the Fokker-Planck equations with quadratic drift and diffusion coefficients by using the quasi-invariant asymptotic limit method [7]. Specifically, the stationary wealth distribution of susceptible (recovered) agents fL(w), L{S,R} in this work satisfies an ordinary differential equation in the form

    σ2d2dw2[w2fL(w)]+ddw[(bw2+˜aLwc)fL(w)]=0, (1.4)

    where the non-negative coefficients σ, ˜aL, b, and c>0 rely on the parameters involved in the exchange rule and the epidemic environment. The solution of (1.4) is in the form of the product of an inverse gamma function and an exponential function. Since the microscopic interaction of the trait (alcohol consumption) in [29] is not a binary interaction, the stationary distribution in [29] satisfies Eq (1.4) with b0 and c=0. The stationary distribution in [13] satisfies Eq (1.4) with b=0 and c0. Compared with the work in [13], in our work, the new quadratic term bw2 in the drift coefficient of (1.4) is due to the nonlinear value function Φ() adopted in the exchange propensity.

    The contributions of this paper are summarized as follows. 1) We supplement the exchange propensity form in the wealth distribution literature. Compared with the constant exchange propensity (see [6,13,22,36,37]), the varying exchange propensity in our model reflects people's psychological features. Compared with the exchange propensity in [5], which is a monotone function of wealth, we take into account the asymmetry of the agent's trading psychology at different wealth levels. 2) We supplement the description of the steady-state wealth distribution function in the literature. Polk and Boghosian [38] point out that the expression form of the wealth distribution's tail is not universal. Based on the classical wealth exchange CPT model, if the dynamic model is involved in the feedback control, taxation and redistribution implemented by the government, or the heterogeneity of agents, the steady-state wealth distributions are inverse gamma function (see [5,6,13,22,39,40]). Compared with the inverse gamma wealth distribution obtained in [13], the presence of the exponential function part in the solution of (1.4) makes the wealth distribution curve decay faster as w, namely, the slimmer of the tail. This phenomenon corresponds to the decline in the number of super-rich. 3) We verify that the epidemic affects wealth distribution, contact control measures can curb the epidemic and aggravate wealth inequality. Ashraf [41] finds that the increase of COVID-19 confirmed cases has a negative impact on the stock market. Ashraf [2] discovers that social distancing measures are bad for the economy. Dosi et al. [42] point out that COVID-19 and contact controls may aggravate wealth inequality. 4) We illustrate that vaccination can curb the spread of epidemics and help to improve the economy. Hansen and Mano [43] find that vaccination can increase the mobility of the workplace, help to improve the economy and reduce inequality.

    The rest of the paper is constructed as follows. In Section 2, we set up the Boltzmann-type system describing the evolution of wealth distribution involving an epidemic environment, and introduce a wealth exchange mechanism containing the environment and agents' psychology. The macroscopic properties of the wealth exchange model, such as the proportion of each group population and their mean wealth, are discussed in Section 3. We obtain a Fokker-Planck system to describe the evolution of wealth distributions in Section 4, and acquire the steady-state wealth distribution under the background of the SIR model. In Section 5, we introduce the government's contact control measures and vaccination into the Boltzmann-type system of wealth distributions and discuss their impact on epidemics and wealth distributions. In addition, we numerically analyze the effect of agents' trading psychology on wealth distribution and verify the existence of bimodal stationary wealth distribution. Conclusions are given in Section 6.

    In this paper, under the framework of the SIR epidemic model [10,11], we investigate how wealth distribution might evolve under the course of an epidemic. In the SIR model [11], agents are separated into the susceptible (S), infected (I), and recovered (R) categories. The susceptible group refers to individuals who have no immunity and may be infected by the disease, the infected group includes those who are infectious, and the recovered group includes those who are cured or permanently immunized.

    As assumed in the wealth exchange dynamics in [5], we regard that agents are indistinguishable. In addition to the difference of infection status, each agent's state at any time t is characterized by wealth w0. We denote Ω={S,I,R}. Let fL(w,t) with LΩ represent the wealth distribution of agents in group L at time t. In the SIR epidemic model, the birth and mortality factors are not considered, which is a simplification of the actual epidemic dynamics. Then, the whole agent system's wealth distribution is f(w,t)=LΩfL(w,t), and satisfies the normalization condition R+f(w,t)dw=1.

    Following the idea of wealth exchange dynamics in [13], the wealth distribution fL(w,t), LΩ satisfies an integro-differential system of three Boltzmann-type equations

    fS(w,t)t=Π(w,t)fS(w,t)+QS(w,t), (2.1a)
    fI(w,t)t=Π(w,t)fS(w,t)rfI(w,t)+QI(w,t), (2.1b)
    fR(w,t)t=rfI(w,t)+QR(w,t), (2.1c)

    where

    QL(w,t)=JΩ1τLJQ(fL,fJ)(w,t),LΩ,

    is a combination of collision operators, and represents the interaction between heterogeneous agents [22,44]. The collision term Q(fL,fJ) describes the changes in wealth distribution resulting from the microscopic interactions between individuals from groups L and J. The relaxation parameters τLJ (L,JΩ) before the collision operators depend on the behavior patterns of agents and the share of transactions [45], reflecting the impact of the infectious disease on the frequency of wealth exchange.

    In (2.1), the time evolution of fL(w,t) (LΩ) is expressed as the additive coupling of collision process and transport terms. The transport terms Π(w,t)fS(w,t) and rfI(w,t) consider the shift of agents from one category to another, while the change in health status is due to contact with infected persons or medical treatment. In (2.1b) and (2.1c), constant r>0 is the recovery rate and 1/r represents the average infection period [11]. The spread of the epidemic is governed by the local incidence growth rate

    Π(w,t)=R+ρ(w,v,t)fI(v,t)dv,

    where ρ(w,v,t) is the contact rate of two agents possessing wealth w and v at time t.

    Let L(t)=R+fL(w,t)dw, LΩ represents the proportion of agents in group L. In this work, we take ρ(w,v,t)=ρ(t)>ρ0>0, where the constant ρ0 is a lower bound of ρ(t), then Π(w,t)=ρ(t)I(t).

    In the background of an epidemic, we consider the binary wealth exchange model

    w=w[PLH(I(t))+Φ(w¯W)]w+[PJH(I(t))+Φ(v¯W)]v+ηw, (2.2a)
    v=v[PJH(I(t))+Φ(v¯W)]v+[PLH(I(t))+Φ(w¯W)]w+ηv. (2.2b)

    In the wealth exchange rule (2.2), an agent with infection status LΩ and wealth w interacts with another agent with infection status JΩ and wealth v, and their post-trade wealth is w and v, respectively.

    According to (2.2), the change of each agent's wealth in a single interaction comes from two mechanisms, the deterministic exchange part and the random fluctuation caused by market risks. The certain exchange part of each agent's wealth depends on the effect of infectious diseases and the impact of the individual's psychology on the transaction. In terms of a mathematical expression, the exchange propensity of the agent with wealth w and infection state L is represented by PLH(I(t))+Φ(w¯W). Specifically, PL is the exchange propensity of agents with infection state L under normal circumstances, which is the same as that in the CPT model (1.1). H(I(t))1 is a non-increasing function of the infected fraction I(t) and is used to measure the impact of the epidemic on people's participation in economic activities. We take H(I(t))=11+I(t). The value function Φ(w¯W), which measures the psychological impact of an agent's wealth level on his trading decision, is an application of the prospect theory [28]. The constant ¯W represents a reference wealth level, such as average wealth. The uncertainty is represented by the random variable η with mean zero and variance σ. To ensure that the post-trade wealth is nonnegative, we suppose that ηPLH(I(t))+Φ(w¯W)1. In addition, to guarantee that the kinetic equations (2.1) is well posed [13], we assume that

    maxL{S,I,R}{[PLH(I(t))+Φ(w¯W)]2+[1PLH(I(t))Φ(w¯W)]2}+σ<1. (2.3)

    For the variable s0, we consider the value function

    Φ(s)=μeϵ(s1)1νeϵ(s1)+1,ν1, (2.4)

    where the constant μ[0,1) measures the influence of individual psychology on trading decision-making, and the constant 0<ϵ<1 denotes the intensity of the frequency of wealth interaction. For fixed μ, ϵ and s, function |Φ(s)| decreases with respect to parameter ν. (2.4) is a generalization of the value function Φϵ1(s) in [29],

    Φϵ1(s)=μeϵ(s1)1eϵ(s1)+1.

    Compared with Φϵ1(s), parameter ν>1 in (2.4) prevents the possibility that when the wealth is large, the proportion of increased investment is too high, and when the wealth is small, the conservative psychology leads to little investment. The images of function Φ(s) with μ=0.1 and different values of parameters ν and ϵ are presented in Figure 1.

    Figure 1.  (a): The images of function Φ(s) with different values of parameters ν and ϵ. (b): The value of function Φ(s) around the reference point s=1.

    The Eq (2.4) satisfies the properties of the value function in [28], which are described as follows:

    1) Φ(s) monotonically increases with s and has finite upper and lower bounds

    lims+Φ(s)=μνΦ(s)lims0Φ(s)=μν[11+ννeϵ+1]<0. (2.5)

    2) s=1 is the reference point, i.e., Φ(s=1)=0.

    3) In the case of ϵ<logν, we have [Φ(s)]<0 for every s0. Namely, Φ(s) is a concave function on R+. In the case of logν<ϵ<1, s=11ϵlogν(0,1) is the inflection point, and

    [Φ(s)]{>0,s<11ϵlogν,<0,s>11ϵlogν.

    4) Since ν1, we get

    Φ(1+ζ)<Φ(1ζ),Φ(1+ζ)<Φ(1ζ),ζ(0,1).

    Property 4) states that the value function (2.4) is asymmetric to the point s=1, which can also be observed in Figure 1(b). It corresponds to a phenomenon that the decision-making behavior of agents possessing wealth higher than the reference level ¯W is more robust, namely, the fluctuation of decision-making affected by psychology is more gentle. Moreover, this property also indicates that agents with wealth under the reference level ¯W tend to save more wealth.

    According to the boundedness (2.5), the parameters in the binary exchange rule (2.2) satisfy PL+μ/ν<1, ηPL+μ/ν1 and PL+μν(11+ννeϵ+1)>0 for every ϵ(0,1), LΩ. Since μν(1+ννeϵ+11) increases with ϵ, we have PLμe1ν+e, LΩ.

    In (2.1), the Boltzmann-type collision operator Q(fL,fL) (LΩ) denotes the binary interaction of agents with the same infection state L, and Q(fL,fJ) with LJ (L,JΩ) represents the binary interaction of agents with different infection states L and J. For any test function ψ(w)C0(R+), we have [13]

    R+Q(fL,fJ)(w,t)ψ(w)dw=R2+ψ(w)ψ(w)fL(w,t)fJ(v,t)dvdw, (3.1)

    where is the expectation operator with respect to the random variable η.

    We take the relaxation time τLJ=1 (L,JΩ) in (2.1). Then, the weak form of the system (2.1) is

    ddtR+fS(w,t)ψ(w)dw=ρ(t)I(t)R+fS(w,t)ψ(w)dw+˜QS, (3.2a)
    ddtR+fI(w,t)ψ(w)dw=ρ(t)I(t)R+fS(w,t)ψ(w)dwrR+fI(w,t)ψ(w)dw+˜QI, (3.2b)
    ddtR+fR(w,t)ψ(w)dw=rR+fI(w,t)ψ(w)dw+˜QR, (3.2c)

    where

    ˜QL=JΩR+Q(fL,fJ)(w,t)ψ(w)dw,LΩ.

    Substituting ψ(w)=1 into (3.2), we obtain that the fractions of the three agent groups satisfy

    dS(t)dt=ρ(t)S(t)I(t), (3.3a)
    dI(t)dt=ρ(t)S(t)I(t)rI(t), (3.3b)
    dR(t)dt=rI(t) (3.3c)

    and S(t)+I(t)+R(t)1, which is due to the normalization condition of f(w,t). If ρ(t)=ρ is a constant, (3.3) is the classical SIR model, which is mathematically and epidemiologically well-posed [11]. In the SIR model, the contact number γ, which refers to the average number of contacts of an infected person during the period of infection, is equal to the ratio of contact rate ρ(t) to recovery rate r (i.e. γ=ρ(t)/r) [11]. Let γ0=ρ/r. For the classical SIR model (3.3), Hethcote [10] gives the properties of its solution, which is repeated as the following Theorem. Denote L=limt+L(t), fL(w)=limt+fL(w,t) with LΩ.

    Theorem 3.1. ([10]) Let (S(t),I(t)) be a solution of the classical SIR model in

    {(S(t),I(t))|S(t)0,I(t)0,S(t)+I(t)1}.

    If γ0S01, then I(t) decreases to zero as t. If γ0S0>1, then I(t) increases to a maximum Imax=I0+S01/γ0[ln(γ0S0)]/γ0 and then decreases to 0 as t. The susceptible proportion S(t) is a decreasing function and S(0,1/γ0) is the unique root of the equation

    S0+I0S+1γ0lnSS0=0. (3.4)

    Theorem 3.1 implies that the infected fraction I(t) tends to zero in the steady-state (i.e., I=0). Combined with the non-negativity of the distribution function, the wealth distribution of the infected population in the steady-state is zero, i.e., fI(w)=0. Then, in the steady-state, the order moments of wealth distribution of the infected population are zero. When I=0, we have limt+Π(w,t)=0.

    Let mL(t)=R+wfL(w,t)dw (LΩ) represent the mean wealth of group L. According to (2.2), the whole agent system's wealth is conserved in the mean, i.e., w+v=w+v, then LΩmL(t):=m, t0.

    Let EL(t)=R+w2fL(w,t)dw (LΩ) represent the second moment of fL(w,t). Denote mL=limt+mL(t) and EL=limt+EL(t).

    Taking ψ(w)=w and substituting (2.2) into (3.1) arise

    R+Q(fL,fJ)(w,t)wdw=[PLH(I(t))]mL(t)J(t)+[PJH(I(t))]mJ(t)L(t)J(t)R+Φ(w¯W)wfL(w,t)dw+L(t)R+Φ(v¯W)vfJ(v,t)dv.

    Denote

    FL(t):=R+Φ(v¯W)vfL(v,t)dv.

    We get

    dmS(t)dt=ρ(t)I(t)mS(t)+MS(t), (3.5a)
    dmI(t)dt=ρ(t)I(t)mS(t)rmI(t)+MI(t), (3.5b)
    dmR(t)dt=rmI(t)+MR(t), (3.5c)

    where

    ML(t)=H(I(t))L(t)JΩPJmJ(t)PLH(I(t))mL(t)+L(t)JΩFJ(t)FL(t),LΩ.

    If I=0, we have mI=0. Denote FJ=limt+FJ(t). From (3.5a) and (3.5c), the mean wealth mS and mR satisfy

    S(PSmS+PRmR)PSmS+S(FS+FR)FS=0, (3.6a)
    R(PSmS+PRmR)PRmR+R(FS+FR)FR=0, (3.6b)

    where R=1S and mS+mR=m. Since Φ(v¯W) is a nonlinear function of variable v, the mean wealth mS and mR cannot be solved explicitly from (3.6), but their upper and lower bounds can be obtained. The value function (2.4) has an upper and lower bound (2.5), so we have FS[μeϵ1νeϵ+1mS,μνmS] and FR[μeϵ1νeϵ+1mR,μνmR]. Then we obtain

    mS[PR+μeϵ1νeϵ+1DRSSm,PR+μνDSRSm],mR[PS+μeϵ1νeϵ+1DSRRm,PS+μνDRSRm],

    where DSR=S(PR+μν)+R(PS+μeϵ1νeϵ+1) and DRS=S(PR++μeϵ1νeϵ+1)+R(PS+μν).

    The Boltzmann-like system (2.1) describes how wealth distribution evolves under the course of an epidemic, but its explicit solutions are difficult to obtain. Utilizing the quasi-invariant limit method [40], the Boltzmann-type equations are turned into the Fokker-Planck equations. We can use the stationary solution of the Fokker-Planck system to depict the large-time behavior of wealth distribution.

    Letting 0<ϵ1 and employing the scaled quantities

    PJϵPJ,ηϵη,JΩ. (4.1)

    The binary wealth exchange model (2.2) becomes

    ww=[ϵPLH(I(t))+Φ(w¯W)]w+[ϵPJH(I(t))+Φ(v¯W)]v+ϵηw, (4.2a)
    vv=[ϵPJH(I(t))+Φ(v¯W)]v+[ϵPLH(I(t))+Φ(w¯W)]w+ϵηv, (4.2b)

    where L,JΩ.

    The scaled micro wealth exchange model (4.2) indicates that a single interaction arises only small changes in wealth. To preserve the effects of all parameters in the exchange rule (2.2) when taking the limit ϵ0, the agents need to do much more interactions within a time period, that is, to increase the interaction frequency. Therefore, we take τLJϵτLJ, which also makes the evolution of the distributions independent of the scaling parameter ϵ. Then, the weak form of the scaled system (2.1) reads

    ddtR+fS(w,t)ψ(w)dw=R+Π(w,t)fS(w,t)ψ(w)dw+˜QϵS, (4.3a)
    ddtR+fI(w,t)ψ(w)dw=R+Π(w,t)fS(w,t)ψ(w)dwrR+fI(w,t)ψ(w)dw+˜QϵI, (4.3b)
    ddtR+fR(w,t)ψ(w)dw=rR+fI(w,t)ψ(w)dw+˜QϵR, (4.3c)

    where

    ˜QϵL=JΩ1ϵτLJR+Qϵ(fL,fJ)(w,t)ψ(w)dw,LΩ.

    Taking a Taylor expansion of ψ(w) around w, and substituting the expansion into the collision terms on the right of (4.3), we obtain

    1ϵτLJR+Qϵ(fL,fJ)(w,t)ψ(w)dw=1ϵτLJR2+ψ(w)(ww)+ψ(w)2(ww)2fL(w,t)fJ(v,t)dvdw+RLJ(ϵ). (4.4)

    The residual RLJ(ϵ) describes the higher-order terms of ϵ. In fact, for any test function ψ(w) belonging to the second-order H¨older space C2+α0(R+) with α(0,1), we have

    RLJ(ϵ)=1ϵτLJR2+ψ(˜w)ψ(w)2(ww)2fL(w,t)fJ(v,t)dvdw,=O(ϵ1+α),

    where ˜w=θw+(1θ)w for some θ(0,1).

    Using

    limϵ01ϵΦ(s)=limϵ01ϵμeϵ(s1)1νeϵ(s1)+1=μν+1(s1)μν+1, (4.5)

    the limit of (4.4) is expressed as

    limϵ01ϵτLJR+Qϵ(fL,fJ)(w,t)ψ(w)dw=1τLJR+{w[HLJ(w,t)fL(w,t)]+σ22w2[J(t)w2fL(w,t)]}ψ(w)dw, (4.6)

    where

    HLJ(w,t)=[PLH(I(t))+μν+1(w¯W1)]wJ(t)+[PJH(I(t))μν+1]mJ(t)+μ(ν+1)¯WEJ(t).

    Substituting (4.4) into (4.3), setting τLJ=1 (L,JΩ), taking ϵ0 and combining with (4.6), we obtain

    fS(w,t)t=Π(w,t)fS(w,t)w[BS(w,t)fS(w,t)]+122w2[σw2fS(w,t)], (4.7a)
    fI(w,t)t=Π(w,t)fS(w,t)rfI(w,t)w[BI(w,t)fI(w,t)]+122w2[σw2fI(w,t)], (4.7b)
    fR(w,t)t=rfI(w,t)w[BR(w,t)fR(w,t)]+122w2[σw2fR(w,t)], (4.7c)

    where

    BL(w,t)=[PLH(I(t))+μν+1(w¯W1)]w+H(I(t))JΩPJmJ(t)μν+1m+μ(ν+1)¯WJΩEJ(t),LΩ.

    The boundary conditions are

    BL(w,t)fL(w,t)|w=+w=0=0,w[w2fL(w,t)]|w=+w=0=0,t0,LΩ.

    The system (4.7) maintains the memory of the micro-dynamic (2.2) through relevant parameters μ, ν, ¯W, σ and PJ (JΩ).

    As a special case of explicitly finding the steady-state solution of (4.7), we suppose that the contact rate ρ(t)=ρ>0 is a constant. From Theorem 3.1, there are I=0, fI(w)=0 and S is the unique solution of (3.4). The mean wealth mS and mR are bounded and belong to [0,m].

    Proposition 4.1. When the steady-state infected fraction I=0, the moments of the stationary solutions of the Boltzmann-like system (4.3) satisfy the recursive relationship

    μ(ν+1)¯WMn+1,L=((n1)σ2+μν+1PL)Mn,L+(J{S,R}PJmJμmν+1+μ(ν+1)¯WJ{S,R}EJ)Mn1,L, (4.8)

    where

    Mn,L=R+wnfL(w)dw,L{S,R},n=1,2,3,...,

    denotes the n-order moment of the stationary wealth distribution of agents with infection state L.

    Proof. When I=0, we have fI(w)=0 and Mn,I=0.

    For the case of n=1. Substituting ψ(w)=w into (4.3), and using the scaled exchange rule (4.2), then the steady-state mean wealth mL and energy EL satisfy

    (μν+1PL)mLμ(ν+1)Lm+LJ{S,R}PJmJ=μ(ν+1)¯W(ELLJ{S,R}EJ), (4.9)

    which is consistent with (4.8) when n=1.

    When n2, substituting ψ(w)=wn into (4.3) and (4.4), letting ϵ0 and using (4.5), we have

    J{S,R}R2+{[PL+μν+1(w¯W1)]w+[PJ+μν+1(v¯W1)]v}wn1fL(w)fJ(v)dvdw+(n1)σ2J{S,R}R2+wnfL(w)fJ(v)dvdw=0. (4.10)

    Then the recursive relation (4.8) is deduced through a simple calculation of (4.10).

    In the scaling (4.1), condition (2.3) for ϵ0 becomes

    minL{S,I,R}[PL+limϵ01ϵΦ(s)]>σ2. (4.11)

    Using the inequality in (4.5), a sufficient condition for (4.11) is PLμν+1σ2>0 with L{S,I,R}. Employing the H¨older's inequality, we have

    (mL)2LEL,(EL)2mLM3,L,L{S,R}. (4.12)

    Let n=2 in (4.8). Using (4.9) and (4.12), EL has an upper bound

    ELPLμν+1PLσ2μν+1(mL)2L,L{S,R}. (4.13)

    In the case of μ0, according to the recursive formula (4.8) and the boundedness of the first two moments of wealth distributions (see (4.12) and (4.13)), we can obtain the boundedness of higher-order moments of wealth distributions in the stationary situation.

    From (4.7), the stationary distribution fL(w) (L{S,R}) satisfies the ordinary differential equation

    (bw2aLwcL)fL(w)+σ2ddw[w2fL(w)]=0,

    where

    aL=μν+1PL0,b=μ(ν+1)¯W0,cL=μ(ν+1)¯WELL+(PLμν+1)mLL>0.

    From (4.9), we have

    cL=μ(ν+1)¯WELL+(PLμν+1)mLL=J{S,I,R}PJmJμν+1m+μ(ν+1)¯WJ{S,I,R}EJ:=c,

    which is independent of the subscript L. Then the stationary wealth distribution of the susceptible (recovered) group is expressed as

    fL(w)=LCLw2(aLσ)σe2cσ1w2bσw,L{S,R}, (4.14)

    where CL is a regularization parameter such that R+fL(w)dw=L. Note that

    dfL(w)dw=2σ1w2fL(w)[bw2+(σaL)wc].

    Then, fL(w) is a concave function in (0,+) and reaches the maximum value at ˜wL=c/(σaL) in the case of μ=0. When μ0, fL(w) gets the maximum value at ˜wL=[(aLσ)+(aLσ)2+4bc]/(2b).

    The whole stationary wealth distribution is given by

    f(w)=SCSw2(aSσ)σe2cσ1w2bσw+RCRw2(aRσ)σe2cσ1w2bσw. (4.15)

    Proposition 4.2. The combination (4.15) of two unimodal distributions (4.14) is a unimodal or bimodal distribution.

    Proof. Let

    Υ(w)=L{S,R}fL(w)[bw2+(σaL)wc].

    Then

    df(w)dw=2σ1w2Υ(w).

    Using limw0+Υ(w)<0 and limw+Υ(w)>0, thus the function Υ(w) has at least one positive root, which corresponds to the maximum point of f(w). Taking the derivative of Υ(w) with respect to w, we get

    dΥ(w)dw=2σ1w2L{S,R}fL(w)ϕL(w),

    where

    ϕL(w)=b2w4+b(σ2aL)w3+[(σ2aL)(σaL)2bc]w22c(σaL)w+c2. (4.16)

    Since fS(w)0, fR(w)0 and the number of variations in the sign of the polynomial ϕL(w) is 2. Using the Descartes' rule of sign, the number of positive roots of dΥ(w)/dw is 0 or 2. When dΥ(w)/dw has no positive root, the function Υ(w) has only on positive root. When dΥ(w)/dw has two positive roots, the function Υ(w) has three positive roots, corresponding to two maximum points and one minimum point of f(w), respectively.

    The distribution (4.14) is the product of an inverse-gamma function and an exponential function, which is equivalent to

    fL(w)=~CLgL(w;aL,c,σ)h(w;b,σ), (4.17)

    where

    ~CL=LCLσ2bΓ(12aLσ)(2cσ)2aLσ1,gL(w;aL,c,σ)=1Γ(12aLσ)(2cσ)12aLσw2aLσ2e2cσ1w,h(w;b,σ)=2bσe2bσw

    and Γ() is the Gamma function. Note that gL(w;aL,c,σ) is the density of the inverse-gamma distribution IGL(12aLσ,2cσ), and h(w;b,σ) is the density of the exponential distribution E(2bσ).

    It is fascinating to note that the appearance of the exponential function part (i.e., h(w;b,σ)) is mainly due to the function Φ() in (2.2). When the psychological factors are not considered in the wealth exchange (i.e., μ=0), (4.14) becomes an inverse-gamma function, which is the same as the stationary wealth distribution in [13], showing polynomial decay when w. The decomposition form (4.17) suggests that, due to the exponential function h(w;b,σ), the tail of the wealth distribution (4.15) is slimmer than that of the inverse gamma distribution curve under appropriate parameters, and corresponds to a society with fewer super-rich people.

    Under the framework of the SIR epidemic dynamic, by coupling the binary wealth exchange rule (2.2) with the Boltzmann-type dynamic system (2.1), we obtain the stationary wealth distribution (4.15), which is impacted by the epidemic-related parameters and the value function (2.4). In this part, we introduce the government contact control measures and vaccination into the kinetic system, and analyze the impact of different measures on epidemic dynamics and wealth distribution. Finally, in a fixed epidemic background, we explore the influence of the value function (2.4) on the stationary wealth distribution, and verify the possible situation that the whole stationary wealth distribution exists double peaks.

    The Gini coefficient takes value in [0,1] and measures wealth inequality. A larger Gini coefficient indicates a more unequal wealth distribution. The Gini coefficient is equal to the ratio of the area between the equality line and the Lorentz curve to the area below the equality line. Define the Lorenz curve as [40]

    L(F(w))=w0vf(v)dv,F(w)=w0f(v)dv,

    then the Gini coefficient is

    Gini=1210L(F(w))dF(w).

    In the following simulations, if there is no special declaration, we always take ρ=0.3, I0=0.01, S0=0.99, PS=0.075, PR=0.15, m=1, σ=0.1, ¯W=1 and ν=3.

    Considering that the government takes non-drug containment measures to control the spread of infectious diseases. We take ρ(t)=ρκI(t)>0, where the constant κ[0,min{ρ/I(t)}) measures the strength of contact control. Then, (3.3) is rewritten as

    dS(t)dt=[ρκI(t)]S(t)I(t), (5.1a)
    dI(t)dt=[ρκI(t)]S(t)I(t)rI(t), (5.1b)
    dR(t)dt=rI(t). (5.1c)

    System (5.1) is an example of the implicit behavioral SIR model [46], and the contact rate ρ(t) decreases with the infected fraction I(t). When κ=0, (5.1) becomes the classical SIR model in [10]. When κ0, compared with the classical SIR model, a nonlinear term κS(t)I2(t) appears in (5.1). The contact number γ1=[ρκI(t)]/rρ/r varies with the infected fraction I(t). Because of 0<ρκI(t)ρ, S(t)0 is monotonically decreasing. Similar to Theorem 3.1, the infected fraction in the steady-state is zero, i.e., I=0, as verified in Figure 2(a). Then, the wealth distribution of the infected group is zero in the steady-state, and the whole wealth distribution is still in the form of (4.15), in which S and R are the stationary solutions of (5.1).

    Figure 2.  Epidemic dynamics and wealth distribution with different values of κ and r. (a): The solid line denotes susceptible proportion and the dotted line indicates infected proportion. (b): The wealth distributions in epidemic backgrounds of (a). (c): The Lorentz curves of the wealth distributions in (b).

    Figure 2 depicts the epidemic dynamics and the wealth distribution with different values of parameters κ and r. We take μ=0. The parameter value ρ=0.3 and r=0.04 are close to the epidemiological parameters estimated in [14], which are fitted from the COVID-19 data before the lockdown in three European countries (France, Italy and Spain). Figure 2(a) shows that with the increase of the recover rate r or the contact control strength κ, the peak value of the infected fraction becomes smaller, and more agents keep the uninfected state. In particular, when r=0.25, more than half of the susceptible people have the opportunity to remain uninfected during the epidemic.

    The Gini coefficients of the wealth distributions in Figure 2(b) are Gini(r=0.04,κ=0)=0.3127, Gini(r=0.15,κ=0)=0.3739, Gini(r=0.25,κ=0)=0.4257, Gini(r=0.15,κ=0.5)=0.3901 and Gini(r=0.15,κ=1)=0.3989. In the epidemic backgrounds in Figure 2(a), the wealth distribution curves and Lorentz curves in Figure 2(b) and their corresponding Gini coefficients show that the increase in r or κ leads the wealth distribution curve shifts to the left, and aggravates the wealth inequality. Combined with Figure 2(a), a reasonable explanation for this phenomenon is that when the contact number γ1 is small, the susceptible agents in the steady-state take a large proportion. Affected by the conservative exchange psychology of susceptible agents, that is, the exchange tendency of susceptible individuals is less than the tendency of recovered agents, the inequality of wealth distribution becomes worse.

    One possible way to deal with the negative effect in Section 5.1.1 is vaccination. Through vaccination, the susceptible agent transforms directly into the recovered person. Compared with (2.1), we introduce a term Ξ(w,t)fS(w,t) to represent the transfer of agents from the susceptible group to the recovered group due to vaccination. The Boltzmann-type system (2.1) is rewritten as

    fS(w,t)t=Π(w,t)fS(w,t)Ξ(w,t)fS(w,t)+QS(w,t), (5.2a)
    fI(w,t)t=Π(w,t)fS(w,t)rfI(w,t)+QI(w,t), (5.2b)
    fR(w,t)t=rfI(w,t)+Ξ(w,t)fS(w,t)+QR(w,t), (5.2c)

    in which we take the transfer rate Ξ(w,t)=R+θ(t)fI(v,t)dv. To explore the effect of vaccination on the wealth distribution, we take the contact rate ρ(t)=ρ as a constant and θ(t)=βΨ{tT0}. The constant β>0 represents the vaccination rate, T0 is the time of starting vaccination and Ψ{tT0} denotes the indicator function on {t|tT0}. Integrating the Eqs (5.2) over R+ yields

    dS(t)dt=[ρ+θ(t)]S(t)I(t), (5.3a)
    dI(t)dt=ρS(t)I(t)rI(t), (5.3b)
    dR(t)dt=[r+θ(t)S(t)]I(t). (5.3c)

    Since θ(t)0, the consideration of vaccination does not affect the steady-state infected fraction I=0, which is verified in Figure 3(a). Therefore, the stationary solution obtained from (5.2) has the same form as (4.15), while the susceptible and recovered fractions S and R are calculated from (5.3).

    Figure 3.  The impact of vaccination on epidemic and wealth distribution. (a): The solid line denotes the susceptible proportion, the dashed line indicates the infected proportion and the dotted line represents the recovered proportion. (b): The wealth distributions in the epidemic backgrounds of (a). (c): The Lorentz curves of the wealth distributions in (b).

    The impact of vaccination on epidemic and wealth distribution is shown in Figure 3, in which we take T0=30, r=0.15 and μ=0. Figure 3 indicates that as the vaccination rate β increases, more agents become recovered. The total number of infected patients declines, and the distribution of wealth shifts to the right, reflecting an improvement in wealth inequality. The Gini coefficients of the wealth distributions in Figure 3(b) are Gini(β=0)=0.3739, Gini(β=0.3)=0.3551 and Gini(β=0.7)=0.3395. Therefore, according to the simulations in Figure 3, we infer that vaccination plays a role in preventing and controlling the epidemic and improving the economy. This change can not only effectively control the spread of the epidemic and reduce the infected fraction, but also have a positive impact on reducing wealth inequality.

    In the exchange mechanism (2.2), the exchange propensity of agents is affected by their psychology, which is measured by the value function (2.4). The stationary wealth distribution of susceptible (infected) populations is obtained in the form of (4.14), which is the product of an inverse-gamma function and an exponential function (see (4.17)). It is different from the inverse-gamma steady-state distribution obtained from the usual socio-economic dynamic models [6,13].

    In Figure 4, we compare the wealth distribution f(w) with different μ. Moreover, to verify the existence of bimodal distribution, we simulate the distribution f(w) with different values of the risk parameter σ. We take PR=0.2 and choose the epidemic background corresponding to a recovery rate r=0.25. The Gini coefficients of the wealth distributions in Figure 4(a) are Gini(μ=0)=0.4476, Gini(μ=0.001)=0.4444, Gini(μ=0.01)=0.4258, Gini(μ=0.05)=0.3856 and Gini(μ=0.08)=0.3654. The Gini coefficients of the wealth distributions in Figure 4(b) are Gini(μ=0)=0.2989, Gini(μ=0.001)=0.2982, Gini(μ=0.01)=0.2923, Gini(μ=0.05)=0.2712 and Gini(μ=0.08)=0.2591.

    Figure 4.  The impact of value function (2.4) on the wealth distribution.

    Figure 4 indicates that with the increase of psychological influence (i.e., the increase of μ), more agents are at the middle wealth level, the number of agents of both low and high wealth levels has declined. The Gini coefficient of different risk parameter values decreases with the increase of parameter μ. It also verifies the improvement of wealth inequality. Additionally, Figure 4(b) illustrates that the wealth distribution's tail becomes slimmer with the increase of μ, which corresponds to a society with fewer super-rich people. From the perspective of mathematical analysis, the larger the value of μ, the smaller the shape parameter 12aL/σ of the inverse-gamma function gL(w;aL,c,σ). This corresponds to a fatter tail. Therefore, the existence of exponential function h(w;b,σ) plays a key role in thinning the tail.

    Real economic behavior is complex and is affected by various factors, such as the market environment and the psychology of traders. Under the background of an epidemic, we utilizes the method of mixed rarefied gas dynamics to investigate the distribution of wealth. In the wealth exchange mechanism, the impact of agents' psychology on trading decisions is expressed by a value function, which satisfies the properties of the prospect theory [28]. Under the SIR epidemic, we obtain that the steady-state wealth distribution of the susceptible (recovered) group is the product of an inverse-gamma function and an exponential function, showing a single peak. The emergence of the exponential function part is caused by the nonlinear utility function (2.4). We prove and numerically verify that the wealth distribution of the whole agent system presents a bimodal distribution with appropriate parameters.

    An increase in the recovery rate or the strength of contact control helps to curb the epidemic, keeping more people uninfected and reducing the peak value of the infected fraction. However, these measures are imperfect and may lead to economic recession, because the conservative trading psychology of susceptible agents caused by the fear of the virus is not changed. Vaccination, which transfers the susceptible person directly into a recovered individual, is numerically verified to have a positive impact on curbing epidemics and reducing wealth inequality. In addition, numerical simulations state that, with the increase of the psychological effect of agents, the population in the middle wealth level is increased, the Gini coefficient is decreased, and the tail of the multi-agent system's wealth distribution becomes thinner. These results indicate a reduction in the super-rich and wealth inequality.

    This research is supported by the National Natural Science Foundation of China (No. 11471263). The authors are very grateful to the reviewers for their valuable and meaningful comments of the paper.

    The authors declare there is no conflict of interest.



    [1] G. J. Tearney, M. E. Brezinski and B. E. Bouma, In vivo endoscopic optical biopsy with optical coherence tomography, Science, 276 (1997), 2037–2039.
    [2] R. William and Hendee, The impact of future technology on oncologic diagnosis: Oncologic imaging and diagnosis, Int. J. Radiat. Oncol. Biol. Phys., 9 (1983), 1851–1865.
    [3] A. Heidenreich, F. Desgrandschamps and F. Terrier, Modern approach of diagnosis and management of acute flank pain: Review of all imaging modalities, Eur. Urol., 41 (2002), 351–362.
    [4] R. E. Bunge and C. L. Herman, Usage of diagnostic imaging procedures: A nationwide hospital study, Radiology, 163 (1987), 569–573.
    [5] G. B. A. Quekel, G. H. Kessels and R. Goei, Miss rate of lung cancer on the chest radiograph in clinical practice, Chest, 115 (1999), 720–724.
    [6] F. Li, S. Shusuke and A. Hiroyuki, Lung cancers missed at low-dose helical CT screening in a general population: Comparison of clinical, histopathologic, and imaging findings, Radiology, 225 (2002), 673–683.
    [7] Q. Li, F. Li and S. Kenji, Computer-aided diagnosis in thoracic CT, Semin. Ultrasound. Ct Mr, 26 (2005), 357–363.
    [8] K. Suzuki, I. Sheu, M. Epstein, et al., An MTANN CAD for detection of polyps in false-negative CT colonography cases in a large multicenter clinical trial: Preliminary results, in Medical Imaging 2008: Computer-Aided Diagnosis, Med. Imaging. Int. Soc. Opt. Photonics., (2008).
    [9] L. Ralph, Attempts to use computers as diagnostic aids in medical decision making: A thirty-year experience, Perspect. Biol. Med., 35(1992), 207–219.
    [10] K. Doi, Current status and future potential of computer-aided diagnosis in medical imaging, Br. J. Radiol., 78(2005), S3–S19.
    [11] K. Doi, Computer-aided diagnosis in medical imaging: Historical review, current status and future potential, Comput. Med. Imaging Graph., 31 (2007), 198–211.
    [12] L. G. Maryellen, P. C. Heang and B. John, Anniversary paper: History and status of CAD and quantitative image analysis: The role of Medical Physics and AAPM, Med. Phys., 35 (2008), 5799–5820.
    [13] K. Doi, H. Macmahon, S. Katsuragawa, et al., Computer-aided diagnosis in radiology: Potential and pitfalls, Eur. J. Radiol., 31 (1999), 97–109.
    [14] K. Kerlikowske, P. A. Carney, B. Geller, et al., Performance of screening mammography among women with and without a first-degree relative with breast cancer, Ann. Intern. Med., 133 (2000), 855–863.
    [15] H. Sittek, K. Herrmann, C. Perlet, et al., Computer-aided diagnosis in mammography, Der Radiologe, 37 (1997), 610–616.
    [16] R. Takahashi and Y. Kajikawa, Computer-aided diagnosis: A survey with bibliometric analysis, Int. J. Med. Inf., 101 (2017), 58–67.
    [17] A. Mansoor, U. Bagci, B. Foster, et al., Segmentation and image analysis of abnormal lungs at CT: Current approaches, challenges, and future trends, Radiographics, 35 (2015), 1056–1076.
    [18] S. Kenji, Computer-aided detection of lung cancer, in image-based computer-assisted radiation therapy, Springer, (2017), 9–40.
    [19] A. El-Baz, G. M. Beache, G. Gimel'Farb, et al., Computer-aided diagnosis systems for lung cancer: Challenges and methodologies, Int. J. Biomed. Imaging, 2013 (2013), 1–46.
    [20] M. Nishio and C. Nagashima, Computer-aided diagnosis for lung cancer: Usefulness of nodule heterogeneity, Acad. Radiol., 24 (2017), 328–336.
    [21] M. Kawagishi, B. Chen, D. Furukawa, et al., A study of computer-aided diagnosis for pulmonary nodule: Comparison between classification accuracies using calculated image features and imaging findings annotated by radiologists, Int. J. Comput. Assist. Radiol. Surg., 12 (2017), 1–10.
    [22] A. O. D. C. Filho, A. C. Silva, A. C. D. Paiva, et al., Computer-aided diagnosis of lung nodules in computed tomography by using phylogenetic diversity, genetic algorithm, and SVM, J. Digit. Imaging, 30 (2017), 812–822.
    [23] Y. Nomura, T. Higaki, M. Fujita, et al., Effects of iterative reconstruction algorithms on computer-assisted detection (CAD) software for lung nodules in ultra-low-dose CT for lung cancer screening, Acad. Radiol., 24 (2017), 124–130.
    [24] M. Liang, W. Tang, D. M. Xu, et al., Low-dose CT screening for lung cancer: Computer-aided detection of missed lung cancers, Radiology, 281 (2016), 279–288.
    [25] D. Shen, G. Wu and H. I. Suk, Deep learning in medical image analysis, Annu. Rev. Biomed. Eng., 19 (2017), 221–248.
    [26] Q. Song, L. Zhao, X. Luo, et al., Using deep learning for classification of lung nodules on computed tomography images, J. Healthcare Eng., 2017 (2017), 1–7.
    [27] Y. Lecun, L. Bottou, Y. Bengio, et al., Gradient-based learning applied to document recognition, Proc. IEEE, 86 (1998), 2278–2324.
    [28] K. Alex, S. Ilya and E. H. Geoffrey, ImageNet classification with deep convolution neural networks, 25th International Conference on Neural Information Processing Sys tems, Curran Associates Inc., (2012), 1097–1105. Available from: https://dl.acm.org/ci tation.cfm?id=2999257.
    [29] T. Xiao, J. X. Zhang, K. Y. Yang, et al., Error-driven Incremental learning in deep convolutional neural network for large-scale image classification, ACM Multimedia, (2014), 177–186.
    [30] C. Szegedy, W. Liu, Y. Q. Jia, et al., Going Deeper with Convolutions, 2015 IEEE Conference on Computer Vision and Pattern Recognition (CVPR), IEEE, (2015), 1–9. Available from: https://ieeexplore.ieee.org/document/7298594.
    [31] S. T. Wu, S. H. Zhong and Y. Liu, Deep residual learning for image steganalysis, Multimedia. Tools. Appl., 77 (2017), 10437–10453.
    [32] K. M. He, X. Y. Zhang, S. Q. Ren, et al., Spatial Pyramid Pooling in Deep Convolutional Networks for Visual Recognition, in European Conference on Computer Vision (ECCV) 2014, Springer, (2014), 346–361.
    [33] H. Greenspan, B. V. Ginneken and R. M. Summers, Guest Editorial Deep Learning in Medical Imaging: Overview and Future Promise of an Exciting New Technique, IEEE Trans. Med. Imaging, 35 (2016), 1153–1159.
    [34] D. Wang, A. Khosla, R. Gargeya, et al., Deep Learning for Identifying Metastatic Breast Cancer, ArXiv 2016, (2016).
    [35] D. Kumar, A. Wong and D. A. Clausi, Lung Nodule Classification Using Deep Features in CT Images, 12th Conference on Computer and Robot Vision, IEEE, (2015), 133–138. Available from: https://ieeexplore.ieee.org/document/7158331.
    [36] F. Liu, C. Y. Wee, H. Chen, et al., Inter-modality relationship constrained multi-modality multi-task feature selection for Alzheimer's Disease and mild cognitive impairment identification, Neuroimage, 84 (2014), 466–475.
    [37] H. I. Suk, S. W. Lee and D. Shen, Hierarchical feature representation and multimodal fusion with deep learning for AD/MCI diagnosis, Neuroimage, 101 (2014), 569–582.
    [38] S. Liu, S. D. Liu, W. D. Cai, et al., Early diagnosis of Alzheimer's disease with deep learning, 11th International Symposium on Biomedical Imaging (ISBI), IEEE, (2014), 1015–1018. Available from: https://ieeexplore.ieee.org/abstract/document/6868045.
    [39] H. Fujita and D. Cimr, Computer Aided detection for fibrillations and flutters using deep convolutional neural network, Inf. Sci., 486 (2019), 231–239.
    [40] L. C. S. Afonso, G. H. Rosa, C. R. Pereira, et al., A recurrence plot-based approach for Parkinson's disease identification, Future Gener. Comput. Syst., 94 (2019), 282–292.
    [41] W. Li, Y. Zhao, X. Chen, et al., Detecting Alzheimer's Disease on Small Dataset: A Knowledge Transfer Perspective, IEEE J. Biomed. Health. Inf., 23 (2019), 1234–1242.
    [42] L. Martin, J. Jendeberg, P. Thunberg, et al., Computer aided detection of ureteral stones in thin slice computed tomography volumes using Convolutional Neural Networks, Comput. Biol. Med., 97 (2018), 153–160.
    [43] I. Sajid, M. U. Ghani, T. Saba, et al., Brain tumor segmentation in multi-spectral MRI using convolutional neural networks (CNN), Microsc. Res. Tech., 81 (2018), 419–427.
    [44] F. Z. Liao, L. Ming, L. Zhe, et al., Evaluate the Malignancy of Pulmonary Nodules Using the 3D Deep Leaky Noisy-or Network, IEEE Trans. Neural Netw. Learn. Syst., 14 (2017), 1–12.
    [45] A. Rajkomar, S. Lingam, A. G. Taylor, et al., High-throughput classification of radiographs using deep convolutional neural networks, J. Digit. Imaging, 30 (2017), 95–101.
    [46] Z. N. Yan, Y. Q. Zhan, Z. G. Peng, et al., Multi-Instance Deep Learning: Discover Discriminative Local Anatomies for Bodypart Recognition, IEEE Trans. Med. Imaging, 35 (2016), 1332–1343.
    [47] H. Pratt, F. Coenen, D. M. Broadbent, et al., Convolutional Neural Networks for Diabetic Retinopathy, Procedia. Comput. Sci., 90 (2016), 200–205.
    [48] M. Gao, U. Bagci, L. Lu, et al., Holistic classification of CT attenuation patterns for interstitial lung diseases via deep convolutional neural networks, Comput. Methods Biomech. Biomed. Eng. Imaging Vis., 6 (2016), 1–6.
    [49] H. C. Shin, H. R. Roth, M. Gao, et al., Deep Convolutional Neural Networks for Computer-Aided Detection: CNN Architectures, Dataset Characteristics and Transfer Learning, IEEE Trans. Med. Imaging, 35 (2016), 1285–1298.
    [50] O. Ronneberger, P. Fischer and T. Brox, U-Net: Convolutional Networks for Biomedical Image Segmentation, in MICCAI 2015, Springer, (2015), 234–241.
    [51] O. F. Ahmad, A. Soares, E. B. Mazomenos, et al., Artificial intelligence and computer-aided diagnosis in colonoscopy: Current evidence and future directions, Lancet. Gastroenterol. Hepatol., 41 (2019), 71–80.
    [52] I. González-Díaz, DermaKNet: Incorporating the Knowledge of Dermatologists to Convolutional Neural Networks for Skin Lesion Diagnosis, IEEE J. Biomed. Health. Inf., 23 (2019), 547–559.
    [53] P. R. Jeyaraj, E. R. J. J. o. C. R. Samuel Nadar and C. Oncology, Computer-assisted medical image classification for early diagnosis of oral cancer employing deep learning algorithm, J. Cancer Res. Clin. Oncol., 145 (2019), 829–837.
    [54] U. Raghavendra, H. Fujita, S. V. Bhandary, et al., Deep convolution neural network for accurate diagnosis of glaucoma using digital fundus images, Inf. Sci., 441 (2018), 41–49.
    [55] U. Raghavendra, H. Fujita, A. Gudigar, et al., Automated technique for coronary artery disease characterization and classification using DD-DTDWT in ultrasound images, Biomed. Signal Process Control, 40 (2018), 324–334.
    [56] E. Hosseini-Asl, M. Ghazal, A. Mahmoud, et al., Alzheimer's disease diagnostics by a 3D deeply supervised adaptable convolutional network, Front Biosci (Landmark Ed), 23 (2018), 584–596.
    [57] A. Farooq, S. M. Anwar, M. Awais, et al., A deep CNN based multi-class classification of Alzheimer's disease using MRI, 2017 IEEE International Conference on Imaging System and Techniques (IST), IEEE, (2018), 182–187. Available from: https://ieeexplore.ieee.org/document/8261460.
    [58] G. V. Tulder and M. D. Bruijne, Combining Generative and Discriminative Representation Learning for Lung CT Analysis With Convolutional Restricted Boltzmann Machines, IEEE Trans. Med. Imaging, 35 (2016), 1262–1272.
    [59] M. Anthimopoulos, S. Christodoulidis, L. Ebner, et al., Lung Pattern Classification for Interstitial Lung Diseases Using a Deep Convolutional Neural Network, IEEE Trans. Med. Imaging, 35 (2016), 1207–1216.
    [60] A. Jalalian, S. Mashohor, R. Mahmud, et al., Foundation and methodologies in computer-aided diagnosis systems for breast cancer detection, EXCLI J, 16 (2017), 113–137.
    [61] M. L. Giger, N. Karssemeijer and J. A. Schnabel, Breast image analysis for risk assessment, detection, diagnosis, and treatment of cancer, Annu. Rev. Biomed. Eng., 15 (2013), 327–357.
    [62] Q. H. Huang, F. B. Yang, L. Z. Liu, et al., Automatic segmentation of breast lesions for interaction in ultrasonic computer-aided diagnosis, Inf. Sci., 314 (2015), 293–310.
    [63] T. C. Chiang, Y. S. Huang, R. T. Chen, et al., Tumor Detection in Automated Breast Ultrasound Using 3-D CNN and Prioritized Candidate Aggregation, IEEE Trans. Med. Imaging, 38 (2018), 240–249.
    [64] R. K. Samala, H. Chan, L. Hadjiiski, et al., Breast Cancer Diagnosis in Digital Breast Tomosynthesis: Effects of Training Sample Size on Multi-Stage Transfer Learning Using Deep Neural Nets, IEEE Trans. Med. Imaging, 38 (2019), 686–696.
    [65] A. S. Becker, M. Marcon, S. Ghafoor, et al., Deep Learning in Mammography: Diagnostic Accuracy of a Multipurpose Image Analysis Software in the Detection of Breast Cancer, Invest. Radiol., 52 (2017), 434–440.
    [66] X. R. Zhou, T. Kano, H. Koyasu, et al., Automated assessment of breast tissue density in non-contrast 3D CT images without image segmentation based on a deep CNN, in Medical Imaging 2017: Computer-Aided Diagnosis, Proc. SPIE, (2017).
    [67] T. Kooi, G. B. Van, N. Karssemeijer, et al., Discriminating Solitary Cysts from Soft Tissue Lesions in Mammography using a Pretrained Deep Convolutional Neural Network, Med. Phys., 44 (2017), 1017–1027.
    [68] A. B. Ayelet, L. Karlinsky, S. Alpert, et al., A Region Based Convolutional Network for Tumor Detection and Classification in Breast Mammography, in Deep Learning and Data Labeling for Medical Applications, Springer, (2016), 197–205.
    [69] J. G. Posada, D. M. Zapata and O. L. Q. Montoya, Detection and Diagnosis of Breast Tumors using Deep Convolutional Neural Networks, Conference Proceedings of the XVI I Latin American Conference on Automatic Control (2016), 11-17. Available from: http s://pdfs.semanticscholar.org/9566/d1f27a0e5f926827d3eaf8546dab51e40e21.pdf.
    [70] R. K. Samala, H. P. Chan, L. Hadjiiski, et al., Mass detection in digital breast tomosynthesis: Deep convolutional neural network with transfer learning from mammography, Med. Phys., 43 (2016), 6654.
    [71] N. Dhungel, G. Carneiro and A. P. Bradley, The Automated Learning of Deep Features for Breast Mass Classification from Mammograms, in MICCAI 2016,Springer, (2016), 106–114.
    [72] Y. J. Zhou, J. X. Xu, Q. G. Liu, et al., A Radiomics Approach with CNN for Shear-wave Elastography Breast Tumor Classification, IEEE Trans. Biomed. Eng., 65 (2018), 1935–1942.
    [73] F. Gao, T. Wu, J. Li, et al., SD-CNN: A Shallow-Deep CNN for Improved Breast Cancer Diagnosis, Comput Med Imaging Graph, 70 (2018), 53–62.
    [74] J. Li, M. Fan, J. Zhang, et al., Discriminating between benign and malignant breast tumors using 3D convolutional neural network in dynamic contrast enhanced MR images, in Medical Imaging 2017: Imaging Informatics for Healthcare, Research, and Applications, Proc. SPIE, (2017).
    [75] T. Kooi, G. Litjens, B. V. Ginneken, et al., Large scale deep learning for computer aided detection of mammographic lesions, Med. Image. Anal., 35 (2017), 303–312.
    [76] R. Samala, H. P. Chan, L. Hadjiiski, et al., Deep-learning convolution neural network for computer-aided detection of microcalcifications in digital breast tomosynthesis, in Medical Imaging 2016: Computer-Aided Diagnosis, Proc. SPIE, (2016).
    [77] D. M. Parkin, Global cancer statistics in the year 2000, Lancet Oncol., 2 (2001), 533–543.
    [78] A. Motohiro, H. Ueda, H. Komatsu, et al., Prognosis of non-surgically treated, clinical stage I lung cancer patients in Japan, Lung Cancer, 36 (2002), 65–69.
    [79] K. L. Hua, C. H. Hsu, S. C. Hidayati, et al., Computer-aided classification of lung nodules on computed tomography images via deep learning technique, Onco. Targets Ther., 8 (2015), 2015–2022.
    [80] Z. H. Shi, H. Hao, M. H. Zhao, et al., A deep CNN based transfer learning method for false positive reduction, Multimed. Tools Appl., 78 (2018), 1017–1033.
    [81] F. Ciompi, B. D. Hoop, S. J. V. Riel, et al., Automatic classification of pulmonary peri-fissural nodules in computed tomography using an ensemble of 2D views and a convolutional neural network out-of-the-box, Med. ImageAnal., 26 (2015), 195–202.
    [82] M. Nishio, O. Sugiyama, M. Yakami, et al., Computer-aided diagnosis of lung nodule classification between benign nodule, primary lung cancer, and metastatic lung cancer at different image size using deep convolutional neural network with transfer learning, PLoS One, 13 (2018), e0200721.
    [83] G. Savitha and P. Jidesh, Lung Nodule Identification and Classification from Distorted CT Images for Diagnosis and Detection of Lung Cancer, in Machine Intelligence and Signal Analysis, Springer, (2019), 11–23.
    [84] X. Z. Zhao, L. Y. Liu, S. Qi, et al., Agile convolutional neural network for pulmonary nodule classification using CT images, Int. J. Comput. Assist Radiol. Surg., 13 (2018), 585–595.
    [85] J. Ding, A. Li, Z. Q. Hu, et al., Accurate Pulmonary Nodule Detection in Computed Tomography Images Using Deep Convolutional Neural Networks, in MICCAI 2017,Springer, (2017), 559–567.
    [86] Q. Dou, H. Chen, Y. M. Jin, et al., Automated Pulmonary Nodule Detection via 3D ConvNets with Online Sample Filtering and Hybrid-Loss Residual Learning, in MICCAI 2017,Springer, (2017), 630–638.
    [87] J. Z. Cheng, D. Ni, Y. H. Chou, et al., Computer-Aided Diagnosis with Deep Learning Architecture: Applications to Breast Lesions in US Images and Pulmonary Nodules in CT Scans, Sci. Rep., 6 (2016), 24454.
    [88] K. Liu and G. Kang, 3D multi-view convolutional neural networks for lung nodule classification, PLoS One, 12 (2017), e0188290.
    [89] R. Dey, Z. J. Lu and H. Yi, Diagnostic Classification Of Lung Nodules Using 3D Neural Networks, 2018 IEEE 15th International Symposium on Biomedical Imaging (ISBI), IEEE, (2018), 774–778. Available from: https://ieeexplore.ieee.org/document/8363687.
    [90] D. Anton, K. Ramil, K. Adil, et al., Large Residual Multiple View 3D CNN for False Positive Reduction in Pulmonary Nodule Detection, 2017 IEEE Conference on Computational Intelligence in Bioinformatics and Computational Biology (CIBCB), IEEE, (2017). Available from: https://ieeexplore.ieee.org/document/8058549.
    [91] W. Li, P. Cao, D. Z. Zhao, et al., Pulmonary Nodule Classification with Deep Convolutional Neural Networks on Computed Tomography Images, Comput. Math. Method. Med., 2016 (2016), 1–7.
    [92] R. L. Siegel, K. D. Miller and A. Jemal, Cancer Statistics, 2017, CA Cancer J. Clin., 67 (2017), 7–30.
    [93] R. Chou, J. M. Croswell, D. Tracy, et al., Screening for prostate cancer: A review of the evidence for the U.S. Preventive Services Task Force, Ann. Intern. Med., 137 (2011), 55–73.
    [94] A. Rampun, L. Zheng, P. Malcolm, et al., Computer-aided detection of prostate cancer in T2-weighted MRI within the peripheral zone, Phys. Med. Biol., 61 (2016), 4796–4825.
    [95] W. Li, J. Li, K. V. Sarma, et al., Path R-CNN for Prostate Cancer Diagnosis and Gleason Grading of Histological Images, IEEE Trans. Med. Imaging, 38 (2018), 945–954.
    [96] E. Leng, J. C. Henriksen, A. E. Rizzardi, et al., Signature maps for automatic identification of prostate cancer from colorimetric analysis of H&E and IHC-stained histopathological specimens, Sci. Rep., 9 (2019), 6992.
    [97] Q. Chen, X. Xu, S. L. Hu, et al., A transfer learning approach for classification of clinical significant prostate cancers from mpMRI scans, in Medical Imaging 2017: Computer-Aided Diagnosis, Proc. SPIE, (2017).
    [98] Y. Song, Y. D. Zhang, X. Yan, et al., Computer-aided diagnosis of prostate cancer using a deep convolutional neural network from multiparametric MRI, J. Magn. Reson. Imaging, 48 (2018), 1570–1577.
    [99] Z. Wang, C. Liu, D. Cheng, et al., Automated Detection of Clinically Significant Prostate Cancer in mp-MRI Images Based on an End-to-End Deep Neural Network, IEEE Trans. Med. Imaging, 37 (2018), 1127–1139.
    [100] J. Ishioka, Y. Matsuoka, S. Uehara, et al., Computer-aided diagnosis of prostate cancer on magnetic resonance imaging using a convolutional neural network algorithm, BJU Int., 122 (2018), 411–417.
    [101] S. Kohl, D. Bonekamp, H.P. Schlemmer, et al., Adversarial Networks for the Detection of Aggressive Prostate Cancer, in ArXiv, (2017). Available from: https://arxiv.org/abs/17 02.08014.
    [102] X. Yang, C. Y. Liu, Z. W. Wang, et al., Co-trained convolutional neural networks for automated detection of prostate cancer in multi-parametric MRI, Med. Image Anal., 42 (2017), 212–227.
    [103] T. K. Jin and S. M. Hewitt, Nuclear Architecture Analysis of Prostate Cancer via Convolutional Neural Networks, IEEE Access, 5 (2017), 18526–18533.
    [104] X. Wang, W. Yang, J. Weinreb, et al., Searching for prostate cancer by fully automated magnetic resonance imaging classification: Deep learning versus non-deep learning, Sci. Rep., 7 (2017), 15415.
    [105] S. F. Liu, H. X. Zheng, Y. Feng, et al., Prostate Cancer Diagnosis using Deep Learning with 3D Multiparametric MRI, in Medical Imaging 2017: Computer-Aided Diagnosis, Proc. SPIE, (2017).
    [106] M. H. Le, J. Y. Chen, L. Wang, et al., Automated diagnosis of prostate cancer in multi-parametric MRI based on multimodal convolutional neural networks, Phys. Med. Biol., 62 (2017), 6497–6514.
    [107] X. Yang, Z. W. Wang, C. Y. Liu, et al., Joint Detection and Diagnosis of Prostate Cancer in Multi-parametric MRI Based on Multimodal Convolutional Neural Networks, in MICCAI 2017,Springer, (2017), 426–434.
    [108] M. F. McNitt-Gray, S. G. Armato, C. R. Meyer, et al., The Lung Image Database Consortium (LIDC) data collection process for nodule detection and annotation, Acad. Radiol., 14 (2007), 1464–1474.
    [109] A. P. Reeves, A. M. Biancardi, D. Yankelevitz, et al., A public image database to support research in computer aided diagnosis, Conf. Proc. IEEE Eng. Med. Biol. Soc., 2009(2009), 3715–3718.
    [110] K. S. Man, C. Ramachandran, A. Yianni, et al., Automatic pectoral muscle segmentation on mediolateral oblique view mammograms, IEEE Trans. Med. Imaging, 23 (2004), 1129–1140.
    [111] D. Saraswathi and E. Srinivasan, An ensemble approach to diagnose breast cancer using fully complex-valued relaxation neural network classifier, Int. J. Biomed. Eng. Technol., 15 (2014), 243–260.
    [112] M. Lamard, G. Cazuguel, G. Quellec, et al., Content Based Image Retrieval based on Wavelet Transform coefficients distribution, 2007 29th Annual International Conference of the IEEE Engineering in Medicine and Biology Society, IEEE, (2007). Available from: https://ieeexplore.ieee.org/document/4353347.
    [113] G. D. Tourassi, in Intelligent Paradigms for Healthcare Enterprises, Current Status of Computerized Decision Support Systems in Mammography, Springer, (2005), 173–208.
    [114] R. M. Rangayyan, F. J. Ayres and J. E. L. Desautels, A review of computer-aided diagnosis of breast cancer: Toward the detection of subtle signs, J. Franklin Inst., 344 (2007), 312–348.
    [115] M. Sundaram, K. Ramar, N. Arumugam, et al., Histogram Modified Local Contrast Enhancement for mammogram images, Appl. Soft. Comput., 11 (2011), 5809–5816.
    [116] P. M. Bolton, S. L. James, J. M. Davidson, et al., Proceedings: Diagnostic and prognostic significance of immune competence testing in patients with breast cancer, Br. J. Surg., 61 (1974), 325–326.
    [117] N. Pérez, M. A. Guevara and A. Silva, Improving Breast Cancer Classification with Mammography, supported on an appropriate Variable Selection Analysis, in Medical Imaging 2013: Computer-Aided Diagnosis, Proc. SPIE, (2013).
    [118] T. Messay, R. C. Hardie and T. R. Tuinstra, Segmentation of pulmonary nodules in computed tomography using a regression neural network approach and its application to the Lung Image Database Consortium and Image Database Resource Initiative dataset, Med. Image Anal., 22 (2015), 48–62.
    [119] W. S. Wang, J. W. Luo, X. D. Yang, et al., Data analysis of the Lung Imaging Database Consortium and Image Database Resource Initiative, Acad. Radiol., 22 (2015), 488–495.
    [120] Y. Rowena, C. I. Henschke, D. F. Yankelevitz, et al., CT screening for lung cancer: Alternative definitions of positive test result based on the national lung screening trial and international early lung cancer action program databases, Radiology, 273 (2014), 591–596.
    [121] M. Oudkerk and M. A. Heuvelmans, Screening for lung cancer by imaging: The Nelson study, JBR-BTR, 96 (2013), 163–166.
    [122] Z. Y. Ru, X. Xie, H. J. d. Koning, et al., NELSON lung cancer screening study, Cancer Imaging, 11 (2011), S79–S84.
    [123] G. B. Van, A. V. D. Van, T. Duindam, et al., Comparing and combining algorithms for computer-aided detection of pulmonary nodules in computed tomography scans: The ANODE09 study, Med. Image Anal., 14 (2010), 707–722.
    [124] L. Geert, D. Oscar, B. Jelle, et al., Computer-aided detection of prostate cancer in MRI, IEEE Trans. Med. Imaging, 33 (2014), 1083–1092.
    [125] K. W. Clark, B. A. Vendt, K. E. Smith, et al., The Cancer Imaging Archive (TCIA): Maintaining and Operating a Public Information Repository, J. Digit. Imaging, 26 (2013), 1045–1057.
    [126] V. M. Gonçalves, M. E. Delamaro and F. L. S. Nunes, A systematic review on the evaluation and characteristics of computer-aided diagnosis systems, Rev. Bras. Eng. Bioméd., 30 (2014), 355–383.
    [127] J. Ma, F. Wu, J. Zhu, et al., A pre-trained convolutional neural network based method for thyroid nodule diagnosis, Ultrasonics, 73 (2017), 221–230.
    [128] W. Sun, T. B. Tseng, J. Zhang, et al., Enhancing deep convolutional neural network scheme for breast cancer diagnosis with unlabeled data, Comput. Med. Imaging Graph., 57 (2017), 4–9.
    [129] W. L. Chen, Y. Zhang, J. J. He, et al., Prostate Segmentation using 2D Bridged U-net, ArXiv 2018, (2018).
    [130] F. Milletari, N. Navab and S. A. Ahmadi, V-Net: Fully Convolutional Neural Networks for Volumetric Medical Image Segmentation, 2016 Fourth International Conference on 3D Vision (3DV), IEEE, (2016). Available from: https://ieeexplore.ieee.org/document/7785132.
    [131] S. Hussain, S. M. Anwar and M. Majid, Segmentation of glioma tumors in brain using deep convolutional neural network, Neurocomputing, 282 (2017), 248–261.
    [132] R. Caruana, in Machine Learning, Multitask Learning, Springer, (1997), 41–75.
    [133] I. Guyon, G. Dror, V. Lemaire, et al., Unsupervised and transfer learning challenge, The 2011 International Joint Conference on Neural Networks, IEEE, (2011).Available from: https://ieeexplore.ieee.org/document/6033302.
    [134] R. J. Gillies, P. E. Kinahan and H. Hricak, Radiomics: Images Are More than Pictures, They Are Data, Radiology, 278 (2016), 563–577.
    [135] T. Tran and R. Kavuluru, Predicting Mental Conditions Based on "History of Present Illness" in Psychiatric Notes with Deep Neural Networks, J. Biomed. Inf., 75 (2017), S138–S148.
  • This article has been cited by:

    1. JI-HUAN HE, QIAN YANG, CHUN-HUI HE, HAI-BIN LI, EERDUN BUHE, PULL-IN STABILITY OF A FRACTAL MEMS SYSTEM AND ITS PULL-IN PLATEAU, 2022, 30, 0218-348X, 10.1142/S0218348X22501857
  • Reader Comments
  • © 2019 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(35405) PDF downloads(3905) Cited by(129)

Figures and Tables

Figures(2)  /  Tables(8)

Other Articles By Authors

/

DownLoad:  Full-Size Img  PowerPoint
Return
Return

Catalog