This paper studies the dynamics of a network-based SIS epidemic model with nonmonotone incidence rate. This type of nonlinear incidence can be used to describe the psychological effect of certain diseases spread in a contact network at high infective levels. We first find a threshold value for the transmission rate. This value completely determines the dynamics of the model and interestingly, the threshold is not dependent on the functional form of the nonlinear incidence rate. Furthermore, if the transmission rate is less than or equal to the threshold value, the disease will die out. Otherwise, it will be permanent. Numerical experiments are given to illustrate the theoretical results. We also consider the effect of the nonlinear incidence on the epidemic dynamics.

In this paper, we analyze the minimization of seminorms ∥L · ∥ on R^n under the constraint of a bounded I-divergence D(b,H·) for rather general linear operators H and L. The I-divergence is also known as Kullback–Leibler divergence and appears in many models in imaging science, in particular when dealing with Poisson data but also in the case of multiplicative Gamma noise. Often H represents, e.g., a linear blur operator and L is some discrete derivative or frame analysis operator. A central part of this paper consists in proving relations between the parameters of I-divergence constrained and penalized problems. To solve the I-divergence constrained problem, we consider various first-order primal–dual algorithms which reduce the problem to the solution of certain proximal minimization problems in each iteration step. One of these proximation problems is an I-divergence constrained least-squares problem which can be solved based on Morozov’s discrepancy principle by a Newton method. We prove that these algorithms produce not only a sequence of vectors which converges to a minimizer of the constrained problem but also a sequence of parameters which converges to a regularization parameter so that the corresponding penalized problem has the same solution. Furthermore, we derive a rule for automatically setting the constraint parameter for data corrupted by multiplicative Gamma noise. The performance of the various algorithms is finally demonstrated for different image restoration tasks both for images corrupted by Poisson noise and multiplicative Gamma noise.

Adult stem cells, which exist throughout the body, multiply by cell division to replenish dying cells or to promote regeneration to repair damaged tissues. To perform these functions during the lifetime of organs or tissues, stem cells need to maintain their populations in a faithful distribution of their epigenetic states, which are suscepti- ble to stochastic fluctuations during each cell division, unexpected injury, and potential genetic mutations that occur during many cell divisions. However, it remains unclear how the three processes of differentiation, proliferation, and apoptosis in regulating stem cells collectively manage these challenging tasks. Here, without consid- ering molecular details, we propose a genetic optimal control model for adult stem cell regeneration that includes the three fundamental processes, along with cell division and adaptation based on differ- ential fitnesses of phenotypes. In the model, stem cells with a distri- bution of epigenetic states are required to maximize expected performance after each cell division. We show that heteroge- neous proliferation that depends on the epigenetic states of stem cells can improve the maintenance of stem cell distributions to create balanced populations. A control strategy during each cell division leads to a feedback mechanism involving heterogeneous proliferation that can accelerate regeneration with less fluctuation in the stem cell population. When mutation is allowed, apoptosis evolves to maximize the performance during homeostasis after multiple cell divisions. The overall results highlight the importance of cross-talk between genetic and epigenetic regulation and the performance objectives during homeostasis in shaping a desirable heterogeneous distribution of stem cells in epigenetic states.

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