We study optimal sustainable policies in a benchmark logistic world (where both population and technological progress follow logistic laws of motion) subject to a pollution ceiling. The main policy in the hands of the benevolent planner is pollution abatement, ultimately leading to the control of a dirtiness index as in the early literature of the limits to growth literature. Besides inclusion of demographic dynamics, we also hypothesize that population size affects negatively the natural regeneration or assimilation rate, as a side product of human activities (like increasing pollution, deforestation,...). We first characterize optimal sustainable policies. Under certain conditions, the planner goes to the pollution ceiling value and stays on, involving a more stringent environmental policy and a sacrifice in terms of consumption per capita. Second, we study how the sustainable problem is altered when we depart from the logistic world by considering exponential technical progress (keeping population growth logistic). It’s shown that, as expected, introducing such an asymmetry widens the margins of optimal policies as sustainable environmental policies are clearly less stringent under exponential technical progress. Third, we connect our model to the data, using in particular UN population projections.

We study the structure of the spectrum of the infinite XXZ quantum spin chain, ananisotropic version of the Heisenberg model. The XXZ chain Hamiltonian preserves thenumber of down spins (or particle number), allowing to represent it as a direct sum ofN-particleinteracting discrete Schrödinger-type operators restricted to the fermionic subspace. Inthe Ising phase of the model we use this representation to give a detailed determinationof the band and gap structure of the spectrum at low energy. In particular, we show thatat sufficiently strong anisotropy the so-called droplet bands are separated from higherspectral bands uniformly in the particle number. Our presentation of all necessarybackground is self-contained and can serve as an introduction to the mathematical theoryof the Heisenberg and XXZ quantum spin chains.

A reaction–diffusion replicator equation is studied. A novel method to apply theprinciple of global regulation is used to write down a model with explicit spatialstructure. Properties of stationary solutions together with their stability are analyzedanalytically, and relationships between stability of the rest points of thenon-distributed replicator equation and the distributed system are shown. In particular,we present the conditions on the diffusion coefficients under which the non-distributedreplicator equation can be used to describe the number and stability of the stationarysolutions to the distributed system. A numerical example is given, which shows that thesuggested modeling framework promotes the system’s persistence, i.e., a scenario ispossible when in the spatially explicit system all the interacting species survive whereassome of them go extinct in the non-distributed one.

This paper presents numerical results based on a macroscopic blood coagulation modelcoupled with a non-linear viscoelastic model for blood flow. The system of governingequations is solved using a central finite-volume scheme for space discretization and anexplicit Runge-Kutta time-integration. An artificial compressibility method is used toresolve pressure and a non-linear TVD filter is applied for stabilization. A simple testcase of flowing blood over a clotting surface in a straight 3D vessel is solved. This workpresents a significant extension of the previous studies [10] and [9].

When modeling the spread of infectious diseases, it is important to incorporate riskbehavior of individuals in a considered population. Not only risk behavior, but also thenetwork structure created by the relationships among these individuals as well as thedynamical rules that convey the spread of the disease are the key elements in predictingand better understanding the spread. In this work we propose the weighted randomconnection model, where each individual of the population is characterized by twoparameters: its position and risk behavior. A goal is to model the effect that theprobability of transmissions among individuals increases in the individual risk factors,and decays in their Euclidean distance. Moreover, the model incorporates a combined riskbehavior function for every pair of the individuals, through which the spread can bedirectly modeled or controlled. We derive conditions for the existence of an outbreak ofinfectious diseases in this model. Our main result is the almost sure existence of aninfinite component in the weighted random connection model. We use results on the randomconnection model and site percolation in Z2.

A two dimensional two-delays differential system modeling the dynamics of stem-like cellsand white-blood cells in Chronic Myelogenous Leukemia is considered. All three types ofstem cell division (asymmetric division, symmetric renewal and symmetric differentiation)are present in the model. Stability of equilibria is investigated and emergence ofperiodic solutions of limit cycle type, as a result of a Hopf bifurcation, is eventuallyshown. The stability of these limit cycles is studied using the first Lyapunovcoefficient.

This work is devoted to analyze a numerical scheme for the approximation of the linear heat equation’s controls. It is known that, due to the regularizing effect, the efficient computation of the null controls for parabolic type equations is a difficult problem. A possible cure for the bad numerical behavior of the approximating controls consists of adding a singular perturbation depending on a small parameter ε which transforms the heat equation into a wave equation. A space discretization of step h leads us to a system of ordinary differential equations. The aim of this paper is to show that there exists a sequence of exact controls of the corresponding perturbed semi-discrete systems which converges to a control of the original heat equation when both h (the mesh size) and ε (the perturbation parameter) tend to zero.

The problem of transformation of quasimonochromatic wavetrains of surface gravity waveswith narrow spatial-temporal spectra on the bottom shelf is considered in the linearapproximation. By means of numerical modeling, the transmission and reflectioncoefficients are determined as functions of the depth ratio and wave number (frequency) ofan incident wave. The approximation formulae are proposed for the coefficients of wavetransformation. The characteristic features of these formulae are analyzed. It is shownthat the numerical results agree quite satisfactorily with the proposed approximationformulae.

An overview of a general approach for mathematical modeling of evolving heterogeneouspopulations using a wide class of selection systems and replicator equations (RE) ispresented. The method allows visualizing evolutionary trajectories of evolvingheterogeneous populations over time, while still enabling use of analytical tools ofbifurcation theory. The developed theory involves introducing escort systems of auxiliary“keystone" variables, which reduce complex multi-dimensional inhomogeneous models tolow dimensional systems of ODEs that in many cases can be investigated analytically. Inaddition to a comprehensive theoretical framework, a set of examples of the method’sapplicability to questions ranging from preventing the tragedy of the commons to cancertherapy is presented.

A stenosis is the narrowing of the artery, this narrowing is usually the result of theformation of an atheromatous plaque infiltrating gradually the artery wall, forming a bumpin the ductus arteriosus. This arterial lesion falls within the general context ofatherosclerotic arterial disease that can affect the carotid arteries, but also thearteries of the heart (coronary), arteries of the legs (PAD), the renal arteries... It cancause a stroke (hemiplegia, transient paralysis of a limb, speech disorder, sailing beforethe eye). In this paper we study the blood-plaque and blood-wall interactions using afluid-structure interaction model. We first propose a 2D analytical study of thegeneralized Navier-Stokes equations to prove the existence of a weak solution forincompressible non-Newtonian fluids with non standard boundary conditions. Then, coupled,based on the results of the theoretical study approach is given. And to form a realisticmodel, with high accuracy, additional conditions due to fluid-structure coupling areproposed on the border undergoing inetraction. This coupled model includes (a) a fluidmodel, where blood is modeled as an incompressible non-Newtonian viscous fluid, (b) asolid model, where the arterial wall and atherosclerotic plaque will be treated as nonlinear hyperelastic solids, and (c) a fluid-structure interaction (FSI) model whereinteractions between the fluid (blood) and structures (the arterial wall and atheromatousplaque) are conducted by an Arbitrary Lagrangian Eulerian (ALE) method that allowsaccurate fluid-structure coupling.

The projection method is a simple way of constructing functions and filters byintegrating multidimensional functions and filters along parallel superplanes in the spacedomain. Equivalently expressed in the frequency domain, the projection method constructs anew function by simply taking a cross-section of the Fourier transform of amultidimensional function. The projection method is linked to several areas such as boxsplines in approximation theory and the projection-slice theorem in image processing. Inthis paper, we shall systematically study and discuss the projection method in the area ofmultidimensional framelet and wavelet analysis. We shall see that the projection methodnot only provides a painless way for constructing new wavelets and framelets but also is auseful analysis tool for studying various optimal properties of multidimensional refinablefunctions and filters. Using the projection method, we shall explicitly and easilyconstruct a tight framelet filter bank from every box spline filter having at least orderone sum rule. As we shall see in this paper, the projection method is particularlysuitable to be applied to frequency-based nonhomogeneous framelets and wavelets in anydimensions, and the periodization technique is a special case of the projection method forobtaining periodic wavelets and framelets from wavelets and framelets on Euclidean spaces.

Properties of blood cells and their interaction determine their distribution in flow. Itis observed experimentally that erythrocytes migrate to the flow axis, platelets to thevessel wall, and leucocytes roll along the vessel wall. In this work, a three-dimensionalmodel based on Dissipative Particle Dynamics method and a new hybrid (discrete-continuous)model for blood cells is used to study the interaction of erythrocytes with platelets andleucocytes in flow. Erythrocytes are modelled as elastic highly deformable membranes,while platelets and leucocytes as elastic membranes with their shape close to a sphere.Separation of erythrocytes and platelets in flow is shown for different values ofhematocrit. Erythrocyte and platelet distributions are in a good qualitative agreementwith the existing experimental results. Migration of leucocyte to the vessel wall and itsrolling along the wall is observed.

In this paper, an SIS (susceptible-infected-susceptible)-type epidemic propagation isstudied on a special class of 3-regular graphs, called modified cycle graphs. The modifiedcycle graph is constructed from a cycle graph with N nodes by connecting nodei to thenode i +d in a way that every node has exactly three links.Monte-Carlo simulations show that the propagation process depends on the value ofd in anon-monotone way. A new theoretical model is developed to explain this phenomenon. Thisreveals a new relation between the spreading process and the average path length in thegraph.

The stochastic dynamics of chemical reactions can be accurately described by chemicalmaster equations. An approximated time-evolution equation of the Langevin type has beenproposed by Gillespie based on two explicit dynamical conditions. However, whennumerically solve these chemical Langevin equations, we often have a small stopping time–atime point of having an unphysical solution–in the case of low molecular numbers. Thispaper proposes an approach to simulate stochasticities in chemical reactions withdeterministic delay differential equations. We introduce a deterministic Brownian motiondescribed by delay differential equations, and replace the Gaussian noise in the chemicalLangevin equations by the solutions of these deterministic equations. This modificationcan largely increase the stopping time in simulations and regain the accuracy as in thechemical Langevin equations. The novel aspect of the present study is to apply thedeterministic Brownian motion to chemical reactions. It suggests a possible direction ofdeveloping a hybrid method of simulating dynamic behaviours of complex gene regulationnetworks.

Increasing experimental evidence suggests that epigenetic and microenvironmental factors play a key role in cancer progression. In this respect, it is now generally recognized that the immune system can act as an additional selective pressure, which modulates tumor development and leads, through cancer immunoediting, to the selection for resistance to immune effector mechanisms. This may have serious implications for the design of effective anti-cancer protocols. Motivated by these considerations, we present a mathematical model for the dynamics of cancer and immune cells under the effects of chemotherapy and immunity-boosters. Tumor cells are modeled as a population structured by a continuous phenotypic trait, that is related to the level of resistance to receptor-induced cell death triggered by effector lymphocytes. The level of resistance can vary over time due to the effects of epigenetic modifications. In the asymptotic regime of small epimutations, we highlight the ability of the model to reproduce cancer immunoediting. In an optimal control framework, we tackle the problem of designing effective anti-cancer protocols. The results obtained suggest that chemotherapeutic drugs characterized by high cytotoxic effects can be useful for treating tumors of large size. On the other hand, less cytotoxic chemotherapy in combination with immunity-boosters can be effective against tumors of smaller size. Taken together, these results support the development of therapeutic protocols relying on combinations of less cytotoxic agents and immune-boosters to fight cancer in the early stages.

Nothing is more fundamental to life than the ability to reproduce and duplicate theinformation cells store in their genomes. The mechanism of duplication of DNA has beenconserved from prokaryotes to eukaryotes. The aim of the study was to quantify whichevolutionary forces could produce the pattern of genome replication architecture observedin present-day organisms. This was achieved using an evolutionary simulation, combiningrandom genome sequence shuffling, mutation, selection and the mathematical modeling of DNAreplication. We have found parameter values which explained evolutionary pressures of DNAreplication in E.coli, P.calidifontis and S.cerevisae. Surprisingly, the results of the evolutionary simulation suggeststhat for a fixed cost per replication origin it is more advantageous for genomes to reducethe number of replication origins under increasing uncertainty in origin activationtiming.

In this work we propose a method for analysis of postsurgical haemodynamics after femoralartery treatment of occlusive vascular disease. Patient specific reconstruction algorithmof 1D core network based on MRI data is proposed as a tool for such analysis. Along withpresurgical ultrasound data fitting it provides effective personalizing predictive methodthat is validated with clinical observations.

We consider the spread of an infectious disease on a heterogeneous metapopulation definedby any (correlated or uncorrelated) network. The infection evolves under transmission,recovery and migration mechanisms. We study some spectral properties of a connectivitymatrix arising from the continuous-time equations of the model. In particular we show thatthe classical sufficient condition of instability for the disease-free equilibrium, wellknown for the particular case of uncorrelated networks, works also for the general case.We give also an alternative condition that yields a more accurate estimation of theepidemic threshold for correlated (either assortative or dissortative) networks.

A general framework for age-structured predator-prey systems is introduced. Individualsare distinguished into two classes, juveniles and adults, and several possibleinteractions are considered. The initial system of partial differential equations isreduced to a system of (neutral) delay differential equations with one or two delays.Thanks to this approach, physically correct models for predator-prey with delay areprovided. Previous models are considered and analysed in view of the above results. ARosenzweig-MacArthur model with delay is presented as an example.

In mammalian cells, the p53 pathway regulates the response to a variety of stresses, including oncogene activation, heat and cold shock, and DNA damage. Here we explore a mathematical model of this pathway, composed of a system of partial differential equations. In our model, the p53 pathway is activated by a DNA-compromising event of short duration. As is typical for mathematical models of the p53 pathway, our model contains a negative feedback loop representing interactions between the p53 and Mdm2 proteins. A novel feature of our model is that we combine a spatio-temporal approach with the appearance and repair of DNA damage. We investigate the behaviour of our model through numerical simulations. By ignoring the possibility of DNA repair, we first explore the scenario in which the cell has a very inefficient DNA repair mechanism. We find that spatio-temporal oscillations in p53 and Mdm2 may occur, consistent with experimental data. We then allow p53 to be directly involved in repairing DNA damage, since experimental evidence suggests this can happen. We find that oscillations in p53 and Mdm2 can still occur, but their amplitude damps down quickly as the DNA damage is repaired. Finally, we find that a minor change to the location of the DNA damage can notably change the spatial distribution of p53 within the nucleus. We discuss the biological implications of our results.