In this paper we outline the hyperbolic system of governing equationsdescribing one-dimensional blood flow in arterial networks. Thissystem is numerically discretised using a discontinuous Galerkinformulation with a spectral/hp element spatial approximation. Weapply the numerical model to arterial networks in theplacenta. Starting with a single placenta we investigate the velocity waveformin the umbilical artery and its relationship with the distalbifurcation geometry and the terminal resistance. We then present resultsfor the waveform patterns and the volume fluxes throughout a simplifiedmodel of the arterial placental network in a monochorionic twin pregnancy with an arterio-arterial anastomosis and an arterio-venous anastomosis. Theeffects of varying the time period of the two fetus' heart beats, increasing the input flux of one fetus and the role ofterminal resistance in the network are investigated and discussed. The results show that the main features of the in vivo, physiological waves are captured by thecomputational model and demonstrate the applicability of themethods to the simulation of flows in arterial networks.

Vasculogenesis and angiogenesis are two different mechanisms for bloodvessel formation. Angiogenesis occurs when new vessels sprout from pre-existing vasculature in response to external chemical stimuli. Vasculogenesis occurs via the reorganization of randomly distributed cells into a blood vessel network. Experimental modelsof vasculogenesis have suggested that the cells exert traction forcesonto the extracellular matrix and that these forces may playan important role in the network forming process.In order to study the role of the mechanical and chemical forcesin both of these stages of blood vessel formation, we present amathematical model which assumes that (i) cells exert traction forcesonto the extracellular matrix, (ii) the matrix behaves as a linearviscoelastic material, (iii) the cells move along gradients ofexogenously supplied chemical stimuli (chemotaxis) and (iv) these stimuli diffuse or are uptaken by the cells.We study the equations numerically, present an appropriate finite difference scheme and simulate the formation of vascular networks in a plane. Our results compare very well with experimental observations and suggest that spontaneous formation of networks can be explained via a purely mechanical interaction betweencells and the extracellular matrix. We find that chemotaxis alone is not a sufficient force to stimulate formation of pattern. Moreover, duringvessel sprouting, we find that mechanical forces can help in the formationof well defined vascular structures.

In this work, we address the numerical solution of fluid-structure interaction problems. This issue is particularly difficulty to tackle when the fluid and the solid densities are of the same order, for instance as it happens in hemodynamic applications, since fully implicit coupling schemes are required to ensure stability of the resulting method. Thus, at each time step, we have to solve a highly non-linear coupled system, since the fluid domain depends on the unknown displacement of the structure. Standard strategies for solving this non-linear problems, are fixed point based methods such as Block-Gauss-Seidel (BGS) iterations. Unfortunately, these methods are very CPU time consuming and usually show slow convergence. We propose a modified fixed-point algorithm which combines the standard BGS iterations with a transpiration formulation. Numerical experiments show the great improvement in computing time with respect to the standard BGS method.

We start from a mathematical model which describes the collective motion of bacteria taking into account the underlying biochemistry. This model was first introduced by Keller-Segel [13]. A new formulation of the system of partial differential equations is obtained by the introduction of a new variable (this new variable is similar to the quasi-Fermi level in the framework of semiconductor modelling). This new system of P.D.E. is approximated via a mixed finite element technique. The solution algorithm is then described and finally we give some preliminary numerical results. Especially our method is well adapted to compute the concentration of bacteria.

We propose a quasi-Newton algorithm for solving fluid-structure interaction problems. The basic idea of the method is to build an approximate tangent operator which is cost effective and which takes into account the so-called added mass effect. Various test cases show that the method allows a significant reduction of the computational effort compared to relaxed fixed point algorithms. We present 2D and 3D fluid-structure simulations performed either with a simple 1D structure model or with shells in large displacements.

Bidomain models are commonly used for studying and simulatingelectrophysiological waves in the cardiac tissue. Most of thetime, the associated PDEs are solved using explicit finitedifference methods on structured grids. We propose an implicitfinite element method using unstructured grids for an anisotropicbidomain model. The impact and numerical requirements ofunstructured grid methods is investigated using a test casewith re-entrant waves.

Saccular aneurisms, swelling of a blood vessel,are investigated in order (i) to estimate the development risk ofthe wall lesion, before and after intravascular treatment,assuming that the pressure is the major factor,and (ii) to better plan medical interventions.Numerical simulations, using the finite element method,are performed in three-dimensional aneurisms.Computational meshes are derived from medical imaging datato take into account both between-subject and within-subjectanatomical variability of the diseased vessel segment.The 3D reconstruction is associated with a faceted surface.A geometrical model is then obtained to be finally meshed for a finite element use. The pulsatile flow of incompressible Newtonian blood is illustrated by numerical simulations carried out in two saccular aneurism types, a side- and a terminal-aneurism.High pressure zones are observed in the aneurism cavity,especially in the terminal one.

We derive a constitutive law for the myocardium from the description of both the geometrical arrangement ofcardiomyocytes and their individual mechanical behaviour. We model a set of cardiomyocytes by a quasiperiodic discretelattice of elastic bars interacting by means of moments. We work in a large displacement framework and we use a discretehomogenization technique. The macroscopic constitutive law is obtained through the resolution of anonlinear self-equilibrum system of the discrete lattice reference cell.

Our purpose is to estimate numerically the influence of particles on the global viscosity of fluid–particle mixtures. Particles are supposed to rigid, and the surrounding fluid is newtonian. The motion of the mixture is computed directly, i.e. all the particle motions are computed explicitly. Apparent viscosity, based on the force exerted by the fluid on the sliding walls, is computed at each time step of the simulation.In order to perform long–time simulations and still control the solid fraction, we assume periodicity of the flow in the shear direction.Direct simulations are based on the so–called Arbitrary Lagrangian Eulerian approach, which we adapted to make it suitable to periodic domains.As a first step toward modelling of interacting red cells in the blood, we propose a simple model of circular particles submitted to an attractive force which tends to form aggregates.

We consider a simple model for the immune systemin which virus are able to undergo mutations and are in competitionwith leukocytes. These mutations are related to several other concepts which havebeen proposed in the literature like those of shape or ofvirulence – a continuous notion. For a given species, the system admits aglobally attractive critical point. We prove that mutations do not affect thispicture for small perturbations and under strong structural assumptions.Based on numerical and theoretical arguments, we also examine how, releasing these assumptions, the system can blow-up.

A hyperelastic constitutive law, for use in anatomically accurate finite element models ofliving structures, is suggested for the passive and the active mechanical properties of incompressiblebiological tissues. This law considers the passive and active states as a same hyperelastic continuummedium, and uses an activation function in order to describe the whole contraction phase.The variational and the FE formulations are also presented, and the FE code has been validatedand applied to describe the biomechanical behavior of a thick-walled anisotropic cylinder underdifferent active loading conditions.