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Register a new userAnalysis and simulations of a Viscoelastic Model of Angiogenesis
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The work analyzes a one-dimensional viscoelastic model of blood vessel growth under nonlinear friction with surroundings, and provides numerical simulations for various growing cases. For the nonlinear differential equations, two sufficient conditions are proven to guarantee the global existence of biologically meaningful solutions. Examples with breakdown solutions are captured by numerical approximations. Numerical simulations demonstrate this model can reproduce angiogenesis experiments under various biological conditions including blood vessel extension without proliferation and blood vessel regression.
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This paper studies the following system of differential equations modeling tumor angiogenesis in a bounded smooth domain $Omega subset mathbb{R}^N$ ($N=1,2$): $$label{0} left{begin{array}{ll} p_t=Delta p- ablacdotp p(displaystylefrac alpha {1+c} abla c+rho abla w)+lambda p(1-p),,& xin Omega, t>0, c_t=Delta c-c-mu pc,, &xin Omega, t>0, w_t= gamma p(1-w),,& xin Omega, t>0, end{array}right. $$ where $alpha, rho, lambda, mu$ and $gamma$ are positive parameters. For any reasonably regular initial data $(p_0, c_0, w_0)$, we prove the global boundedness ($L^infty$-norm) of $p$ via an iterative method. Furthermore, we investigate the long-time behavior of solutions to the above system under an additional mild condition, and improve previously known results. In particular, in the one-dimensional case, we show that the solution $(p,c,w)$ converges to $(1,0,1)$ with an explicit exponential rate as time tends to infinity.
There is currently limited understanding of the role played by haemodynamic forces on the processes governing vascular development. One of many obstacles to be overcome is being able to measure those forces, at the required resolution level, on vessels only a few micrometres thick. In the current paper, we present an in silico method for the computation of the haemodynamic forces experienced by murine retinal vasculature (a widely used vascular development animal model) beyond what is measurable experimentally. Our results show that it is possible to reconstruct high-resolution three-dimensional geometrical models directly from samples of retinal vasculature and that the lattice-Boltzmann algorithm can be used to obtain accurate estimates of the haemodynamics in these domains. We generate flow models from samples obtained at postnatal days (P) 5 and 6. Our simulations show important differences between the flow patterns recovered in both cases, including observations of regression occurring in areas where wall shear stress gradients exist. We propose two possible mechanisms to account for the observed increase in velocity and wall shear stress between P5 and P6: i) the measured reduction in typical vessel diameter between both time points, ii) the reduction in network density triggered by the pruning process. The methodology developed herein is applicable to other biomedical domains where microvasculature can be imaged but experimental flow measurements are unavailable or difficult to obtain.
To study the effect of stress within the thin amorphous film generated atop Si irradiated by Ar+, we model the film as a viscoelastic medium into which the ion beam continually injects biaxial compressive stress. We find that at normal incidence, the model predicts a steady compressive stress of a magnitude comparable to experiment. However, linear stability analysis at normal incidence reveals that this mechanism of stress generation is unconditionally stabilizing due to a purely kinematic material flow, depending on none of the material parameters. Thus, despite plausible conjectures in the literature as to its potential role in pattern formation, we conclude that beam stress at normal incidence is unlikely to be a source of instability at any energy, supporting recent theories attributing hexagonal ordered dots to the effects of composition. In addition, we find that the elastic moduli appear in neither the steady film stress nor the leading order smoothening, suggesting that the primary effects of stress can be captured even if elasticity is neglected. This should greatly simplify future analytical studies of highly nonplanar surface evolution, in which the beam-injected stress is considered to be an important effect.
We prove the existence of novel, shock-fronted travelling wave solutions to a model of wound healing angiogenesis studied in Pettet et al., IMA J. Math. App. Med., 17, 2000. In this work, the authors showed that for certain parameter values, a heteroclinic orbit in the phase plane representing a smooth travelling wave solution exists. However, upon varying one of the parameters, the heteroclinic orbit was destroyed, or rather cut-off, by a wall of singularities in the phase plane. As a result, they concluded that under this parameter regime no travelling wave solutions existed. Using techniques from geometric singular perturbation theory and canard theory, we show that a travelling wave solution actually still exists for this parameter regime: we construct a heteroclinic orbit passing through the wall of singularities via a folded saddle canard point onto a repelling slow manifold. The orbit leaves this manifold via the fast dynamics and lands on the attracting slow manifold, finally connecting to its end state. This new travelling wave is no longer smooth but exhibits a sharp front or shock. Finally, we identify regions in parameter space where we expect that similar solutions exist. Moreover, we discuss the possibility of more exotic solutions.
We consider a fluid model including viscoelastic and viscoplastic effects. The state is given by the fluid velocity and an internal stress tensor that is transported along the flow with the Zaremba-Jaumann derivative. Moreover, the stress tensor obeys a nonlinear and nonsmooth dissipation law as well as stress diffusion. We prove the existence of global-in-time weak solutions satisfying an energy inequality under general Dirichlet conditions for the velocity field and Neumann conditions for the stress tensor.
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