The time-varying flow in which fluid is withdrawn from or added to a reservoir of infinite or arbitrary finite depth through a point sink or source of variable strength beneath a free surface is considered. Backed up by some analytic work, a numerical method is used, and the results are compared with previous work on steady and unsteady flows. In the case of withdrawal for an impulsively started flow, it is found that the critical flow rate increases with reservoir depth, although it changes little as the depth increases beyond double the sink submergence depth. The largest flow rate at which steady solutions can evolve in source flows follows a similar pattern although at a considerably higher value. Simulations indicate that some of the previously calculated steady state solutions at higher flow rates may be unstable, if they exist at all.

We investigate a non-isothermal diffuse-interface model that describes the dynamics of two-phase incompressible flows with thermo-induced Marangoni effect. The governing PDE system consists of the Navier--Stokes equations coupled with convective phase-field and energy transport equations, in which the surface tension, fluid viscosity and thermal diffusivity are allowed to be temperature dependent functions. First, we establish the existence and uniqueness of local strong solutions when the spatial dimension is two and three. Then, in the two-dimensional case, assuming that the L∞-norm of the initial temperature is suitably bounded with respect to the coefficients of the system, we prove the existence of global weak solutions as well as the existence and uniqueness of global strong solutions.

We study a free boundary problem for the Fisher-KPP equation: ut = uxx + f(u) (g(t) < x < h(t)) with free boundary conditions h′(t) = −ux(t, h(t)) − α and g′(t) = −ux(t, g(t)) + β for 0 < β < α. This problem can model the spreading of a biological or chemical species, where free boundaries represent the spreading fronts of the species. We investigate the asymptotic behaviour of bounded solutions. There are two parameters α0 and α* with 0 < α0 < α* which play key roles in the dynamics. More precisely, (i) in case 0 < β < α0 and 0 < α < α*, we obtain a trichotomy result: (i-1) spreading, i.e., h(t) − g(t) → +∞ and u(t, ⋅ + ct) → 1 with c ∈ (cL, cR), where cL and cR are the asymptotic spreading speed of g(t) and h(t), respectively, (cR > 0 > cL when 0 < β < α < α0; cR = 0 >cL when 0 < β < α = α0; 0 > cR > cL when α0 < α < α* and 0 < β < α0); (i-2) vanishing, i.e., limt→Th(t) = limt→Tg(t) and limt→T u(t, x) = 0, where T is some positive constant; (i-3) transition, i.e., g(t) → −∞, h(t) → −∞, 0 < limt→∞[h(t) − g(t)] < +∞ and u(t, x) → V*(x − c*t) with c* < 0, where V*(x − c*t) is a travelling wave with compact support and which satisfies the free boundary conditions. (ii) in case β ≥ α0 or α ≥ α*, vanishing happens for any solution.

We consider a fully practical finite element approximation of the Cahn–Hilliard–Stokes system:

$$\begin{align*} \gamma \tfrac{\partial u}{\partial t} + \beta v \cdot \nabla u - \nabla \cdot \left( \nabla w \right) & = 0 \,, \quad w= -\gamma \Delta u + \gamma ^{-1} \Psi ' (u) - \tfrac12 \alpha c'(\cdot,u) | \nabla \phi |^2\,, \\ \nabla \cdot (c(\cdot,u) \nabla \phi) & = 0\,,\quad \begin{cases} -\Delta v + \nabla p = \varsigma w \nabla u, \\ \nabla \cdot v = 0, \end{cases} \end{align*}$$

$\mathbb{R}_{>0}$

$\mathbb{R}_{\geq0}$

In this article, we consider the spatial homogenisation of a multi-phase model for avascular tumour growth and response to chemotherapeutic treatment. The key contribution of this work is the derivation of a system of homogenised partial differential equations describing macroscopic tumour growth, coupled to transport of drug and nutrient, that explicitly incorporates details of the structure and dynamics of the tumour at the microscale. In order to derive these equations, we employ an asymptotic homogenisation of a microscopic description under the assumption of strong interphase drag, periodic microstructure, and strong separation of scales. The resulting macroscale model comprises a Darcy flow coupled to a system of reaction–advection partial differential equations. The coupled growth, response, and transport dynamics on the tissue scale are investigated via numerical experiments for simple academic test cases of microstructural information and tissue geometry, in which we observe drug- and nutrient-regulated growth and response consistent with the anticipated dynamics of the macroscale system.