The paper is concerned with an extension of the classical relation between the flame speed and the curvature-flow stretch, valid only for high Lewis numbers (diffusively stable flames). At low Lewis numbers the corresponding flame-flow system suffers short-wavelength instability, making the associated initial value problem ill-posed. In this study the difficulty is resolved by incorporation of higher-order effects. As a result one ends up with a reduced model based on a coupled system of second-order dynamic equations for the flame interface and its temperature. As an illustration the new model is applied for description of diffusively unstable stagnation-point flow flames.

The present work is a continuation of previous studies of premixed gas flames spreading through a space-periodic array of large-scale vorticities, and is motivated by the experimentally known phenomenon of flame extinction by turbulence. The prior work dealt with the strongly non-stoichiometric limit where the reaction rate is controlled by a single (deficient) reactant. In the present study the discussion is extended over a physically more realistic formulation based on a bimolecular reaction involving two reactants with different molecular diffusivities, and where the mixture equivalence ratio is utilized as a control param- eter. The flow-field is considered as prescribed and unaffected by combustion. The results obtained show that the dual influence of the large-scale turbulence on premixed combustion (flame speed enhancement followed by its reduction and extinction), and higher resilience of turbulent flames at lower Lewis numbers, are not actually related to the multiple-scale nature of the flow-field; the effects may well be captured within the framework of a one-scale flame-flow interaction scheme.


We study the influence of natural convection on stability of reaction fronts in porous media. The model consists of the heat equation, of the equation for the depth of conversion and of the equations of motion under the Darcy law. Linear stability analysis of the problem is fulfilled, the stability boundary is found. Direct numerical simulations are performed and compared with the linear stability analysis.

A numerical study of a two-dimensional model for premixed gas combustion in a narrow, semi-infinite channel with no-slip boundary condition is performed. The work is motivated by recent theoretical advances revealing the major role of hydraulic resistance in deflagration-to-detonation transition, one of the central yet still inadequately understood phenomena of gaseous combustion. The work is a continuation and extension of recently reported results over non-isothermal boundary conditions, wider channels, and lower incipient flame velocities, closer to those of real life explosives.

Gaseous detonation is a phenomenon with very complicated dynamics which has been studied extensively by physicists, mathematicians and engineers for many years. Despite many efforts the problem is far from a complete resolution. Recently the theory of subsonic detonation that occurs in highly resistant porous media was proposed in [4]. This theory provides a model which is realistic, rich and suitable for a mathematical study. In particular, the model is capable of describing the transition from a slowly propagating deflagration wave to the fast detonation wave. This phenomena is known as a deflagration to detonation transition and is one of the most challenging issues in combustion theory. In this paper we will present some recent mathematical results concerning initiation of reaction in porous media, existence and uniqueness of traveling fronts, quenching and propagation.

Theoretical framework for linear stability of an anomalous sub-diffusive activator-inhibitor system is set. Generalized Turing instability conditions are found to depend on anomaly exponents of various species. In addition to monotonous instability, known from normal diffusion, in an anomalous system oscillatory modes emerge. For equal anomaly exponents for both species the type of unstable modes is determined by the ratio of the reactants' diffusion coefficients. When the ratio exceeds its normal critical value, the monotonous modes become stable, whereas oscillatory instability persists until the anomalous critical value is also exceeded. An exact formula for the anomalous critical value is obtained. It is shown that in the short wave limit the growth rate is a power law of the wave number. When the anomaly exponents differ, disturbance modes are governed by power laws of the distinct exponents. If the difference between the diffusion anomaly exponents is small, the splitting of the power law exponents is absent at the leading order and emerges only as a next-order effect. In the short wave limit the onset of instability is governed by the anomaly exponents, whereas the ratio of diffusion coefficients influences the complex growth rates. When the exponent of the inhibitor is greater than that of the activator, the system is always unstable due to the inhibitor enhanced diffusion relatively to the activator. If the exponent of the activator is greater, the system is always stable. Existence of oscillatory unstable modes is also possible for waves of moderate length.

We study the existence and some properties of travelling waves in partially degenerate reaction-diffusion systems. Such systems may for example describe intracellular calcium dynamics in the presence of immobile buffers. In order to prove the wave existence, we first consider the non degenerate case and then pass to the limit as some of the diffusion coefficient converge to zero. The passage to the limit is based on a priori estimates of solutions independent of the values of the diffusion coefficients. The wave uniqueness is also proved.

In this work we study the inflammatory process resulting in the development of atherosclerosis. We develop a one- and two-dimensional models based on reaction-diffusion systems to describe the set up of a chronic inflammatory response in the intima of an artery vessel wall. The concentration of the oxidized low density lipoproteins (ox-LDL) in the intima is the critical parameter of the model. Low ox-LDL concentrations do not lead to a chronic inflammatory reaction. Intermediate ox-LDL concentrations correspond to a bistable system and can lead to a travelling wave propagation corresponding to a chronic inflammatory reaction. In this case the disease development depends on the initial condition. If the concentration of monocytes in the intima is sufficiently high, which can be caused by an inflammation related to other factors, then the development of atherosclerosis can start. Otherwise, the system returns to the stable disease free equilibrium. High ox-LDL concentrations correspond to a monostable system and even a small perturbation of the non inflammatory case leads to a travelling wave propagation which corresponds to a chronic inflammatory response.

Atherosclerosis always develops in plaques, and the reasons are not clear. We test the hypothesis that plaque morphology results from a self-perpetuating propagating process driven by macrophages (Mphs). A computer model of atherogenesis was written in which the computer screen represents a surface view of a flattened area of an arterial wall on which greatly accelerated atherogenesis is depicted. Rate of Mph recruitment from blood monocytes is set as a steeply rising function of the number of Mphs locally present. Smooth muscle accumulation depends on Mph number, Mphs have a probability of death/loss, and lipid accumulation results directly from the death of Mphs. The program runs in reiterative cycles. From an initially normal wall, fatty streak-like foci of Mphs form at random sites, which may progress or regress. Some develop into progressive focal lesions resembling advanced plaques, which are Mph-rich and have a central fibrous cap-like central region of smooth muscle cells. Lipid accumulates centrally in them. To investigate a fetal origin of atherosclerosis, the simulation was initially loaded with Mphs: lesion development was greatly enhanced. These results strongly resemble atherosclerosis in vivo, and support the Mph-dependent hypothesis of spreading plaque growth.