No Arabic abstract
A theory of fractional kinetics of glial cancer cells is presented. A role of the migration-proliferation dichotomy in the fractional cancer cell dynamics in the outer-invasive zone is discussed an explained in the framework of a continuous time random walk. The main suggested model is based on a construction of a 3D comb model, where the migration-proliferation dichotomy becomes naturally apparent and the outer-invasive zone of glioma cancer is considered as a fractal composite with a fractal dimension $frD<3$.
We study the dynamics of a thick polar epithelium subjected to the action of both an electric and a flow field in a planar geometry. We develop a generalized continuum hydrodynamic description and describe the tissue as a two component fluid system. The cells and the interstitial fluid are the two components and we keep all terms allowed by symmetry. In particular we keep track of the cell pumping activity for both solvent flow and electric current and discuss the corresponding orders of magnitude. We study the growth dynamics of tissue slabs, their steady states and obtain the dependence of the cell velocity, net cell division rate, and cell stress on the flow strength and the applied electric field. We find that finite thickness tissue slabs exist only in a restricted region of phase space and that relatively modest electric fields or imposed external flows can induce either proliferation or death.
We investigate a model of cell division in which the length of telomeres within the cell regulate their proliferative potential. At each cell division the ends of linear chromosomes change and a cell becomes senescent when one or more of its telomeres become shorter than a critical length. In addition to this systematic shortening, exchange of telomere DNA between the two daughter cells can occur at each cell division. We map this telomere dynamics onto a biased branching diffusion process with an absorbing boundary condition whenever any telomere reaches the critical length. As the relative effects of telomere shortening and cell division are varied, there is a phase transition between finite lifetime and infinite proliferation of the cell population. Using simple first-passage ideas, we quantify the nature of this transition.
Continuous time random Walk model has been versatile analytical formalism for studying and modeling diffusion processes in heterogeneous structures, such as disordered or porous media. We are studying the continuous limits of Heterogeneous Continuous Time Random Walk model, when a random walk is making jumps on a graph within different time-length. We apply the concept of a generalized master equation to study heterogeneous continuous-time random walks on networks. Depending on the interpretations of the waiting time distributions the generalized master equation gives different forms of continuous equations.
We present a generic model of cell motility generated by acto-myosin contraction of the cell cortex. We identify analytically dynamical instabilities of the cortex and show that they trigger spontaneous cortical flows which in turn can induce cell migration in 3-dimensional (3D) environments as well as bleb formation. This contractility--based mechanism, widely independent of actin treadmilling, appears as an alternative to the classical picture of lamellipodial motility on flat substrates. Theoretical predictions are compared to experimental data of tumor cells migrating in 3D matrigel and suggest that this mechanism could be a general mode of cell migration in 3D environments.
In a well-stirred system undergoing chemical reactions, fluctuations in the reaction propensities are approximately captured by the corresponding chemical Langevin equation. Within this context, we discuss in this work how the Kramers escape theory can be used to predict rare events in chemical reactions. As an example, we apply our approach to a recently proposed model on cell proliferation with relevance to skin cancer [P.B. Warren, Phys. Rev. E {bf 80}, 030903 (2009)]. In particular, we provide an analytical explanation for the form of the exponential exponent observed in the onset rate of uncontrolled cell proliferation.