Oncolytic virus (OV) therapy is a promising treatment for cancer due to the OVs selective ability to infect and replicate inside cancer cells, thus killing them, without harming healthy cells. In this work, we present a new non-local multiscale moving boundary model for the spatio-temporal cancer-OV interactions. This model explores an important double feedback loop that links the macro-scale dynamics of cancer-virus interactions and the micro-scale dynamics of proteolytic activity taking place at the tumour interface. The cancer cell-cell and cell-matrix interactions are assumed to be nonlocal, while the cell-virus interactions are assumed local. With the help of this model we investigate computationally various cancer treatment scenarios involving oncolytic viruses (i.e., the effect of injecting the OV inside the tumour, or outside it). Moreover, we investigate the effect of different cell-cell and cell-matrix interaction strengths on the success of OV spreading throughout the tumour, and the effect of constant or density-dependent virus diffusion coefficients on viral spread.

<abstract><p>In this study we investigate computationally tumour-oncolytic virus (OV) interactions that take place within a heterogeneous extracellular matrix (ECM). The ECM is viewed as a mixture of two constitutive phases, namely a fibre phase and a non-fibre phase. The multiscale mathematical model presented here focuses on the nonlocal cell-cell and cell-ECM interactions, and how these interactions might be impacted by the infection of cancer cells with the OV. At macroscale we track the kinetics of cancer cells, virus particles and the ECM. At microscale we track (i) the degradation of ECM by matrix degrading enzymes (MDEs) produced by cancer cells, which further influences the movement of tumour boundary; (ii) the re-arrangement of the microfibres that influences the re-arrangement of macrofibres (i.e., fibres at macroscale). With the help of this new multiscale model, we investigate two questions: (i) whether the infected cancer cell fluxes are the result of local or non-local advection in response to ECM density; and (ii) what is the effect of ECM fibres on the the spatial spread of oncolytic viruses and the outcome of oncolytic virotherapy.</p></abstract>

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Outlined here is an innovative method for characterizing a layer of microelongated semiconductor material under excitation. Fractional time derivatives of a heat equation with a rotational field are used to probe the model during photo-excitation processes. Micropolar-thermoelasticity theory, which the model implements, introduces the microelongation scalar function to characterize the processes occurring inside the microelements. When the microelongation parameters are considered following the photo-thermoelasticity theory, the model investigates the interaction scenario between optical-thermo-mechanical waves under the impact of rotation parameters. During electronic and thermoelastic deformation, the key governing equations have been reduced to dimensionless form. Laplace and Fourier's transformations are used to solve this mathematical problem. Isotropic, homogeneous, and linear microelongated semiconductor medium's general solutions to their respective fundamental fields are derived in two dimensions (2D). To get complete solutions, several measurements must be taken at the free surface of the medium. As an example of numerical modeling of the important fields, we will use the silicon (Si) material’s physicomechanical characteristics. Several comparisons were made using different values of relaxation time and rotation parameters, and the results were graphically shown.

In this study we investigate computationally tumour-oncolytic virus (OV) interactions that take place within a heterogeneous ExtraCellular Matrix (ECM). The ECM is viewed as a mixture of two constitutive phases, namely a fibre phase and a non-fibre phase. The multiscale mathematical model presented here focuses on the nonlocal cell-cell and cell-ECM interactions, and how these interactions might be impacted by the infection of cancer cells with the OV. At macroscale we track the kinetics of cancer cells, virus particles and the ECM. At microscale we track (i) the degradation of ECM by matrix degrading enzymes (MDEs) produced by cancer cells, which further influences the movement of tumour boundary; (ii) the re-arrangement of the microfibres that influences the re-arrangement of macrofibres (i.e., fibres at macroscale). With the help of this new multiscale model, we investigate two questions: (i) whether the infected cancer cell fluxes are the result of local or non-local advection in response to ECM density; and (ii) what is the effect of ECM fibres on the the spatial spread of oncolytic viruses and the outcome of oncolytic virotherapy.