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In this work, we highlight the influence of the material uncertainties (magnetic permeability, electric conductivity of a Mn-Zn ferrite core, and electric permittivity of wire insulation) on the RLC parameters of a wound inductor extracted from the finite element method. To that end, the finite element method is embedded in a Monte Carlo simulation. We show that considering mentioned different material properties as real random variables, leads to significant variations in the distributions of the RLC parameters.

The paper introduces a new approach to kriging based multi-objective optimization by utilizing a local probability of improvement as the infill sampling criterion and the nearest neighbor check to ensure diversification and uniform distribution of Pareto fronts. The proposed method is computationally fast and linearly scalable to higher dimensions.

The evolutionary dynamics of a system of cancerous cells in a model of chronic myeloid leukemia (CML) is investigated by a statistical approach. Cancer progression is explored by applying a Monte Carlo method to simulate the stochastic behavior of cell reproduction and death in a population of blood cells which can experience genetic mutations. In CML front line therapy is represented by the tyrosine kinase inhibitor imatinib which strongly affects the reproduction of leukemic cells only. In this work, we analyze the effects of a targeted therapy on the evolutionary dynamics of normal, first-mutant and cancerous cell populations. Several scenarios of the evolutionary dynamics of imatinib-treated leukemic cells are described as a consequence of the efficacy of the different modeled therapies. We show how the patient response to the therapy changes when an high value of the mutation rate from healthy to cancerous cells is present. Our results are in agreement with clinical observations. Unfortunately, development of resistance to imatinib is observed in a proportion of patients, whose blood cells are characterized by an increasing number of genetic alterations. We find that the occurrence of resistance to the therapy can be related to a progressive increase of deleterious mutations., Submitted to Central European Journal of Physics