No abstract

The complexity of cancer has motivated the development of different approaches to understand the dynamics of this large group of diseases. One that may allow us to better comprehend the behavior of cancer cells, in both short- and long-term, is mathematical modelling through ordinary differential equations. Several ODE mathematical models concerning tumor evolution and immune response have been formulated through the years, but only a few may exhibit chaotic attractors and oscillations such as stable limit cycles and periodic orbits; these dynamics are not that common among cancer systems. In this paper, we apply the Localization of Compact Invariant Sets (LCIS) method and Lyapunov stability theory to investigate the global dynamics and the main factors involved in tumor growth and immune response for a chaotic-cancer system presented by Itik and Banks in 2010. The LCIS method allows us to compute what we define as the localizing domain, which is formulated by the intersection of all lower and upper bounds of each cells population in the nonnegative octant, R+,03. Bounds of this domain are given by inequalities in terms of the system parameters. Then, we apply Lyapunov stability theory and LaSalle’s invariance principle to establish existence conditions of a global attractor. The latter implies that given any nonnegative initial condition, all trajectories will go to the largest compact invariant set (a stable equilibrium point, limit cycles, periodic orbits, or a chaotic attractor) located either inside or at the boundaries of the localizing domain. In order to complement our analysis, numerical simulations are performed throughout the paper to illustrate all mathematical results and to better explain their biological implications.

No abstract

Type-1 diabetes mellitus (T1DM) is an autoimmune disease that has an impact on mortality due to the destruction of insulin-producing pancreatic β -cells in the islets of Langerhans. Over the past few years, the interest in analyzing this type of disease, either in a biological or mathematical sense, has relied on the search for a treatment that guarantees full control of glucose levels. Mathematical models inspired by natural phenomena, are proposed under the prey–predator scheme. T1DM fits in this scheme due to the complicated relationship between pancreatic β -cell population growth and leukocyte population growth via the immune response. In this scenario, β -cells represent the prey, and leukocytes the predator. This paper studies the global dynamics of T1DM reported by Magombedze et al. in 2010. This model describes the interaction of resting macrophages, activated macrophages, antigen cells, autolytic T-cells, and β -cells. Therefore, the localization of compact invariant sets is applied to provide a bounded positive invariant domain in which one can ensure that once the dynamics of the T1DM enter into this domain, they will remain bounded with a maximum and minimum value. Furthermore, we analyzed this model in a closed-loop scenario based on nonlinear control theory, and proposed bases for possible control inputs, complementing the model with them. These entries are based on the existing relationship between cell–cell interaction and the role that they play in the unchaining of a diabetic condition. The closed-loop analysis aims to give a deeper understanding of the impact of autolytic T-cells and the nature of the β -cell population interaction with the innate immune system response. This analysis strengthens the proposal, providing a system free of this illness—that is, a condition wherein the pancreatic β -cell population holds and there are no antigen cells labeled by the activated macrophages.