scholarly journals A Class of Solutions for the Hybrid Kinetic Model in the Tumor-Immune System Competition

2013 ◽  
Vol 2013 ◽  
pp. 1-11 ◽  
Author(s):  
Carlo Cattani ◽  
Armando Ciancio

In this paper, the hybrid kinetic models of tumor-immune system competition are studied under the assumption of pure competition. The solution of the coupled hybrid system depends on the symmetry of the state transition density which characterizes the probability of successful occurrences. Thus by defining a proper transition density function, the solutions of the hybrid system are explicitly computed and applied to a classical (realistic) model of competing populations.

2017 ◽  
Vol 2017 ◽  
pp. 1-7
Author(s):  
Yong-Ki Ma

The transition density function plays an important role in understanding and explaining the dynamics of the stochastic process. In this paper, we incorporate an ergodic process displaying fast moving fluctuation into constant volatility models to express volatility clustering over time. We obtain an analytic approximation of the transition density function under our stochastic process model. Using perturbation theory based on Lie–Trotter operator splitting method, we compute the leading-order term and the first-order correction term and then present the left and right skew scenarios through numerical study.


2012 ◽  
Vol 2012 ◽  
pp. 1-6 ◽  
Author(s):  
Carlo Cattani ◽  
Armando Ciancio

A hybrid model, on the competition tumor cells immune system, is studied under suitable hypotheses. The explicit form for the equations is obtained in the case where the density function of transition is expressed as the product of separable functions. A concrete application is given starting from a modified Lotka-Volterra system of equations.


2019 ◽  
Vol 14 (02) ◽  
pp. 101-114 ◽  
Author(s):  
Vladimir P. Zhdanov

The understanding of the interplay between cancer and the immune system is still limited. Herein, I focus on two aspects of this interplay. First, I propose a kinetic model describing the likely role of the immune system in the lifetime risk of cancer at the level of the whole human population. For each tissue, the risk is predicted to be influenced by the heterogeneity of the population and to depend exponentially on time. The expression for the risk does not, however, depend explicitly on the total number of divisions of the corresponding stem cells. For this reason, the correlation with the latter number can only be indirect. Second, using another kinetic framework, I describe how the growth of a few tumors can depend on their interaction via the immune system. The analysis shows that depending on specific details, the tumors of different sizes tend either to reach the same size or remain to be of different sizes.


Author(s):  
Vladimir P. Zhdanov

AbstractOne of the suggested ways of the use of nanoparticles in virology implies their association with and subsequent deactivation of virions. The conditions determining the efficiency of this approach in vivo are now not clear. Herein, I propose the first kinetic model describing the corresponding processes and clarifying these conditions. My analysis indicates that nanoparticles can decrease concentration of infected cells by a factor of one order of magnitude, but this decrease itself (without feedback of the immune system) is insufficient for full eradication of infection. It can, however, induce delay in the progress of infection, and this delay can help to form sufficient feedback of the immune system.


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