Abstract
We use d'Aspremont and Jacquemin's strategic optimal R&D investment in a duopoly Cournot competition model to construct myopic optimal discrete and continuous R&D dynamics. We show that for some high initial production costs, the success or failure of a firm is very sensitive to small variations in its initial R&D investment strategies.

Abstract
We consider a Bertrand duopoly model with unknown costs. The firms' aim is to choose the price of its product according to the well-known concept of Bayesian Nash equilibrium. The chooses are made simultaneously by both firms. In this paper, we suppose that each firm has two different technologies, and uses one of them according to a certain probability distribution. The use of either one or the other technology affects the unitary production cost. We show that this game has exactly one Bayesian Nash equilibrium. We analyse the advantages, for firms and for consumers, of using the technology with highest production cost versus the one with cheapest production cost. We prove that the expected profit of each firm increases with the variance of its production costs. We also show that the expected price of each good increases with both expected production costs, being the effect of the expected production costs of the rival dominated by the effect of the own expected production costs.

Abstract
For a spatial stochastic epidemic model we investigate in the pair approximation scheme the differential equations for the moments. The basic reinfection model of susceptible-infected-recovered-reinfected or SIRI type is analysed, its phase transition lines calculated analytically in this pair approximation.

Abstract
The consequences of regulatory T cell (Treg) inhibition of interleukine 2 secretion are examined by mathematical modelling. We determine the analytic formula that describes the fine balance between Regulatory T cells and T cells at controlled and immune response equilibrium states. We demonstrate that cytokine dependent growth exhibits a quorum T cell population threshold that determines if immune responses develop on activation. We determine the analytic formulas of T cell proliferation thresholds that allow us to study the sensibility of the quorum growth thresholds controlling immune responses.

Abstract
We study a mathematical model of immune response by T cells where the regulatory T cells (Treg) inhibit interleukin 2 secretion. The bystander proliferation to an immune response is modelled. We consider an asymmetry reflecting that the difference between the growth and death rates can be higher for the active T cells and Tregs than for the inactive. This asymmetry leads to a better understanding of the bystander proliferation. An exposure to a pathogen results in an increased proliferation rate of the bystander T cells. If the population of the bystander T cells becomes large enough, autoimmunity can arise, eventually after a long transient period.

Abstract
The consequences of regulatory T cell (Treg) inhibition of interleukine 2 secretion are examined by mathematical modelling. We demonstrate that cytokine dependent growth exhibits quorum T cell population thresholds that determine whether immune responses develop on activation and whether the immune system returns to a control state. We study the effects in the quorum T cell population thresholds, by the T cell maximum growth rate, by the growth rate ratio between Tregs and T cells, by the value of the secretion rate of cytokines, and by the effectiveness of T cell secretion inhibition by Tregs.