HighlightsAflatoxins toxicity model has been developed.Tracing aflatoxins concentration in foods and feeds at various stages is shown.The need to use experimental data is suggested.Satisfactory harmonization of acceptable threshold levels of aflatoxins in foods and feeds could be drawn.

In this paper, we formulated a mathematical model that studies the dynamics of HIV/ AIDS in Turkey from 1985 to 2016. We find two equilibrium points, disease free equilibrium and endemic equilibrium. Global stability analysis of the equilibria was conducted using Lyapunov function which depends on the basic reproduction ratio R 0 . If R 0 \ 1, the disease free equilibrium point is globally asymptotically stable, and if R 0 C 1 the endemic equilibrium point is globally asymptotically stable. We computed and predicted the basic reproduction ratios across all the years. It was found out that there were flaws in the exact values of R 0 which is related to the poor registration system of HIV/AIDS in Turkey. Hence, there is need for the government to improve the system in order to cover the actual cases of the disease. The increase of the basic reproduction ratio over the years also shows the need for the relevant authorities to adopt appropriate control measures in combating the disease.

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This paper aims to study the dynamics of immune suppressors/checkpoints, immune system, and BCG in the treatment of superficial bladder cancer. Programmed cell death protein-1 (PD-1), cytotoxic T-lymphocyte-associated antigen 4 (CTLA4), and transforming growth factor-beta (TGF-β) are some of the examples of immune suppressors/checkpoints. They are responsible for deactivating the immune system and enhancing immunological tolerance. Moreover, they categorically downregulate and suppress the immune system by preventing and blocking the activation of T-cells, which in turn decreases autoimmunity and enhances self-tolerance. In cancer immunotherapy, the immune checkpoints/suppressors prevent and block the immune cells from attacking, spreading, and killing the cancer cells, which leads to cancer growth and development. We formulate a mathematical model that studies three possible dynamics of the treatment and establish the effects of the immune checkpoints on the immune system and the treatment at large. Although the effect cannot be seen explicitly in the analysis of the model, we show it by numerical simulations.

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