13 research outputs found

    Adversarial Control in a Delay Tolerant Network

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    Abstract. We consider a multi-criteria control problem that arises in a delay tolerant network with two adversarial controllers: the source and the jammer. The source’s objective is to choose transmission probabilities so as to maximize the probability of successful delivery of some content to the destination within a deadline. These transmissions are subject to interference from a jammer who is a second, adversarial type controller, We solve three variants of this problem: (1) the static one, where the actions of both players, u and w, are constant in time; (2) the dynamic open loop problem in which all policies may be time varying, but inde-pendent of state, the number of already infected mobiles; and (3) the dynamic closed-loop feedback policies where actions may change in time and may be specified as functions of the current value of the state (in which case we look for feedback Nash equilibrium). We obtain some ex-plicit expressions for the solution of the first game, and some structural results as well as explicit expressions for the others. An interesting out-come of the analysis is that the latter two games exhibit switching times for the two players, where they switch from pure to mixed strategies and vice versa. Some numerical examples included in the paper illustrate the nature of the solutions

    Pancreatic beta cell protection/regeneration with phytotherapy

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    Although currently available drugs are useful in controlling early onset complications of diabetes, serious late onset complications appear in a large number of patients. Considering the physiopathology of diabetes, preventing beta cell degeneration and stimulating the endogenous regeneration of islets will be essential approaches for the treatment of insulin-dependent diabetes mellitus. The current review focused on phytochemicals, the antidiabetic effect of which has been proved by pancreatic beta cell protection/regeneration. Among the hundreds of plants that have been investigated for diabetes, a small fraction has shown the regenerative property and was described in this paper. Processes of pancreatic beta cell degeneration and regeneration were described. Also, the proposed mechanisms for the protective/regenerative effects of such phytochemicals and their potential side effects were discussed

    Down-Regulation of SIRT1 Expression by mir-23b Contributes to Lipid Accumulation in HepG2 Cells

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    Non-alcoholic fatty liver disease is one of the main causes of chronic liver disease and therefore is currently considered a major public health problem. Sirtuin 1 (SIRT1) is an NAD-dependent deacetylase enzyme that contributes in the regulation of metabolic processes and protects against lipid accumulation in hepatocytes. Its expression is potentially regulated by microRNAs which attach to the 3� untranslated region (3�-UTR) of their target mRNA. HepG2 cells were incubated by glucose to induce lipid accumulation and were subsequently transfected with mir-23b mimic and inhibitor. Real-time PCR was used for measuring the expression of mir-23b and SIRT1 mRNA. Cell survival assay and intracellular triglyceride measurement were performed using colorimetric methods. Determination of SIRT1 protein level and activity were done by western blot and fluorometric analysis, respectively. The interaction of miR-23b with 3�-UTR of SIRT1 mRNA was confirmed by dual luciferase. miR-23b mimic inhibited gene and protein expression of SIRT1, while the inhibitor of miR-23b significantly elevated the expression levels of SIRT1 mRNA and protein. The results showed that the 3�-UTR of SIRT1 mRNA is a direct target for miR-23b. The intracellular triglyceride level was increased following the inhibition of SIRT1 in transfected HepG2 cell by miR-23b mimic. Cell viability was decreased in response to miR-23b upregulation compared to control cells. miR-23b reduces the expression and activity of SIRT1 and therefore may be a causative factor in the enhancement of lipid accumulation in HepG2 cells. © 2019, Springer Science+Business Media, LLC, part of Springer Nature
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