Reliability and Makespan Optimization of Hardware Task Graphs in Partially Reconfigurable Platforms

This paper addresses the problem of reliability and makespan optimization of hardware task graphs in reconfigurable platforms by applying fault tolerance (FT) techniques to the running tasks based on the exploration of the Pareto set of solutions. In the presented solution, in contrast to the existing approaches in the literature, task graph scheduling, tasks parallelism, reconfiguration delay, and FT requirements are taken into account altogether. This paper first presents a model for hardware task graphs, task prefetch and scheduling, reconfigurable computer, and a fault model for reliability. Then, a mathematical model of an integer nonlinear multi-objective optimization problem is presented for improving the FT of hardware task graphs, scheduled in partially reconfigurable platforms. Experimental results show the positive impacts of choosing the FT techniques selected by the proposed solution, which is named Pareto-based. Thus, in comparison to nonfault-tolerant designs or other state-of-the-art FT approaches, without increasing makespan, about 850% mean time to failure (MTTF) improvement is achieved and, without degrading reliability, makespan is improved by 25%. In addition, experiments in fault-varying environments have demonstrated that the presented approach outperforms the existing state-of-the-art adaptive FT techniques in terms of both MTTF and makespan

Tumor-necrosis factor impairs CD4(+) T cell-mediated immunological control in chronic viral infection

Persistent viral infections are characterized by the simultaneous presence of chronic inflammation and T cell dysfunction. In prototypic models of chronicity-infection with human immunodeficiency virus (HIV) or lymphocytic choriomeningitis virus (LCMV)-we used transcriptome-based modeling to reveal that CD4(+) T cells were co-exposed not only to multiple inhibitory signals but also to tumor-necrosis factor (TNF). Blockade of TNF during chronic infection with LCMV abrogated the inhibitory gene-expression signature in CD4(+) T cells, including reduced expression of the inhibitory receptor PD-1, and reconstituted virus-specific immunity, which led to control of infection. Preventing signaling via the TNF receptor selectively in T cells sufficed to induce these effects. Targeted immunological interventions to disrupt the TNF-mediated link between chronic inflammation and T cell dysfunction might therefore lead to therapies to overcome persistent viral infection