Laxity dynamics and LLF schedulability analysis on multiprocessor platforms

LLF (Least Laxity First) scheduling, which assigns a higher priority to a task with a smaller laxity, has been known as an optimal preemptive scheduling algorithm on a single processor platform. However, little work has been made to illuminate its characteristics upon multiprocessor platforms. In this paper, we identify the dynamics of laxity from the system’s viewpoint and translate the dynamics into LLF multiprocessor schedulability analysis. More specifically, we first characterize laxity properties under LLF scheduling, focusing on laxity dynamics associated with a deadline miss. These laxity dynamics describe a lower bound, which leads to the deadline miss, on the number of tasks of certain laxity values at certain time instants. This lower bound is significant because it represents invariants for highly dynamic system parameters (laxity values). Since the laxity of a task is dependent of the amount of interference of higher-priority tasks, we can then derive a set of conditions to check whether a given task system can go into the laxity dynamics towards a deadline miss. This way, to the author’s best knowledge, we propose the first LLF multiprocessor schedulability test based on its own laxity properties. We also develop an improved schedulability test that exploits slack values. We mathematically prove that the proposed LLF tests dominate the state-of-the-art EDZL tests. We also present simulation results to evaluate schedulability performance of both the original and improved LLF tests in a quantitative manner.

Mathematical model for HIV dynamics in HIV-specific helper cells

In this paper we study a delay mathematical model for the dynamics of HIV in HIV-specific CD4 + T helper cells. We modify the model presented by Roy and Wodarz in 2012, where the HIV dynamics is studied, considering a single CD4 + T cell population. Non-specific helper cells are included as alternative target cell population, to account for macrophages and dendritic cells. In this paper, we include two types of delay: (1) a latent period between the time target cells are contacted by the virus particles and the time the virions enter the cells and; (2) virus production period for new virions to be produced within and released from the infected cells. We compute the reproduction number of the model, R0, and the local stability of the disease free equilibrium and of the endemic equilibrium. We find that for values of R0<1, the model approaches asymptotically the disease free equilibrium. For values of R0>1, the model approximates asymptotically the endemic equilibrium. We observe numerically the phenomenon of backward bifurcation for values of R0⪅1. This statement will be proved in future work. We also vary the values of the latent period and the production period of infected cells and free virus. We conclude that increasing these values translates in a decrease of the reproduction number. Thus, a good strategy to control the HIV virus should focus on drugs to prolong the latent period and/or slow down the virus production. These results suggest that the model is mathematically and epidemiologically well-posed.