An OpenEaagles Framework Extension for Hardware-in-the-Loop Swarm Simulation

Unmanned Aerial Vehicle (UAV) swarm applications, algorithms, and control strategies have experienced steady growth and development over the past 15 years. Yet, to this day, most swarm development efforts have gone untested and thus unimplemented. Cost of aircraft systems, government imposed airspace restrictions, and the lack of adequate modeling and simulation tools are some of the major inhibitors to successful swarm implementation. This thesis examines how the OpenEaagles simulation framework can be extended to bridge this gap. This research aims to utilize Hardware-in-the-Loop (HIL) simulation to provide developers a functional capability to develop and test the behaviors of scalable and modular swarms of autonomous UAVs in simulation with high confidence that these behaviors will prop- agate to real/live ight tests. Demonstrations show the framework enhances and simplifies swarm development through encapsulation, possesses high modularity, pro- vides realistic aircraft modeling, and is capable of simultaneously accommodating four hardware-piloted swarming UAVs during HIL simulation or 64 swarming UAVs during pure simulation

Accelerated in vivo proliferation of memory phenotype CD4+ T-cells in human HIV-1 infection irrespective of viral chemokine co-receptor tropism.

CD4(+) T-cell loss is the hallmark of HIV-1 infection. CD4 counts fall more rapidly in advanced disease when CCR5-tropic viral strains tend to be replaced by X4-tropic viruses. We hypothesized: (i) that the early dominance of CCR5-tropic viruses results from faster turnover rates of CCR5(+) cells, and (ii) that X4-tropic strains exert greater pathogenicity by preferentially increasing turnover rates within the CXCR4(+) compartment. To test these hypotheses we measured in vivo turnover rates of CD4(+) T-cell subpopulations sorted by chemokine receptor expression, using in vivo deuterium-glucose labeling. Deuterium enrichment was modeled to derive in vivo proliferation (p) and disappearance (d*) rates which were related to viral tropism data. 13 healthy controls and 13 treatment-naive HIV-1-infected subjects (CD4 143-569 cells/ul) participated. CCR5-expression defined a CD4(+) subpopulation of predominantly CD45R0(+) memory cells with accelerated in vivo proliferation (p = 2.50 vs 1.60%/d, CCR5(+) vs CCR5(-); healthy controls; P<0.01). Conversely, CXCR4 expression defined CD4(+) T-cells (predominantly CD45RA(+) naive cells) with low turnover rates. The dominant effect of HIV infection was accelerated turnover of CCR5(+)CD45R0(+)CD4(+) memory T-cells (p = 5.16 vs 2.50%/d, HIV vs controls; P<0.05), naïve cells being relatively unaffected. Similar patterns were observed whether the dominant circulating HIV-1 strain was R5-tropic (n = 9) or X4-tropic (n = 4). Although numbers were small, X4-tropic viruses did not appear to specifically drive turnover of CXCR4-expressing cells (p = 0.54 vs 0.72 vs 0.44%/d in control, R5-tropic, and X4-tropic groups respectively). Our data are most consistent with models in which CD4(+) T-cell loss is primarily driven by non-specific immune activation