Ad hoc wireless networks can be quickly deployed to provide wireless communication services in areas without pre-established infrastructure of base stations. Since delivering signals between sources and destinations is a primary function of ad hoc networks, the design and analysis of ad hoc networks are also a task of signal processing. In this paper, we review some of the major results on maximum throughput of ad hoc networks. Both single-hop ad hoc networks and multi-hop ad hoc networks are considered. In particular, we show examples of how to maximize the throughput of a large ad hoc network through a closed-loop analysis of two medium access control (MAC) schemes: synchronous array method (SAM) and asynchronous array method (AAM). Both omni-directional antennas and directional antennas are examined. This study illustrates an importance of the interplays between signal processing, information theory and networking protocols.

Apolipoprotein (apo) E4 is a risk factor for heart disease, Alzheimer's disease, and other forms of neurodegeneration, but the underlying mechanisms are unknown. Domain interaction, a structural property that distinguishes apoE4 from apoE2 and apoE3, results in more rapid turnover and lower plasma levels of apoE4. To determine whether domain interaction affects brain apoE levels, we analyzed brain homogenates from human apoE3 and apoE4 knock-in mice, wild-type mice, and Arg-61 apoE mice, in which domain interaction was introduced by gene targeting. As determined on Western blots, the hemibrain, cortex, hippocampus, and cerebellum of knock-in mice had 30 - 40% lower levels of apoE4 than apoE3, and Arg-61 mice had 25 - 50% lower apoE levels than wild-type mice. In the CSF, Arg-61 apoE level was 40% lower than the wild-type level. Arg-61 apoEmRNA levels were similar to or slightly higher than wild-type apoEmRNA levels. Thus, the lower Arg-61 apoE levels were not attributable to decreased mRNA levels. In culture medium from heterozygous Arg-61/wild-type and apoE4/apoE3 primary astrocytes, Arg-61 apoE and apoE4 levels were lower than wild-type apoE and apoE3, respectively, suggesting that primary astrocytes secrete lower amounts of Arg-61 apoE and apoE4. These results demonstrate that domain interaction is responsible for the lower levels of both human apoE4 and mouse Arg-61 apoE in mouse brain. Cells may recognize apoE4 and Arg-61 apoE as misfolded proteins and target them for degradation or accumulation. Thus, degradation/accumulation or lower levels of apoE4 may contribute to the association of apoE4 with Alzheimer's disease.