Access Point Association Coordination in Densely Deployed 802.11 Wireless Networks

Dense deployment of wireless local area network (WLAN) access points (APs) is an important part of the next generation Wi-Fi and standardization (802.11ax) efforts are underway. Increasing demand for WLAN connectivity motivates such dense deployments, especially in geographical areas with large numbers of users, such as stadiums, large enterprises, multi-tenant buildings, and urban cities. Although densification of WLAN APs guarantees coverage, it is susceptible to increased interference and uncoordinated association of stations (STAs) to APs, which degrade network throughput. Therefore, to improve network throughput, algorithms are proposed in this thesis to optimally coordinate AP associations in the presence of interference. In essence, coordination of APs in dense WLANs (DWLANs) is achieved through coordination of STAs' associations with APs. While existing approaches suggest tuning of APs' beacon powers or using transmit power control (TPC) for association control, here, the signal-to-interference-plus-noise ratio (SINRs) of STAs and the clear channel assessment (CCA) threshold of the 802.11 MAC protocol are employed. The proposed algorithms in this thesis enhance throughput and minimize coverage holes inherent in cell breathing and TPC techniques by not altering the transmit powers of APs, which determine cell coverage. Besides uncoordinated AP associations, unnecessary frequent transmission deferment is envisaged as another problem in DWLANs due to the clear channel assessment aspect of the carrier sensing multiple access collision avoidance (CSMA/CA) scheme in 802.11 standards and the short spatial reuse distance between co-channel APs. To address this problem in addition to AP association coordination, an algorithm is proposed for CCA threshold adjustment in each AP cell, such that CCA threshold used in one cell mitigates transmission deferment in neighboring cells. Performance evaluation reveals that the proposed association optimization algorithms achieve significant gain in throughput when compared with the default strongest signal first (SSF) association scheme in the current 802.11 standard. Also, further gain in throughput is observed when the CCA threshold adjustment is combined with the optimized association. Results show that when STA-AP association is optimized and CCA threshold is adjusted in each cell, throughput improves. Finally, transmission delay and the number of packet re-transmissions due to collision and contention significantly decrease.

ENVIRONMENTAL INFLUENCES AND EPIGENETIC MECHANISMS IN RISK FOR DEPRESSION

Genetic and environmental factors interact to influence vulnerability for internalizing psychopathology, including Major Depressive Disorder (MDD). The mechanisms that account for how environmental stress can alter biological systems are not yet well understood yet are critical to develop more accurate models of vulnerability and targeted interventions. Epigenetic influences, and more specifically, DNA methylation, may provide a mechanism by which stress could program gene expression, thereby altering key systems implicated in depression, such as frontal-limbic circuitry and its critical role in emotion regulation. This thesis investigated the role of environmental factors from infancy and throughout the lifespan affecting the serotonergic (5-HT) system in the vulnerability to and treatment of depression and anxiety and potential underlying DNA methylation processes. First, we investigated the contributions of additive genetic vs. environmental factors on an early trait phenotype for depression (negative emotionality) in infants and their stability over time in the first 2 years of life. We provided evidence of the substantial contributions of both genetic and shared environmental factors to this trait, as well as genetically- and environmentally- mediated stability and innovation. Second, we studied how childhood environmental stress is associated with peripheral DNA methylation of the serotonin transporter gene, SLC6A4, as well as long-term trajectories of internalizing behaviours. There was a relationship between childhood psychosocial adversity and SLC6A4 methylation in males, as well as between SLC6A4 methylation and internalizing trajectory in both sexes. Third, we investigated changes in emotion processing and epigenetic modification of the SLC6A4 gene in depressed adolescents before and after Mindfulness-Based Cognitive Therapy (MBCT). The alterations from pre- to post-treatment in connectivity between the ACC and other network regions and SLC6A4 methylation suggested that MBCT may work to optimize the connectivity of brain networks involved in cognitive control of emotion as well as also normalize the relationship between SLC6A4 methylation and activation patterns in frontal-limbic circuitry. Our results from these three studies strengthen the theory that environmental influences are critical in establishing early vulnerability factors for MDD, driving epigenetic processes, and altering brain processes as an individual undergoes treatment, or experiences relapse.