An Energy-efficient Rate Adaptive Media Access Protocol (RA-MAC) for Long-lived Sensor Networks

We introduce an energy-efficient Rate Adaptive Media Access Control (RA-MAC) algorithm for long-lived Wireless Sensor Networks (WSNs). Previous research shows that the dynamic and lossy nature of wireless communications is one of the major challenges to reliable data delivery in WSNs. RA-MAC achieves high link reliability in such situations by dynamically trading off data rate for channel gain. The extra gain that can be achieved reduces the packet loss rate which contributes to reduced energy expenditure through a reduced numbers of retransmissions. We achieve this at the expense of raw bit rate which generally far exceeds the application’s link requirement. To minimize communication energy consumption, RA-MAC selects the optimal data rate based on the estimated link quality at each data rate and an analytical model of the energy consumption. Our model shows how the selected data rate depends on different channel conditions in order to minimize energy consumption. We have implemented RA-MAC in TinyOS for an off-the-shelf sensor platform (the TinyNode) on top of a state-of-the-art WSN Media Access Control Protocol, SCP-MAC, and evaluated its performance by comparing our implementation with the original SCP-MAC using both simulation and experiment

Pathogenesis of HIV-associated sensory neuropathy: evidence from in vivo and in vitro experimental models

HIV-associated sensory neuropathy (HIV-SN) is a frequent neurological complication of HIV infection and its treatment with some antiretroviral drugs. We review the pathogenesis of the viral- and drug-induced causes of the neuropathy, and its primary symptom, pain, based on evidence from in vivo and in vitro models of HIV-SN. Viral coat proteins mediate nerve fibre damage and hypernociception through direct and indirect mechanisms. Direct interactions between viral proteins and nerve fibres dominate axonal pathology, while somal pathology is dominated by indirect mechanisms that occur secondary to virus-mediated activation of glia and macrophage infiltration into the dorsal root ganglia. The treatment-induced neuropathy and resulting hypernociception arise primarily from drug-induced mitochondrial dysfunction, but the sequence of events initiated by the mitochondrial dysfunction that leads to the nerve fibre damage and dysfunction are still unclear. Overall, the models that have been developed to study the pathogenesis of HIV-SN, and hypernociception associated with the neuropathy, are reasonable models and have provided useful insights into the pathogenesis of HIV-SN. As new models are developed they may ultimately lead to identification of therapeutic targets for the prevention or treatment of this common neurological complication of HIV infection

TNF-block genotypes influence susceptibility to HIV-associated sensory neuropathy in Indonesians and South Africans

HIV-associated sensory neuropathy (HIV-SN) is a disabling complication of HIV disease and antiretroviral therapies (ART). Since stavudine was removed from recommended treatment schedules, the prevalence of HIV-SN has declined and associated risk factors have changed. With stavudine, rs1799964*C (TNF-1031) associated with HIV-SN in Caucasians and Indonesians but not in South Africans. Here, we investigate associations between HIV-SN and rs1799964*C and 12 other polymorphisms spanning TNF and seven neighboring genes (the TNF-block) in Indonesians (n = 202; 34/168 cases) and South Africans (n = 75; 29/75 cases) treated without stavudine. Haplotypes were derived using fastPHASE and haplotype networks built with PopART. There were no associations with rs1799964*C in either population. However, rs9281523*C in intron 10 of BAT1 (alternatively DDX39B) independently associated with HIV-SN in Indonesians after correcting for lower CD4 T-cell counts and \u3e500 copies of HIV RNA/mL (model p = 0.0011, Pseudo R2 = 0.09). rs4947324*T (between NFKBIL1 and LTA) independently associated with reduced risk of HIV-SN and shared haplotype 1 (containing no minor alleles) associated with increased risk of HIV-SN after correcting for greater body weight, a history of tuberculosis and nadir CD4 T-cell counts (model: p = 0.0003, Pseudo R2 = 0.22). These results confirm TNF-block genotypes influence susceptibility of HIV-SN. However, critical genotypes differ between ethnicities and with stavudine use

Priority areas for cannabis and cannabinoid product research in South Africa

No abstract available

Resilience.HIVPain v0.1.3

Updated activity and random forest plots to be publication-ready

Bad Science: torture numbers and they will tell you anything

Bad Science: Torture numbers and they will tell you anything. Presented at the 8th Annual Congress of PainSA, Muldersdrift, South Africa, 2015. <div><br></div><div>The presentation covers the issue of paper retractions, and the dual problems of publication bias, and poor data study design, analysis and reporting to low study reproducibility and replicability, and increasing rate of retractions.<br></div