Redesign of Turbo Magazine Feature Article

This project contains a feature article redesign for Turbo Magazine. This project addresses the current state of the magazine, the relative history of the magazine, and the audience of the magazine, and how to address the needs of the magazine in a redesign

New Upper Bounds on the Distance Domination Numbers of Grids

In his 1992 Ph.D. thesis Chang identified an efficient way to dominate m-by-n grid graphs and conjectured that his construction gives the most efficient dominating sets for relatively large grids. In 2011 Goncalves, Pinlou, Rao, and Thomasse proved Chang\u27s conjecture, establishing a closed formula for the domination number of a grid. In March 2013, Fata, Smith and Sundaram established upper bounds for the k-distance domination numbers of grid graphs by generalizing Chang\u27s construction of dominating sets to k-distance dominating sets. In this paper we use algebraic and geometric arguments to improve the upper bounds established by Fata, Smith, and Sundaram for the k-distance domination numbers of grids

Innate immune modulation induced by EBV lytic infection promotes endothelial cell inflammation and vascular injury in scleroderma

Microvascular injury is considered an initial event in the pathogenesis of scleroderma and endothelial cells are suspected of being the target of the autoimmune process seen in the disease. EBV has long been proposed as a trigger for autoimmune diseases, including scleroderma. Nevertheless, its contribution to the pathogenic process remains poorly understood. In this study, we report that EBV lytic antigens are detected in scleroderma dermal vessels, suggesting that endothelial cells might represent a target for EBV infection in scleroderma skin. We show that EBV DNA load is remarkably increased in peripheral blood, plasma and circulating monocytes from scleroderma patients compared to healthy EBV carriers, and that monocytes represent the prominent subsets of EBV-infected cells in scleroderma. Given that monocytes have the capacity to adhere to the endothelium, we then investigated whether monocyte-associated EBV could infect primary human endothelial cells. We demonstrated that endothelial cells are infectable by EBV, using human monocytes bound to recombinant EBV as a shuttle, even though cell-free virus failed to infect them. We show that EBV induces activation of TLR9 innate immune response and markers of vascular injury in infected endothelial cells and that up-regulation is associated with the expression of EBV lytic genes in infected cells. EBV innate immune modulation suggests a novel mechanism mediating inflammation, by which EBV triggers endothelial cell and vascular injury in scleroderma. In addition, our data point to up-regulation of EBV DNA loads as potential biomarker in developing vasculopathy in scleroderma. These findings provide the framework for the development of novel therapeutic interventions to shift the scleroderma treatment paradigm towards antiviral therapies