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How will a virus propagate in a real network? How long does it take to disinfect a network given particular values of infection rate and virus death rate? What is the single best node to immunize? Answering these questions is essential for devising network-wide strategies to counter viruses. In addition, viral propagation is very similar in principle to the spread of rumors, information, and "fads," implying that the solutions for viral propagation would also offer insights into these other problem settings. We answer these questions by developing a nonlinear dynamical system (NLDS) that accurately models viral propagation in any arbitrary network, including real and synthesized network graphs. We propose a general epidemic threshold condition for the NLDS system: we prove that the epidemic threshold for a network is exactly the inverse of the largest eigenvalue of its adjacency matrix. Finally, we show that below the epidemic threshold, infections die out at an exponential rate. Our epidemic threshold model subsumes many known thresholds for special-case graphs (e.g., Erdös-Rényi, BA powerlaw, homogeneous). We demonstrate the predictive power of our model with extensive experiments on real and synthesized graphs, and show that our threshold condition holds for arbitrary graphs. Finally, we show how to utilize our threshold condition for practical uses: It can dictate which nodes to immunize; it can assess the effects of a throttling policy; it can help us design network topologies so that they are more resistant to viruses.

The obesity epidemic is a global issue and shows no signs of abating, while the cause of this epidemic remains unclear. Marketing practices of energy-dense foods and institutionally-driven declines in physical activity are the alleged perpetrators for the epidemic, despite a lack of solid evidence to demonstrate their causal role. While both may contribute to obesity, we call attention to their unquestioned dominance in program funding and public efforts to reduce obesity, and propose several alternative putative contributors that would benefit from equal consideration and attention. Evidence for microorganisms, epigenetics, increasing maternal age, greater fecundity among people with higher adiposity, assortative mating, sleep debt, endocrine disruptors, pharmaceutical iatrogenesis, reduction in variability of ambient temperatures, and intrauterine and intergenerational effects, as contributing factors to the obesity epidemic are reviewed herein. While the evidence is strong for some contributors such as pharmaceutical-induced weight gain, it is still emerging for other reviewed

The mechanisms linking human immunodeficiency virus replication to the progressive immunodeficiency of acquired immune deficiency syndrome are controversial, particularly the relative contribution of CD4+ T cell destruction. Here, we used the simian immunodeficiency virus (SIV) model to investigate the relationship between systemic CD4+ T cell dynamics and rapid disease progression. Of 18 rhesus macaques (RMs) infected with CCR5-tropic SIVmac239 (n = 14) or CXCR4-tropic SIVmac155T3 (n = 4), 4 of the former group manifested end-stage SIV disease by 200 d after infection. In SIVmac155T3 infections, naive CD4+ T cells were dramatically depleted, but this population was spared by SIVmac239, even in rapid progressors. In contrast, all SIVmac239-infected RMs demonstrated substantial systemic depletion of CD4+ memory T cells by day 28 after infection. Surprisingly, the extent of CD4+ memory T cell depletion was not, by itself, a strong predictor of rapid progression. However, in all RMs destined for stable infection, this depletion was countered by a striking increase in production of short-lived CD4+ memory T cells, many of which rapidly migrated to tissue. In all rapid progressors (P < 0.0001), production of these cells initiated but failed by day 42 of infection, and tissue delivery of new CD4+ memory T cells ceased. Thus, although profound depletion of tissue CD4+ memory T cells appeared to be a prerequisite for early pathogenesis, it was the inability to respond to this depletion with sustained production of tissue-homing CD4+ memory T cells that best distinguished rapid progressors, suggesting that mechanisms of the CD4+ memory T cell generation play a crucial role in maintaining immune homeostasis in stable SIV infection.

Graphene has attracted a lot of research interest owing to its exotic properties and a wide spectrum of potential applications. Chemical vapor deposition (CVD) from gaseous hydrocarbon sources has shown great promises for large-scale graphene growth. However, high growth temperature, typically 1000 °C, is required for such growth. Here we demonstrate a revised CVD route to grow graphene on Cu foils at low temperature, adopting solid and liquid hydrocarbon feedstocks. For solid PMMA and polystyrene precursors, centimeter-scale monolayer graphene films are synthesized at a growth temperature down to 400 °C. When benzene is used as the hydrocarbon source, monolayer graphene flakes with excellent quality are achieved at a growth temperature as low as 300 °C. The successful low-temperature growth can be qualitatively understood from the first principles calculations. Our work might pave a way to an undemanding route for economical and convenient graphene growth.