9 research outputs found

    Linking stroke mortality with air pollution, income, and greenness in northwest Florida: an ecological geographical study

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    <p>Abstract</p> <p>Background</p> <p>Relatively few studies have examined the association between air pollution and stroke mortality. Inconsistent and inclusive results from existing studies on air pollution and stroke justify the need to continue to investigate the linkage between stroke and air pollution. No studies have been done to investigate the association between stroke and greenness. The objective of this study was to examine if there is association of stroke with air pollution, income and greenness in northwest Florida.</p> <p>Results</p> <p>Our study used an ecological geographical approach and dasymetric mapping technique. We adopted a Bayesian hierarchical model with a convolution prior considering five census tract specific covariates. A 95% credible set which defines an interval having a 0.95 posterior probability of containing the parameter for each covariate was calculated from Markov Chain Monte Carlo simulations. The 95% credible sets are (-0.286, -0.097) for household income, (0.034, 0.144) for traffic air pollution effect, (0.419, 1.495) for emission density of monitored point source polluters, (0.413, 1.522) for simple point density of point source polluters without emission data, and (-0.289,-0.031) for greenness. Household income and greenness show negative effects (the posterior densities primarily cover negative values). Air pollution covariates have positive effects (the 95% credible sets cover positive values).</p> <p>Conclusion</p> <p>High risk of stroke mortality was found in areas with low income level, high air pollution level, and low level of exposure to green space.</p

    Linking stroke mortality with air pollution, income, and greenness in northwest Florida: an ecological geographical study-3

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    Ty is equal to the value of the kernel surface at the raster cell center.<p><b>Copyright information:</b></p><p>Taken from "Linking stroke mortality with air pollution, income, and greenness in northwest Florida: an ecological geographical study"</p><p>http://www.ij-healthgeographics.com/content/7/1/20</p><p>International Journal of Health Geographics 2008;7():20-20.</p><p>Published online 1 May 2008</p><p>PMCID:PMC2396612.</p><p></p

    Linking stroke mortality with air pollution, income, and greenness in northwest Florida: an ecological geographical study-0

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    Rid represents a census unit). Right: Cell values of the environment exposure (red represents human activity area). The mean exposure value is 87 for red cells, and 77 for the whole census unit.<p><b>Copyright information:</b></p><p>Taken from "Linking stroke mortality with air pollution, income, and greenness in northwest Florida: an ecological geographical study"</p><p>http://www.ij-healthgeographics.com/content/7/1/20</p><p>International Journal of Health Geographics 2008;7():20-20.</p><p>Published online 1 May 2008</p><p>PMCID:PMC2396612.</p><p></p

    The Escherichia coli GTPase ObgE modulates hydroxyl radical levels in response to DNA replication fork arrest

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    Obg proteins are universally conserved GTP-binding proteins that are essential for viability in bacteria. Homologs in different organisms are involved in various cellular processes, including DNA replication. The goal of this study was to analyse the structure-function relationship of Escherichia coli ObgE with regard to DNA replication in general and sensitivity to stalled replication forks in particular. Defined C-terminal chromosomal deletion mutants of obgE were constructed and tested for sensitivity to the replication inhibitor hydroxyurea. The ObgE C-terminal domain was shown to be dispensable for normal growth of E. coli. However, a region within this domain is involved in the cellular response to replication fork stress. In addition, a mutant obgE over-expression library was constructed by error-prone PCR and screened for increased hydroxyurea sensitivity. ObgE proteins with substitutions L159Q, G163V, P168V, G216A or R237C, located within distinct domains of ObgE, display dominant-negative effects leading to hydroxyurea hypersensitivity when over-expressed. These effects are abolished in strains with a single deletion of the iron transporter TonB or combined deletions the toxin/antitoxin modules RelBE/MazEF, strains both of which have been shown to be involved in a pathway that stimulates hydroxyl radical formation following hydroxyurea treatment. Moreover, the observed dominant-negative effects are lost in the presence of the hydroxyl radical scavenger thiourea. Together, these results indicate involvement of hydroxyl radical toxicity in ObgE-mediated protection against replication fork stress.status: publishe

    Obg and membrane depolarization are part of a microbial bet-hedging strategy that leads to antibiotic tolerance

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    Within bacterial populations, a small fraction of persister cells is transiently capable of surviving exposure to lethal doses of antibiotics. As a bet-hedging strategy, persistence levels are determined both by stochastic induction and by environmental stimuli, called responsive diversification. Little is known on the mechanisms that link the low frequency of persisters to environmental signals. Our results support a central role for the conserved GTPase Obg in determining persistence in Escherichia coli in response to nutrient starvation. Obg-mediated persistence requires the stringent response alarmone (p)ppGpp and proceeds through transcriptional control of the hokB-sokB type I toxin-antitoxin module. In individual cells, increased Obg levels induce HokB expression, which in turn results in a collapse of the membrane potential, leading to dormancy. Obg also controls persistence in Pseudomonas aeruginosa and thus constitutes a conserved regulator of antibiotic tolerance. Combined, our findings signify an important step towards unravelling shared genetic mechanisms underlying persistence.publisher: Elsevier articletitle: Obg and Membrane Depolarization Are Part of a Microbial Bet-Hedging Strategy that Leads to Antibiotic Tolerance journaltitle: Molecular Cell articlelink: http://dx.doi.org/10.1016/j.molcel.2015.05.011 content_type: article copyright: Copyright © 2015 Elsevier Inc. All rights reserved.status: publishe

    Obg and membrane depolarization are part of a microbial bet-hedging strategy that leads to antibiotic tolerance

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    Within bacterial populations, a small fraction of per-sister cells is transiently capable of surviving exposure to lethal doses of antibiotics. As a bet-hedging strategy, persistence levels are determined both by stochastic induction and by environmental stimuli called responsive diversification. Little is known about the mechanisms that link the low frequency of per-sisters to environmental signals. Our results support a central role for the conserved GTPase Obg in determining persistence in Escherichia coli in response to nutrient starvation. Obg-mediated persistence requires the stringent response alarmone (p) ppGpp and proceeds through transcriptional control of the hokB-sokB type I toxin-antitoxin module. In individual cells, increased Obg levels induce HokB expression, which in turn results in a collapse of the membrane potential, leading to dormancy. Obg also controls persistence in Pseudomonas aeruginosa and thus constitutes a conserved regulator of antibiotic tolerance. Combined, our findings signify an important step toward unraveling shared genetic mechanisms underlying persistence
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