21 research outputs found

    Adult populations of each Lao province in 2005 [15].

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    <p>Adult populations of each Lao province in 2005 <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0044545#pone.0044545-National1" target="_blank">[15]</a>.</p

    Estimated percentage beneficial effect on each infection of individual empirical treatments.

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    <p>Inclusion threshold: percentage of all febrile cases of diseases treatable by each individual empirical treatment that must be exceeded for the inclusion of that treatment in an empirical protocol.</p

    Graphs illustrating the model predictions of the effect of spatial heterogeneity given the baseline input values in Tables (1, 2, 3).

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    <p>The mean predicted numbers of appropriate treatments if a protocol based on the Vientiane epidemiology is applied nationally is plotted in Graph (a) for a range of values for national and regional variation. The 2.5% and 97.5% prediction intervals are plotted in Graphs (c) and (e). The mean additional numbers of appropriate treatments (i.e. the potential impact) predicted if a spatially explicit treatment protocol based on the incidence not only in Vientiane but also in three sentinel provinces were applied is plotted in Graph (b) for the same range of national and regional variation. The 2.5% and 97.5% prediction intervals are plotted in Graphs (c) and (f).</p

    Network representation of genes differentially expressed in melioidosis.

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    <p>‘Canonical’ pathways (such as those presented in a standard biochemistry textbook) are manually curated collections of protein interactions arranged in a manner that aids human understanding, and as artificial constructs the boundaries between pathways are subjective. Pathways that are conceptually distinct often have proteins in common and overlap, so in modular analysis, multiple pathways may collapse into a single module, causing other pathways and relationships to gain prominence. These two networks (<b>A</b> and <b>B</b>) represent those genes that are differentially expressed in melioidosis. For simplicity of presentation, we have used only a subset of genes in these networks. The top 221 upregulated genes (as ranked by <i>p</i>-value) are presented in <b>A</b>, and the top 155 downregulated genes are in <b>B</b>. The same clusters were found in an analysis of the whole gene set and those results are presented in <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0054961#pone-0054961-t002" target="_blank">Tables 2</a> & <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0054961#pone-0054961-t003" target="_blank">3</a>. <b>Network </b><b>A</b>. IFN-γ, TNF-α, IL-12 signalling pathways cluster together with the glypican network in the centre of the graph, but the complement/chemokine receptor (<b>cluster 1</b>), inflammasome (<b>cluster 2</b>) and Toll-like receptor pathways come to prominence in this analysis (<b>cluster 3</b>). <b>Network B</b>. IFN-γ, TGF-β and TNF signalling again cluster in the middle of the network. The two most prominent clusters are ribosomal proteins (<b>cluster 1</b>) and zinc finger proteins (<b>cluster 2</b>).</p

    Genes downregulated in melioidosis and tuberculosis, arranged by pathway.

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    <p>IFN = interferon, IGF = insulin-like growth factor, IL = interleukin, NF-κB = nuclear factor kappa-light-chain-enhancer of activated B cells, PI3K = phosphoinositide 3-kinase, RNA = ribonucleic acid, TGF = transforming growth factor, TNF = tumour necrosis factor.</p><p>Note:– Genes names are those assigned by the HUGO gene nomenclature committee.</p

    The 86-gene signature of tuberculosis is also seen in melioidosis.

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    <p>These heat maps demonstrate the gene expression profiles for two cohorts: (A) melioidosis and (B) tuberculosis. The 86 genes displayed are those identified by Berry <i>et al. </i><a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0054961#pone.0054961-Berry1" target="_blank">[7]</a> as being specific for tuberculosis, after excluding genes differentially regulated in other infections (<i>Staphylococcus aureus</i> and Group A Streptococcus) and inflammatory conditions (adult onset Still’s disease and systemic lupus erythematosus). Each column in the heat map is the gene expression profile of an individual, with control subjects on the left and patients on the right. Each cell within the heat map is the expression of a single gene: orange genes are upregulated and purple genes are downregulated, with expression normalized across the rows. We used this 86-gene signature to cluster study participants into two groups (marked black and red in the coloured banner at the top of each heat map). In the tuberculosis cohort, three controls clustered with the patients, and two patients clustered with the controls. In the melioidosis cohort, the same 86-gene signature also allowed us to distinguish controls and patients, with the exception of four patients who clustered with the controls. Despite the same microarray platform being used, the two cohorts were assayed as separate batches, so the absolute fluorescence intensities are different, making a direct comparison of melioidosis and tuberculosis impossible. All patients were therefore compared to their own controls.</p

    Patient characteristics.

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    a<p>One patient in this group was lost to follow-up following discharge from hospital, and was counted as having survived to discharge.</p><p>Gb = Glibenclamide. Values reported are means, except where stated.</p
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