150 research outputs found

    Public Perceptions on National ID System in Japan

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    <p><b>A) Number of pathways differentially regulated in each transition in each brain region</b>. *Numbers in brackets indicate the number of pathways selectively differentially regulated in that region for a particular transition as compared to the other 2 brain regions. <b>B) Bar plot showing the number of pathways significantly differentially regulated per comparison (FDR < 0.01)</b>. WM = White Matter; FC = Frontal Cortex; BG = Basal Ganglia. Common pathways define pathways significant in at least 2 regions.</p

    Festlegung des Bemessungshochwassers für Anlagen des technischen Hochwasserschutzes

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    Immunoblot analysis of oligodendroglial and myelination markers. (A) Immunoblot analysis of the levels of MBP, CNPase and Olig2 in non-tg and MBP-α-syn tg mice treated with LV-control or LV-CD5-D5-ApoB, and vehicle or lenalidomide. Significant results of three mice per group are shown. (B) Densitometric analysis of the levels of MBP, CNPase and Olig2 in non-tg and MBP-α-syn tg mice treated with LV-control or LV-CD5-D5-ApoB, and vehicle or lenalidomide. Results are presented as average ± SEM. (TIF 1161 kb

    Pathways differentially regulated in multiple brain regions in patients infected with HIV without NCI as compared to uninfected controls.

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    <p>The table shows pathways dysregulated in at least 2 brain regions in patients infected with HIV without NCI compared to uninfected controls. The dataset was interrogated for pathway enrichment using the canonical pathways from the MSigDb C2 collection using GSEA. The GSEA pathway analysis results show gene expression changes involving significant immune activation and neuronal injury even in the absence of clinical NCI. NES: normalized enrichment score; FDR: false discovery rate; WM: White Matter; FC: Frontal Cortex; BG: Basal Ganglia.</p

    Genes differentially expressed in HIV-infected patients without NCI.

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    <p>The heatmap shows the genes in the leading edge of the pathways commonly dysregulated in all 3 brain regions in HIV-infected patients without NCI as compared to uninfected controls. We selected the 54 genes most differentially expressed (t-test, p-value < 0.01) among the list of 128 genes belonging to the leading edges of the significant pathways identified by the GSEA analysis in HIV-infected patients without NCI in comparison with uninfected controls.</p

    Differential regulation of IFN-related pathways in the groups of the NNTC gene expression dataset.

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    <p><b>A) Gene expression evidence of interferon (IFN) activation in HIV-infected patients without NCI</b>. The diagrams show GSEA plots for 3 pathways representative of IFN activation in HIV-infected patients without NCI (group B, left-hand side in the GSEA plot) as compared to uninfected controls (group A, right-hand side). Each pathway was tested in each region independently. WM = White Matter; FC = Frontal Cortex; BG = Basal Ganglia. These pathways are indicative of type I IFN activation and include IFN-related genes in Top) INTERFERON ALPHA BETA SIGNALING, Middle) type II IFN activation (INTERFERON GAMMA SIGNALING), and Bottom) ANTIGEN PRESENTATION FOLDING ASSEMBLY AND PEPTIDE LOADING OF MHC CLASS I, a pathway involving several IFN-regulated MHC class I genes. Significant changes in the expression of the pathways is indicated by the asymmetric distribution of the genes in the geneset (vertical bars) and of the running enrichment score plot (ES) (19). Genes participating in the enrichment (on the left of the leading edge corresponding to the peak of the running enrichment in GSEA) are shown in <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0175316#pone.0175316.g003" target="_blank">Fig 3</a>. B) Differential regulation of IFN-related pathways in the 4 groups of the NNTC gene expression dataset. Significant activation of pathways related to both type I and type II IFN was seen in a brain region-specific pattern in HIV-infected patients without NCI (group B) and in patients with HIVE (group D). Top) INTERFERON ALPHA BETA SIGNALING in the white matter, frontal cortex and basal ganglia; Middle) INTERFERON GAMMA SIGNALING; and Bottom) ANTIGEN PRESENTATION FOLDING ASSEMBLY AND PEPTIDE LOADING OF MHC CLASS I, in the same three regions. Each plot represents the pathway activity (computed as an enrichment score) in the 4 different phenotypes and is annotated with the FDR values of respective GSEA comparisons.</p

    White matter changes in HIV-infected patients with NCI without HIVE.

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    <p>GSEA plots representative of induction of cytokines, chemokines and β-defensins in HIV-infected patients with NCI without HIVE (group C in the NNTC gene expression dataset) as compared to uninfected controls.</p

    Evidence of neuronal injury in HIV-infected patients without NCI.

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    <p><b>A) and B)</b> Downregulation of genes related to neuronal transmission in patients with HIV without NCI (group B, left-hand side in the GSEA plot) vs. uninfected controls (Group A). <b>C)</b> Upregulation of apoptotic-related pathways in the frontal cortex and basal ganglia of HIV-infected patients without NCI (group B).</p

    ) Trypan Blue Exclusion assay for cell survival after 30 min of treatment with inhibitors LY294002, U0126, Bis I, or Gö6983 followed by treatment with FGF2 and/or gp120

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    <p><b>Copyright information:</b></p><p>Taken from "Signalling crosstalk in FGF2-mediated protection of endothelial cells from HIV-gp120"</p><p>BMC Neuroscience 2005;6():8-8.</p><p>Published online 2 Feb 2005</p><p>PMCID:PMC549045.</p><p>Copyright © 2005 Langford et al; licensee BioMed Central Ltd.</p> Trypan Blue Exclusion assay for cell survival after 30 min of treatment with the MEK inhibitor U0126 alone, and followed by exposure to gp120 and/or FGF2 for 24 h. In cells treated with FGF2 and anti-FGF2, HUVEC were exposed to anti-FGF2 antibody for 1 h followed by treatment with FGF2 alone or in combination with gp120. * Indicates a significant difference from control. * = P < 0.05 by One-Way ANOVA with post-hoc Dunnett's when compared to control

    Western blots showing ERK and GSK3β phosphorylation with gp120 alone (lane 2), and with inhibitors (lanes 3–6), FGF2 and gp120 (lane 2), and FGF2 with inhibitors and gp120 (lanes 3–6)

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    <p><b>Copyright information:</b></p><p>Taken from "Signalling crosstalk in FGF2-mediated protection of endothelial cells from HIV-gp120"</p><p>BMC Neuroscience 2005;6():8-8.</p><p>Published online 2 Feb 2005</p><p>PMCID:PMC549045.</p><p>Copyright © 2005 Langford et al; licensee BioMed Central Ltd.</p> Table summarizing data from western blots and showing changes in phosphorylation of ERK and GSK3β. ⇑ Indicates and increase, ⇓ indicates a decrease, – indicates no change

    Immunocomplex kinase assays for ERK and GSK3β activity without FGF2 treatment, or after inhibition with PD98059, U0126, LY29004, Bisindolymaleimide I or Gö6983 followed by FGF2 treatment

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    <p><b>Copyright information:</b></p><p>Taken from "Signalling crosstalk in FGF2-mediated protection of endothelial cells from HIV-gp120"</p><p>BMC Neuroscience 2005;6():8-8.</p><p>Published online 2 Feb 2005</p><p>PMCID:PMC549045.</p><p>Copyright © 2005 Langford et al; licensee BioMed Central Ltd.</p> Inhibitor treatment alone. () Summary of changes in phosphorylation (P) versus changes in activity (Act) of ERK and GSK3β. ⇑ Indicates an increase, ⇓ indicates a decrease, – indicates no change. * = P < 0.05 by One-Way ANOVA with post-hoc Dunnett's when compared to control
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