22 research outputs found

    Hierarchical clustering of gene expression in alewives from the Atlantic (AO) and Lake Michigan (LM) populations.

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    <p>Red color reflects overexpression in LM and blue in AO (intermediate expression is in yellow; lack of expression – in white). A total of 621 genes differentially expressed, genes at 8-fold change were used and Euclidean distance metric with centroid (fast) linkage method was implemented.</p

    List of AO- and LM-specific SNPs.

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    i<p>Reference: <i>Danio rerio</i> CDS;</p>ii<p>Reference: <i>Osmerus mordax</i> CDS;</p>iii<p><i>Esox lucius</i> CDS;</p>iv<p>Reference: <i>Ictalurus punctatus</i> CDS;</p>v<p>G<i>allus gallus</i> (75% identity).</p

    Most populated GO classes (Molecular Function) in the transcriptome assembly.

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    <p>Most populated GO classes (Molecular Function) in the transcriptome assembly.</p

    An example of alignment with a group specific SNP (16S ribosomal RNA gene).

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    <p>An example of alignment with a group specific SNP (16S ribosomal RNA gene).</p

    Most differentially expressed genes between AO and LM (P-values are FDR-corrected).

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    <p>Most differentially expressed genes between AO and LM (P-values are FDR-corrected).</p

    Application of music therapy techniques in cognitive rehabilitation

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    Table listing the genotype fixed in both control group and desiccation group. (XLSX 2892 kb

    Modeling the Role of Peroxisome Proliferator-Activated Receptor γ and MicroRNA-146 in Mucosal Immune Responses to <em>Clostridium difficile</em>

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    <div><p><em>Clostridium difficile</em> is an anaerobic bacterium that has re-emerged as a facultative pathogen and can cause nosocomial diarrhea, colitis or even death. Peroxisome proliferator-activated receptor (PPAR) γ has been implicated in the prevention of inflammation in autoimmune and infectious diseases; however, its role in the immunoregulatory mechanisms modulating host responses to <em>C. difficile</em> and its toxins remains largely unknown. To characterize the role of PPARγ in <em>C. difficile</em>-associated disease (CDAD), immunity and gut pathology, we used a mouse model of <em>C. difficile</em> infection in wild-type and T cell-specific PPARγ null mice. The loss of PPARγ in T cells increased disease activity and colonic inflammatory lesions following <em>C. difficile</em> infection. Colonic expression of IL-17 was upregulated and IL-10 downregulated in colons of T cell-specific PPARγ null mice. Also, both the loss of PPARγ in T cells and <em>C. difficile</em> infection favored Th17 responses in spleen and colonic lamina propria of mice with CDAD. MicroRNA (miRNA)-sequencing analysis and RT-PCR validation indicated that miR-146b was significantly overexpressed and nuclear receptor co-activator 4 (NCOA4) suppressed in colons of <em>C. difficile</em>-infected mice. We next developed a computational model that predicts the upregulation of miR-146b, downregulation of the PPARγ co-activator NCOA4, and PPARγ, leading to upregulation of IL-17. Oral treatment of <em>C. difficile</em>-infected mice with the PPARγ agonist pioglitazone ameliorated colitis and suppressed pro-inflammatory gene expression. In conclusion, our data indicates that miRNA-146b and PPARγ activation may be implicated in the regulation of Th17 responses and colitis in <em>C. difficile</em>-infected mice.</p> </div