North American distribution of native (brown) and non-native (maroon and pink) ranges of alewife (<i>Alosa pseudoharengus</i>) along with the comparison of same-age individuals collected from freshwater Lake Michigan (A) and Atlantic Ocean (B).

<p>Arrows approximate sampling locations. Map is a courtesy of United States Geological Survey.</p

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

<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.

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.

<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).

<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).

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

Application of music therapy techniques in cognitive rehabilitation

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

Additional file 2: Figure S1. of Nucleotide diversity inflation as a genome-wide response to experimental lifespan extension in Drosophila melanogaster

Simulations of heterozygosity decrease under neutral evolution. (PNG 152 kb

Additional file 5: of Experimental evolution of recombination and crossover interference in Drosophila caused by directional selection for stress-related traits

Estimates of the coefficients of coincidence for non-adjacent intervals per replicate and entire variants (selection and control). (PDF 2103 kb

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

<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