Isolated focal lesion in the splenium of the corpus callosum in a patient with acute viral hepatitis A

Mitochondrial dysfunction - Nm vs ctr - FDR5. (XLS 46 kb

Normalized expression profiles of the (A) miR-17-92 cluster and its (B) paralogs in five precursor B cell subsets in adults (solid lines) and children (dotted lines).

<p>All 10 microRNAs followed the same expression profile in both age groups and showed a near inverse pattern with age.</p

Principle component analysis (PCA) of regulated genes.

<p>The clustering represents the overall expression pattern of significantly regulated mRNAs at FDR 0.1% (p-value ≤1.13×10⁻⁴) in five subsets of precursor B cells. Color codes represent the various maturation stages as indicated under the plot. The Partek® Genomics Suite™ program draws the elipsoids encompassing the individual datapoints. Note the dots for the children (spheres) and adults (angular balls) are tightly grouped together.</p

MicroRNA profiles of precursor B cell subsets.

<p>Principle component analysis (PCA) showing the overall expression pattern of 17 microRNAs (18 assays) that were at least once differentially expressed between the various subsets (FDR 10%, p≤0,004). The color codes indicating differentiation stage (right) and age group (left) are explained below.</p

Functional analysis of 1796 differentially expressed mRNAs (FDR 0.1%, p-value≤1.13×10⁻⁴).

<p>Functional analysis of 1796 differentially expressed mRNAs (FDR 0.1%, p-value≤1.13×10⁻⁴).</p

Functional network of up-regulated mRNAs (red) and down-regulated (green) microRNAs during differentiation to PreBII large cells in adults.

<p>Note connection of miR-125b-5p to ID2 and involvement of the hematopoiesis related miR-181a-5p and miR-196a-5p, and the cell cycle regulating miR-24-3p. Note, all the coloured interacting partners in this network were detected in the present study.</p

Cell sorting of precursor B cells subsets from CD10 positively selected cells.

<p>Immunomagnetic selection and subsequent FACS were used to isolate the five populations from pediatric and adult human BM. Shown are the FACS dot plots with sorting gates to obtain CD34⁺CD19⁻ ProB cells, CD34⁺CD19⁺ PreBI cells, CD34⁻CD19⁺CD20^dim PreBII large cells, CD34⁻CD19⁺CD20⁻ PreBII small cells, and CD34⁻CD19⁺CD20^highIgM⁺ Immature B cells.</p

The human ABC transporter pseudogene family: Evidence for transcription and gene-pseudogene interference-4

%, 95%-CI: 65–73%) of the pseudogene transcript levels (lane 3). mRNA levels are normalized to β-actin (yellow bars) and cyclophilin B (blue bars). silencing is associated with a reduction of mRNA expression (84%, p = 0.003, 95%-CI: 76–91%, yellow bar; 82%, p = 0.01, 95%-CI: 72–93%, blue bar, lane 4). A positive control (knock-down of ) is shown (lane 2). Data were obtained from six independent experiments. The relative expression levels before knock-down experiments were set to 100% (lane 1).<p><b>Copyright information:</b></p><p>Taken from "The human ABC transporter pseudogene family: Evidence for transcription and gene-pseudogene interference"</p><p>http://www.biomedcentral.com/1471-2164/9/165</p><p>BMC Genomics 2008;9():165-165.</p><p>Published online 11 Apr 2008</p><p>PMCID:PMC2329642.</p><p></p

Large-scale reduction of tyrosine kinase activities in human monocytes stimulated <i>in vitro</i> with <i>N</i>. <i>meningitidis</i>

<div><p><i>N</i>. <i>meningitidis</i> induces extensive gene expression changes in human monocytes, suggesting that complex networks of signaling pathways are activated during meningococcal sepsis. These effects are modulated by the anti-inflammatory cytokine interleukin-10 (IL-10). To further study changes in signal transduction suggested by mRNA data, we used kinase substrate arrays to identify composite kinase activities induced by lysates from a primary human monocyte model system. Cell lysates were prepared from monocytes treated with the following experimental conditions: 10⁶ <i>N</i>. <i>meningitidis</i>/mL, 25 ng/mL IL-10, 10⁶ <i>N</i>. <i>meningitidis</i>/mL in combination with 25 ng/mL IL-10, and vehicle. Lysates were subjected to kinase activity profiling with Tyrosine Kinase PamChip® arrays containing 144 kinase peptide substrates. In our experimental model, we were not able to detect a statistically significant large-scale change in <i>ex vivo</i> array peptide phosphorylation by lysates from monocytes treated for 15 minutes. Targets of the IL-10 anti-inflammatory response were not identified. A profound inhibition of array peptide phosphorylation by monocytes treated for 60 minutes was identified, suggesting low activity of a large number of kinases associated with different signaling pathways and immune cell functions, including STAT3 activity, Nf-κB and VEGF signaling, and PTEN signaling activity. The peptide representing ZBTB16, which was reduced in phosphorylation by lysates from all three experimental conditions, was in Ingenuity Pathway Analysis identified to be linked to reduced cytokine release and mRNA levels of tumor necrosis factor (TNF), IL-6, and CXCL10. Further studies should investigate changes in tyrosine kinase-mediated signal transduction in human immune cells, in order to evaluate the potential clinical application of kinome profiling in the study of systemic inflammatory responses to pathogens.</p></div

The human ABC transporter pseudogene family: Evidence for transcription and gene-pseudogene interference-0

are the chromosomal localizations (colored arrows) of ABC transporter pseudogenes (right-hand side of each chromosome) and their parental protein-coding genes (left) in the human genome. Pairs of parental genes and pseudogenes are represented by the same arrow color code. Transcribed pseudogenes are green shaded. A close-up view of the ABC transporter pseudogene cluster (30 Mb) on chromosome 16p is shown at the bottom. Arrows indicate the 5'-> 3' orientation of the pseudogenes on chr. 16p and distances between adjacent pseudogenes are detailed (Mb). , and , respectively, represent pseudogenes for which functional counterparts have only been reported in rodents (Abca14, Abca15). The ideogram was generated using the ColoredChromosomes software [41].<p><b>Copyright information:</b></p><p>Taken from "The human ABC transporter pseudogene family: Evidence for transcription and gene-pseudogene interference"</p><p>http://www.biomedcentral.com/1471-2164/9/165</p><p>BMC Genomics 2008;9():165-165.</p><p>Published online 11 Apr 2008</p><p>PMCID:PMC2329642.</p><p></p