DC-LAMP is a membrane bound protein produced by mature activated dendritic cells, while BDCA2 is an antigen produced by immature plasmacytoid dendritic cells (both markers are stained dark brown)

Long disease duration JDM patients displayed a greater overall presence of mature dendritic cells (A) compared to short disease duration JDM patients (C). Greater concentrations of mature dendritic cells were found in perivascular and perifasicular regions compared with the endomysium. Many mature dendritic cells co-expressed plasmacytoid markers (A, B). No substantiated differences were found in the distribution of the BDCA2 positive plasmacytoid dendritic cells in JDM of either long or short disease duration (B, D). Normal pediatric muscle displayed an absence of mature dendritic cells with presence of BDCA2 positive cells (E). Images were taken at 10× on a Leica Upright Light Microscope. Scale bars represent 10 μm.<p><b>Copyright information:</b></p><p>Taken from "Duration of chronic inflammation alters gene expression in muscle from untreated girls with juvenile dermatomyositis"</p><p>http://www.biomedcentral.com/1471-2172/9/43</p><p>BMC Immunology 2008;9():43-43.</p><p>Published online 31 Jul 2008</p><p>PMCID:PMC2529263.</p><p></p

Hematoxylin and eosin (H & E) evaluation of skeletal muscle.

<p>H&E staining was carried out to assess the effect of treatment on inflammation (<b>A</b>), central nucleation (<b>B</b>), and fibers with central nucleation (<b>C</b>). Inflammatory cells were quantified in five non-overlapping fields in gastrocnemius muscle. <i>mdx</i> mice received no treatment (N = 4, 15, and 15) or GC treatment (N = 4, 18, and 16) for 50, 100, or 180 days, respectively. Error bars indicate mean+/- SEM. * p  =  <0.05 and ** p  =  <0.01.</p

Weight of muscles and spleen in untreated and GC-treated mice.

<p>Weight of muscles and spleen in untreated and GC-treated mice.</p

Figure 3

<p><b>Effect of treatments on cardiac function and fibrosis.</b> (<b>A</b>) Ejection fraction (%) and (<b>B</b>) shortening fraction (%) were assessed by echocardiography in mice who received no treatment (N = 30, 21) or GC treatment (N = 25, 19) for 100 or 180 days, respectively. (<b>C</b>) Sirius Red staining of formalin-fixed heart sections was used to estimate collagen content. <i>mdx</i> mice received no treatment (N = 12, 13) or GC treatment (N = 11, 14) for 100 or 180 days, respectively. Error bars indicate mean +/- SEM. **p  = <0.01 and ***p  = <0.001.</p

Figure 1

<p><b>Effect of treatments on body weight.</b> (<b>A</b>) <i>mdx</i> mice received no treatment (N = 84, 83, and 44) or GC treatment (N = 92, 89, and 38) for 50, 100, or 180 days, respectively, *** p = <0.001. (<b>B</b>) Comparison of the % rate change in body weight of untreated and GC-treated mice at 50, 100, and 180 days. The rate at which body weight changed was established in the first 50 days, when the change occurred in the untreated mice at a much faster rate (<0.0001). The rate remained greater than that for the treated mice, but the change over time was the same for both groups. Error bars indicate mean+/- SEM.</p

Grip strength, motor, and behavioral measurements in untreated and GC-treated mice

*<p>Analyzed using quantile regression due to non-normality</p>**<p>Data transformed to conform to normality (total distance, move time, CK level, and cardiac fibrosis were log transformed; EDL weight was square transformed)</p><p>#Significantly different p values for treatment groups</p

Additional file 12: of Proteomic analysis of Medulloblastoma reveals functional biology with translational potential

Figure S8. Expression of HMAG1 isoforms in medulloblastoma tumors. a) Schematic representation of HMGA11 isoforms and Boxplots representing the mRNA expression levels for HMGA1 isoforms. b). Western blot of HMGA1 isoforms in the four medulloblastoma subgroups. Both HMAG1 isoforms are highly expressed in group 3 medulloblastoma. c) Kaplan–Meier survival curve shows that increased levels of HMGA1 are associated with poor survival in Group 3 Medulloblastoma. d) Expression level of HMGA1 is highly correlated with the expression of the oncogene MYC in Group 3 Medulloblastoma. (PDF 1.94 mb

Effect of treatment on open field behavioral (locomotor) activity.

<p>Legend:</p><p>HACTV = total horizontal activity; TOTDIST = total movement distance; MOVTIME = total movement time; RESTIME = total rest time; VACTV = total vertical activity.</p

Non-Invasive MRI and Spectroscopy of <i>mdx</i> Mice Reveal Temporal Changes in Dystrophic Muscle Imaging and in Energy Deficits

<div><p>In Duchenne muscular dystrophy (DMD), a genetic disruption of dystrophin protein expression results in repeated muscle injury and chronic inflammation. Magnetic resonance imaging shows promise as a surrogate outcome measure in both DMD and rehabilitation medicine that is capable of predicting clinical benefit years in advance of functional outcome measures. The <i>mdx</i> mouse reproduces the dystrophin deficiency that causes DMD and is routinely used for preclinical drug testing. There is a need to develop sensitive, non-invasive outcome measures in the <i>mdx</i> model that can be readily translatable to human clinical trials. Here we report the use of magnetic resonance imaging and spectroscopy techniques for the non-invasive monitoring of muscle damage in <i>mdx</i> mice. Using these techniques, we studied dystrophic <i>mdx</i> muscle in mice from 6 to 12 weeks of age, examining both the peak disease phase and natural recovery phase of the <i>mdx</i> disease course. T2 and fat-suppressed imaging revealed significant levels of tissue with elevated signal intensity in <i>mdx</i> hindlimb muscles at all ages; spectroscopy revealed a significant deficiency of energy metabolites in 6-week-old <i>mdx</i> mice. As the <i>mdx</i> mice progressed from the peak disease stage to the recovery stage of disease, each of these phenotypes was either eliminated or reduced, and the cross-sectional area of the <i>mdx</i> muscle was significantly increased when compared to that of wild-type mice. Histology indicates that hyper-intense MRI foci correspond to areas of dystrophic lesions containing inflammation as well as regenerating, degenerating and hypertrophied myofibers. Statistical sample size calculations provide several robust measures with the ability to detect intervention effects using small numbers of animals. These data establish a framework for further imaging or preclinical studies, and they support the development of MRI as a sensitive, non-invasive outcome measure for muscular dystrophy.</p></div

Statistical sample size calculations to detect intervention effects in <i>mdx</i> mice.

<p><i>Abbreviations:</i> NMR Spec, Nuclear Magnetic Resonance spectroscopy; PCr, phosphocreatine; tATP, total adenosine triphosphate; Vol., Volume; WT, wild-type.</p><p>Statistical sample size calculations to detect intervention effects in <i>mdx</i> mice.</p