Brain regions activated or deactivated by working memory task performance.

<p>Anatomical locations of maximal test statistics are specified in {x,y,z} coordinates (mm) in the stereotactic system of the MNI template image and the number of supra-threshold voxels comprising the 4 most significant clusters designated as activated regions and deactivated regions.</p

Task-activated brain regions and the recovery of fractal scaling of endogenous oscillations after task performance.

<p>(a) Within-group map of activated (red) and deactivated (blue) regions from a contrast of <i>n</i>-back versus zero-back (control) trials of the working memory task. Axial slice locations are in mm coordinates of the MNI stereotaxic template. The left of the image is the right of the brain. Threshold for significance was at the cluster level and set such that one false-positive cluster was expected under the null hypothesis (equivalent p = 3.6×10⁻³). (b–e) Post-task recovery of fractal scaling (Δ<i>H</i>) for low and high working memory loads, extracted from activated regions clusters 1–3 and deactivated regions cluster 1 (see <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0006626#pone-0006626-t001" target="_blank">table 1</a> for anatomical description). Error bars are between-subject standard deviations. Note that in the immediate post-task period, values of <i>H</i> were lower than before task performance, indicating a relative loss of long-range autocorrelations or long memory properties in the endogenous dynamics. Endogenous dynamics tended to recover their pre-task parameter values quite slowly over the course of several minutes following completion of the task and the rate of recovery was faster following completion of the less demanding version of the working memory task.</p

Summary of experimental paradigm.

<p>Summary of experimental paradigm.</p

Immunofluorescent staining of primary cortical neurons.

<p>A: p65 expression in primary cortical neurons, showing increased expression with TNF-α and decreased expression with IKK Inhibitor (F = 177.79; p<0.001; df = 2,12). B: NF-κ B expression in a control neuron, using anti-p65 antibody and FITC labelled secondary, NF-κ B expression in a TNF-α stimulated neuron and NF-κ B expression in a TNF-α stimulated neuron with NF-κ B inhibitor. C: The percentage of neurons with anti-p65 staining in the nucleus (F = 30.63; p<0.001; df = 2,14), and D: the levels of fluorescence in each sample where fluorescence is rated between 0 and 3 on the scale bar (F = 17.65; p<0.002; df = 2,57). Molecular weight markers are in kilodaltons (kDa).</p

Quantification of inflammation induced by TNF-α.

<p>Tissue inflammation in Control (Ctrl), 10 ng/ml TNF-α (TNF), TNF-α with IKK Inhibitor (IKK), and TNF-α with sodium salicylate samples (Sodium S). A–C: Measurements at 24, 48, 72 and 96 hour periods in A: frontal lobe, B: temporal region, and C: cerebellum. Data is significant after 24 hours of stimulation. Results are presented as a percentage increase of original value (F = 816.22; p<0.001; df = 3,96). D–F: Confirmation of inflammation with hematoxylin and eosin (H&E) stain. Tissue stimulated with TNF-α 10 ng/ml in frontal lobe (D), temporal region (E) and cerebellum (F). Calibration bars are 50 µm.</p

Quantification of inflammation induced by TNF-α.

<p>Tissue inflammation in Control (Ctrl), 10 ng/ml TNF-α (TNF), TNF-α with IKK Inhibitor (IKK), and TNF-α with sodium salicylate samples (Sodium S). A–C: Measurements at 0.5, 1 and 2 hours stimulation and after TNF-α removal (3 and 4 hours). Results are presented as for <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0039049#pone-0039049-g001" target="_blank">figure 1</a>, data is significant after 2 hours of stimulation (F = 22.53; p = 0.001; df = 3,96). D-F: Plot of % volumetric increase of tissue vs. normalized overall expression of NF-κB p65 from quantification of Western blot samples with a superimposed line of linear regression.</p

Procedural details of volumetric measurements.

<p>Procedural details of volumetric measurements.</p

Additional file 1: of Atypical lateralization of motor circuit functional connectivity in children with autism is associated with motor deficits

Group differences in LIs of individual DMN connections and group differences in LIs of individual visual network connections. (DOCX 83 kb

Resting perfusion map acquired from a single participant, shown in radiological orientation (scale: 0–90 ml/min/100ml).

<p>Resting perfusion map acquired from a single participant, shown in radiological orientation (scale: 0–90 ml/min/100ml).</p

Women show higher perfusion than men and DHEAS correlates negatively with perfusion.

<p>a) Sex difference in whole brain grey matter perfusion: perfusion is higher in women (<i>M</i> = 35.97 ml/min/100 ml, <i>SD</i> = 5.37) than in men (<i>M</i> = 30.47 ml/min/100 ml, <i>SD</i> = 5.91, <i>p</i> = .006). Single dots represent the subjects' individual values. The horizontal line within the boxes indicate medians, the edges of the boxes are the 25^th and 75^th percentiles, and the whiskers represent 1.5 times the interquartile range. b) Sex difference (women > men) in regional perfusion: women show higher regional perfusion than men (<i>p</i> = .004, FWE-corrected). c) Simple regression analysis with whole brain perfusion values as the dependent variable and DHEAS as the only predictor: a significant model was found (<i>p</i> = .007, adjusted <i>R</i>^<i>2</i> = .180) with a standardised β = -.452 for DHEAS. d) DHEAS effects in men and women: DHEAS correlates negatively with regional perfusion in both sexes (<i>p</i> = .004, FWE-corrected). Colour bar in a) and c) denotes a non-parametric <i>t</i> score, given by <i>a1</i>/[standard error(<i>a1</i>)], see <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0135827#sec002" target="_blank">methods</a>. Images are shown in neurological orientation. Slices are at MNI z-coordinates -45, -30, -15, 0, 15, 30, 45, 60, 75 (from top left to bottom right).</p