Trace plots for the Gibbs sampler of the mixture model for T2-hypointensity segmentation of one randomly chosen subject.

<p>Components of (left) and of (right). See text for details.</p

Trace plots of the voxel-wise regression model.

<p>Precision parameters (left) and main effect of age for two selected voxels (right). Corresponding MNI coordinates are (top) and (bottom).</p

Segmentation of simulated T2-hypointensities.

<p>Manually delineated T2-hypointensities were added as an extra class to BrainWebs discrete anatomical model. This way, T1-weighted, T2-weighted and FLAIR images were simulated. Hypointensities were then segmented from the simulated images.</p

Effect of age on T2-hypointensity.

<p>Increasing T2-hypointensity with increasing age is projected onto the mean normalized FLAIR image. Axial slices are indicated in the upper row. Significance is color-coded according to the -value (Panels A and B) and posterior probability (Panel C) as indicated by the bars on the right. A–B) Results derived from the frequentist approach as implemented in SPM8 are shown after application of different statistical thresholds (Panel A, false-discovery rate 0.05; Panel B, uncorrected -value 0.05) and different smoothing kernels (upper rows, 4 mm; lower rows, 8 mm. C) Fully Bayesian inference could not only identify the globus pallidus, substantia nigra, and red nucleus but also the dentate nucleus. This result was largely independent of smoothing although more voxels were identified after smoothing with 4 mm.</p

Segmentation and normalization of T2-hypointensity.

<p>T2-weighted and FLAIR images are first coregistered to the T1-weighted images and then prepared for the segmentation of T2-hypointensities, which includes correction of T2-weighted and FLAIR images for magnetic field inhomogeneity by VBM8 and segmentation of T1-weighted images into the tissue classes of GM, WM, and CSF. These images are then used to segment hypointensities. The resulting T2-hypointensity images are normalized in two steps: First, T1-weighted images are affine normalized and respective parameters applied to FLAIR and T2-hypointensity images. Second, affine normalized T1-weighted and FLAIR images of all subjects are used to produce individual flow fields by DARTEL; these flow fiields are then applied to T2-hypointensity images.</p

Estimated regression coefficients of the simulated data.

<p>Posterior mean image for unsmoothed data of the approach proposed in this paper is shown in the upper left corner. Results of SPM's frequentist and Bayesian implementation are shown in the second and third column for unsmoothed (upper row) and smoothed (lower row) data, respectively. The true parameter image is shown in the lower left corner. The approach proposed in this paper performs best as demonstrated by the MSE and by visual inspection.</p

Time schedule of the treatments and investigations in the three types of experiments performed.

<p>OP, operation; MCAO, medial cerebral artery occlusion.</p

Effect of PPADS on the time course of EEG changes in the delta- and alpha-frequency bands caused by permanent MCAO of rats in four cortical regions up to day 28 after permanent MCAO.

<p>The delta-frequency band is shown in the left panel (<b>A</b>, <b>C</b>, <b>E</b>, <b>G</b>) and the alpha-frequency band in the right panel (<b>B</b>, <b>D</b>, <b>F</b>, <b>H</b>). The inset shows the placement of the four cortical electrodes and the reference electrode. The electrode P2 is located above the expected ischemic area indicated by grey shading, whereas the other electrodes are located above the contralateral parietal cortex (P1) and the respective frontal cortices (F2 and F1). Data are calculated as percental changes of the relative power from baseline measurements and expressed as means ± SEM. (ACSF: n = 7; PPADS: n = 8), * <i>P</i><0.05, ** <i>P</i><0.001 <i>vs.</i> MCAO/ACSF; + <i>P</i><0.05 <i>vs.</i> day 1, # <i>P</i><0.01 <i>vs.</i> basal.</p

Effect of PPADS on the extent of cell death measured at TUNEL-positive cells.

<p>(<b>Aa</b>) The brain slice shows the infarct area at the striatal level of the brain and the caudal and ventral areas in the penumbra counted for TUNEL-positive cells. An example for a cell with deep brown-labelled apoptotic bodies (arrow) is given (<b>Ab</b>; scale bar: 20 µm). Images of caudal areas at day seven after MCAO of TUNEL-immunostained brain slices from animals treated either with ACSF (<b>Ac</b>) or with PPADS (<b>Ad</b>). TUNEL-positive cells are indicated by arrows. (<b>B</b>) The pooled number of TUNEL-positive cells counted on striatal and hippocampal brain slices from animals treated either with ACSF or with PPADS is shown for day 1, day 7 and day 28. * <i>P</i><0.05 <i>vs.</i> MCAO/ACSF treated animals, + <i>P</i><0.05 <i>vs.</i> day 7. (<b>Ca–d</b>) Confocal images of double immunofluorescence to characterize TUNEL-positive cell bodies (yellow-green immunofluorescence) in degenerating neurons (<b>b</b>, red Cy3-immunofluorescence, MAP2-positive), and in astrocytes (<b>d</b>, red Cy3-immunofluorescence, GFAP-positive) in the periinfarct area, seven days after MCAO. The arrows indicate co-expression in the same cell (Scale bars: (a,b) = 20 µm; (c,d) = 10 µm).</p

Effect of PPADS on the infarct volume calculated at days one, seven and 28 after MCAO from volumetric image analysis of T2W MRI.

<p>Examples for the extension of the infarct area at day 7 after MCAO with ACSF and PPADS by T2W MRI (<b>A</b>). Volumes are expressed as means ± SEM (n = 8); * <i>P</i><0.05 <i>vs.</i> MCAO/ACSF (<b>B</b>). The infarct volumes are expressed as means ± SEM (n = 8 each), * <i>P</i><0.05 <i>vs.</i> MCAO/ACSF treated animals, + <i>P</i><0.05 <i>vs.</i> day 1.</p