Spatial activation maps and time courses of the GE and SE HRF upon short visual stimulation.

<p>A) Percent signal change (PSC) map of the visual cortex V1 for the GE (top) and SE (bottom) HRF data with isotropic voxel sizes of 1 mm and 2 mm, respectively. As expected the SE contrast shows reduced sensitivity. B) Closer examination of the cortical surface and pial vasculature on the 0.5 mm T2*-weighted anatomical scan. The cortical surface (white) was manually delineated in 3D and from this surface the cortical depth profiles were computed: black; 0–1 mm, red; 1–2 mm, and green; 2–3 mm. The high-resolution T2*-weighted scan was also used to identify the larger pial draining veins, which were excluded from the GE BOLD analysis. C) GE HRFs across cortical depth (0–1, 1–2, and 2–3 mm) and the SE HRF for a representative subject (subject 4 as indicated in <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0054560#pone-0054560-t001" target="_blank">Table 1</a>). As the GE and SE BOLD do not measure from the exact same vasculature there should be no exact spatial match in their activation patterns from the functional localizer. We therefore focused on the temporal evolution of the estimated HRFs, with the following parameters of interest: onset time, time-to-peak (TTP), full-width-at-half-maximum (FWHM), and maximum percent signal change (PSC). Onset times of the SE and GE HRF in deep gray matter (>1 mm cortical depth) are very comparable while the FWHM and TTP are increased for the GE HRF for all cortical depths indicating that the earlier part of deep gray matter GE HRF is weighted toward microvascular dynamics. Shaded areas denote the standard error of the mean (SEM). The black bar indicates the stimulus onset and duration (250 ms).</p

Box plot of the temporal HRF properties of the GE HRF across the cortical depth and SE HRF across all subjects.

<p>A) Onset time (s), B) TTP (s) C) FWHM (s), and D) PSC (%). Comparing the SE HRF with surface gray matter GE HRF (0–1 mm cortical depth) shows that all temporal properties are significantly increased (P<0.01, Wilcoxon signed–rank test). This indicates that the surface gray matter GE contrast probes a different part of the vascular system upon activation than the SE contrast. Surface gray matter in V1 contains mainly postcapillary veins (diameters ∼70 μm) and much less capillaries (diameters ∼5 μm) than deep gray matter regions <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0054560#pone.0054560-Duvernoy1" target="_blank">[20]</a>. Looking at the deep gray matter GE HRFs (>1 mm cortical depth) and the SE HRF we found that the TTP, FWHM and PSC were all significantly increased for the GE HRF. The onset times, however, did not differ significantly. These findings suggest that the earlier part of the deep gray matter GE HRF is in close correspondence to the SE HRF and hence is weighted towards the microvasculature. ^*** denotes significant difference between the two compartments (Wilcoxon signed–rank test for P<0.01, ** for P<0.05, * for P<0.1).</p

Mean number and range of perforating branches per parent artery identified in the 7T postcontrast TOF-MRA images.

<p>^aIn one patient the posterior communicating artery was absent bilaterally.</p><p>^bOnly scans containing this segment within the FOV were taken into account.</p><p>Mean number and range of perforating branches per parent artery identified in the 7T postcontrast TOF-MRA images.</p

7T TOF-MRA MIP images of different intracranial perforating arteries.

<p><b>On the left (A,C,E) the precontrast images with the corresponding postcontrast images of the same patient on the right (B,D,F)</b>. In B, D and F, longer arterial trajectories can be seen after contrast administration as compared to the corresponding unenhanced image in A, C and E (white boxes). (A and B) Sagittal slab MIP, thickness 10mm; (B and C) sagittal slab MIP, thickness 10mm; (E and F) coronal slab MIP, thickness 10mm. MIP = maximum intensity projection.</p

Typical images of intracranial perforators from different patients, obtained by postcontrast TOF-MRA at 7T.

<p>(A) A medial lenticulostriate artery (arrowhead), arising from the A1 segment of the ACA (transverse slab MIP, thickness 10mm), (B) lateral lenticulostriate arteries arising from the right MCA (arrows) and medial lenticulostriate arteries arising from the left ACA (arrowheads; coronal slab MIP, thickness 10 mm), (C) artery of Percheron (arrowheads), arising from the P1 segment of the PCA (coronal slab MIP, thickness 10mm), (D) perforating branch (arrowheads) arising from the right AChA (sagittal slab MIP, thickness 10mm), (E) thalamoperforating artery (arrowhead), arising from the left PCoA (transverse slab MIP, thickness 6mm), (F) pontine arteries (arrowheads) arising from the BA (transverse slab MIP, thickness 4mm), and (G) the intracranial feeders of the anterior spinal artery (arrows) with an adjacent vein (dashed arrow, transverse slab MIP angulated anterior-posterior in line with the BA, thickness 10mm). ACA = anterior cerebral artery; AChA = anterior choroidal artery; BA = basilar artery; ICA = intracranial carotid artery; MCA = middle cerebral artery; MIP = maximum intensity projection; PCA = posterior cerebral artery; PCoA = posterior communicating artery; P1 = first segment of the PCA; VA = vertebral artery.</p

Relative infarct size determined from histology compared to MRI.

<p>(A) Long axis cross sections through <i>ex vivo</i> ΔUTE images in post-MI mouse hearts obtained from subtraction of a long-TE (4 ms) from a short-TE (21 μs) T2*-weighted image. The left panels show a post-MI heart 2 days after surgery. The right panels show a post-MI heart with a chronic MI 7 days after surgery. A positive contrast is observed in the ΔUTE image, which corresponds to the location of the chronic MI. Corresponding Picrosirius red stained slices showed hardly any collagen in the MI heart 2 days after surgery, whereas excessive replacement fibrosis was present (arrows) in the chronic MI. (B) Correlation between the infarct size as percentage of the total heart volume determined from histology and the <i>ex vivo</i> ΔUTE images of control (n = 3) and MI hearts (n = 8). The solid line is a linear fit.</p

Three-component model fit parameters of UTE signal intensity as function of TE.

<p>Listed parameters are: n = number of mice, fractions of the fast (I_fast), slow (I_slow) and lipid (I_lipid) pool, and the T2*_fast (μs) and T2*_slow (ms) for control hearts, infarct and remote tissue in post-MI hearts, and the TAC hearts. Indicated are:</p><p>* (<i>P</i><0.05)</p><p>† (<i>P</i><0.01)</p><p>‡(<i>P</i><0.001) of the TAC hearts or the remote tissue in post-MI hearts as compared to the control hearts, or between the infarct core and remote tissue in post-MI hearts. The change of T2*_slow in remote tissue of post-MI hearts, as compared to control hearts, did not reach statistical significance (<i>P</i> = 0.09, respectively), so as the change of T2*_slow in TAC hearts as compared to control hearts (<i>P</i> = 0.18).</p><p>Three-component model fit parameters of UTE signal intensity as function of TE.</p

T2*-weighted MR images of a post-MI mouse heart.

<p>Two short-axis and long-axis cross-sections through an <i>in vivo</i> T2*-weighted dataset (TE = 21 μs) of a post-MI mouse heart. Indicated are the right ventricle (RV), left ventricle (LV), the papillary muscles (PM) and some small artefacts (↖). A dark saturation band with low signal intensity is visible in the two long-axis images.</p

<i>In vivo</i> signal difference between long and short-TE.

<p><i>In vivo</i> signal difference between long and short-TE, in control, post-MI and TAC mouse hearts. The signal difference between the short-TE (21 μs) and long-TE images (1.429 ms) is larger for remote and infarct tissue in post-MI hearts, and in TAC hearts, compared to control hearts. * (<i>P</i><0.05) and † (<i>P</i><0.01). Error bars indicate SD.</p

<i>Ex vivo</i> and <i>in vivo</i> signal intensity time curves.

<p>Representative ROI-based T2*-weighted signal intensity curves as a function of echo time (TE) for <i>ex vivo</i> (top row) and <i>in vivo</i> (bottom row) measurements in control hearts, remote tissue and infarct area of the post-MI hearts and the TAC hearts, together with the corresponding model fit (gray line, top row) and lines to guide the eye (bottom row). Signal intensities were normalized to the signal intensity at TE = 21 μs.</p