Phantom images and corresponding spatial response functions.

<p>Images were reconstructed from k-space density weighted (A), Cartesian (B) and unfiltered Cartesian acquisition (C). Spatial response functions (D) were obtained from the edge spread functions indicated by the red bars.</p

Corresponding local activation maxima from second level fixed-effects (FE) analyses of the mean activation evoked by left-hand finger tapping as detected by density weighted and Cartesian EPI in n = 5 subjects.

<p>R … right, SMA … supplementary motor area, G. … gyrus.</p><p>x, y, z …MNI152 coordinates [mm].</p><p>t-stats … statistical t-values.</p>*<p>based on the Havard-Oxford Cortical Structural Atlas (part of FSL).</p

Second-level fixed-effects (FE) fMRI results - Differential contrast.

<p>(A) Revealing a cluster of significantly increased activation detected by k-space density weighted compared to conventional Cartesian EPI for left-hand finger tapping in n = 5 subjects (thresholded using clusters determined by Z>2.3 at a FWER-corrected p≤0.05 and displayed in MNI152 standard space). In the opposite, no areas of increased activation detected by Cartesian over density weighted EPI were found. (B) Time-courses within this cluster (extracted from raw data prior to further processing and averaged across n = 5 subjects) reveal increased percentual BOLD signal changes of density weighted compared to Cartesian EPI for each of the five blocks of the finger-tapping task.</p

Bland-Altman difference plots of quantitative parameter gains.

<p>Gains are plotted on a voxel-to-voxel basis for spatial SNR, temporal SNR and relative signal change (rSC; scaled to the mean Cartesian value) for density weighted (DW) over Cartesian (Cart) EPI in n = 5 subjects. Red solid lines represent the mean difference across voxels and subjects, red dashed lines ±1.96 × the standard deviation (SD; 95% limits of agreement for each comparison). The dotted gray line represents identity (no difference). Average increases in spatial SNR (12.4%, t = 15.68), temporal SNR (5.5%, t = 2.46) and rSC (8.6%, t = 2.63) were consistent and statistically significant (p<0.03125; based on mean within-subject differences). Gray data points and corresponding gray lines in the tSNR plot represent values of one additional subject measured at rest for comparison.</p

Representative slices of the brain of a healthy volunteer.

<p>Images are shown for k-space density weighted (A), Cartesian filtered (B), unfiltered density weighted (C) and unfiltered Cartesian reconstructions (D). Cartesian and density weighted images correspond well in geometry and contrast.</p

Second-level fixed-effects (FE) fMRI results - Mean activation.

<p>Evoked by left-hand finger tapping in n = 5 subjects as detected by density weighted (top) and Cartesian (bottom) EPI acquisitions (all thresholded using clusters determined by Z>2.3 at a FWER-corrected p≤0.05 and projected to the pial surface of the MNI152 template).</p

First-level fMRI results.

<p>Five consecutive slices of the statistical activation images thresholded using clusters (determined by Z>2.3 and a FWER-corrected p≤0.05) of the subject presented in Fig. 4 for the density weighted and the Cartesian acquisition.</p

Cartesian (A) and density weighted acquisition (B) for a typical fMRI experiment.

<p>The MTF (bottom, grey) results from a multiplication of the k-space density <i>ρ(k)</i> (blue, top) with the signal <i>S(k)</i> (green) and the filter <i>f(k)</i> (red).</p

Functional MRI for characterization of renal perfusion impairment and edema formation due to acute kidney injury in different mouse strains

<div><p>Purpose</p><p>The purpose was to characterize acute kidney injury (AKI) in C57BL/6 (B6)- and 129/Sv (Sv)-mice by noninvasive measurement of renal perfusion and tissue edema using functional MRI.</p><p>Methods</p><p>Different severities of AKI were induced in B6- and Sv-mice by renal ischemia reperfusion injury (IRI). Unilateral clamping of the renal pedicle for 35 min (moderate AKI) or 45 min (severe AKI) was done. MRI (7-Tesla) was performed 1, 7 and 28 days after surgery using a flow alternating inversion recovery (FAIR) arterial spin labeling (ASL) sequence. Maps of perfusion and T1-relaxation time were calculated. Relative MRI-parameters of the IRI kidney compared to the contralateral not-clipped kidney were compared between AKI severities and between mouse strains using unpaired t-tests. In addition, fibrosis was assessed by Masson Trichrome and collagen IV staining.</p><p>Results</p><p>After moderate AKI relative perfusion impairment was significantly higher in B6- than in Sv-mice at d7 (55±7% vs. 82±8%, p<0.05) and d28 (76±7% vs. 102±3%, p<0.01). T1-values increased in the early phase after AKI in both mouse strains. T1-increase was more severe after prolonged ischemia times of 45 min compared to 35 min in both mouse strains, measured in the renal cortex and outer stripe of outer medulla. Kidney volume loss (compared to the contralateral kidney) occurred already after 7 days but proceeded markedly towards 4 weeks in severe AKI. Early renal perfusion impairment was predictive for later kidney volume loss. The progression to chronic kidney disease (CKD) in the severe AKI model was similar in both mouse strains as revealed by histology.</p><p>Conclusion</p><p>Quantification of renal perfusion and tissue edema by functional MRI allows characterization of strain differences upon AKI. Renal perfusion impairment was stronger in B6- compared to Sv-animals following moderate AKI. Prolonged ischemia times were associated with more severe perfusion impairment and edema formation in the early phase and progression to CKD within 4 weeks of observation.</p></div

Correlation of MR-parameters on day 7 with histology (collagen IV- and IFTA-score).

<p>The correlation of MR-parameters (ASL in continuous line, T1-mapping in dotted line) on day 7 with scores from histology (collagen IV: upper panel, IFTA: lower panel) is shown for Sv- (left column) and B6-mice (right column).</p