Orta, the aortic arch and onward through the aorta’s principal branches leading to progressive arterial stiffness [4]. These anatomical positions have one common theme; low and oscillatory (multi- or bidirectional) flow patterns, implying that plaque detection 
may be hampered by alterations in blood flow [32]. Proper visualization and quantification of atherosclerotic plaque components in both patients and animal models usually relies heavily on black-blood or bright-blood techniques with saturation slices or double inversion recovery methods [33,34]. However, the required steady state blood saturation can be difficult to maintain in ECG-triggered sequences [18] especially in animal models. In the aortic arch, the prime site of plaque development, and carotid arteries assessment of plaques and vessel wall area becomes even more difficult, because of its proximity to the beating heart which may cause large motion artifacts on top of flow artifacts. Classically, synchronization with the heart cycle, or prospective gating, is done using respiratory and ECG sensors to generate triggering signals [35]. In hemodynamically unstable animals, one needs to monitor the R-R interval closely, or choose this interval conservatively, which means that the total scan time will be longerConclusionWe have shown that retrospectively gated CINE MRI can be used to detect plaque burden and aortic distensibility simultaMRI of Plaque Burden and Vessel Wall Stiffnessneously. Because the method can be used for both black-blood and bright-blood contrast, it is suitable for both gadolinium- and iron oxide based contrast agents. We have shown that in the ApoE2/2 mouse there is a high correlation between aortic stiffness, and plaque load, and both measures can be used to assess atherosclerotic plaque progression and therapeutic interventions.end-systole and end-diastole for 5, 8, 12, 15, 20 and 40 reconstructed cardiac movie frames compared to 10 movie frames. *P,0.05 compared to 10 movie frames. (TIF)Figure S3 Anatomical positioning in the aortic arch. A. Depiction of the BIBS39 position (in green) in the aortic where frames were taken orthogonal to the aortic arch. B. purchase Fexinidazole Schematical depiction of determination of the diameter of the aortic arch using circular cross-sections only. (TIF)Supporting 
InformationFigure S1 Time course of micelles and USPIO. A. Time course of Gd-micelle accumulation in the inner curvature of the aortic arch of ApoE2/2 mice. Contrast to Noise Ratios (CNR) were determined at different time points after intravenous injection of n = 8 mice. B. CNR determined at different time points after USPIO injection in the inner curvature of the aortic arch of n = 8 mice. (TIF) Figure S2 Diameter measurements with different numbers of movie frames. Aortic arch diameter measurements atAuthor ContributionsConceived and designed the experiments: BdA LMvdG GJS HL REP LvdW. Performed the experiments: BdA LMvdG LvdW. Analyzed the data: BdA LMvdG GJS REP LvdW. Contributed reagents/materials/ analysis tools: BdA LMvdG GJS REP LvdW. Wrote the paper: BdA GJS HJL REP LvdW.
Activated T cells and the cytokines they produce are thought to drive the pathogenesis of psoriasis [1]. Cytokines secreted by CD4+ T cells stimulate keratinocytes to proliferate and recruit inflammatory cells into the skin, promoting epidermal hyperplasia and inflammation. Because CD4+ T cells producing the T helper cell type 1 (Th1) cytokine IFN-c are present in large numbers within psoriatic plaques [2], T.Orta, the aortic arch and onward through the aorta’s principal branches leading to progressive arterial stiffness [4]. These anatomical positions have one common theme; low and oscillatory (multi- or bidirectional) flow patterns, implying that plaque detection may be hampered by alterations in blood flow [32]. Proper visualization and quantification of atherosclerotic plaque components in both patients and animal models usually relies heavily on black-blood or bright-blood techniques with saturation slices or double inversion recovery methods [33,34]. However, the required steady state blood saturation can be difficult to maintain in ECG-triggered sequences [18] especially in animal models. In the aortic arch, the prime site of plaque development, and carotid arteries assessment of plaques and vessel wall area becomes even more difficult, because of its proximity to the beating heart which may cause large motion artifacts on top of flow artifacts. Classically, synchronization with the heart cycle, or prospective gating, is done using respiratory and ECG sensors to generate triggering signals [35]. In hemodynamically unstable animals, one needs to monitor the R-R interval closely, or choose this interval conservatively, which means that the total scan time will be longerConclusionWe have shown that retrospectively gated CINE MRI can be used to detect plaque burden and aortic distensibility simultaMRI of Plaque Burden and Vessel Wall Stiffnessneously. Because the method can be used for both black-blood and bright-blood contrast, it is suitable for both gadolinium- and iron oxide based contrast agents. We have shown that in the ApoE2/2 mouse there is a high correlation between aortic stiffness, and plaque load, and both measures can be used to assess atherosclerotic plaque progression and therapeutic interventions.end-systole and end-diastole for 5, 8, 12, 15, 20 and 40 reconstructed cardiac movie frames compared to 10 movie frames. *P,0.05 compared to 10 movie frames. (TIF)Figure S3 Anatomical positioning in the aortic arch. A. Depiction of the position (in green) in the aortic where frames were taken orthogonal to the aortic arch. B. Schematical depiction of determination of the diameter of the aortic arch using circular cross-sections only. (TIF)Supporting InformationFigure S1 Time course of micelles and USPIO. A. Time course of Gd-micelle accumulation in the inner curvature of the aortic arch of ApoE2/2 mice. Contrast to Noise Ratios (CNR) were determined at different time points after intravenous injection of n = 8 mice. B. CNR determined at different time points after USPIO injection in the inner curvature of the aortic arch of n = 8 mice. (TIF) Figure S2 Diameter measurements with different numbers of movie frames. Aortic arch diameter measurements atAuthor ContributionsConceived and designed the experiments: BdA LMvdG GJS HL REP LvdW. Performed the experiments: BdA LMvdG LvdW. Analyzed the data: BdA LMvdG GJS REP LvdW. Contributed reagents/materials/ analysis tools: BdA LMvdG GJS REP LvdW. Wrote the paper: BdA GJS HJL REP LvdW.
Activated T cells and the cytokines they produce are thought to drive the pathogenesis of psoriasis [1]. Cytokines secreted by CD4+ T cells stimulate keratinocytes to proliferate and recruit inflammatory cells into the skin, promoting epidermal hyperplasia and inflammation. Because CD4+ T cells producing the T helper cell type 1 (Th1) cytokine IFN-c are present in large numbers within psoriatic plaques [2], T.
