The purpose of the study was to evaluate the effect of motion compensation by non-rigid registration combined with the Karhunen-Loeve Transform (KLT) filter on the signal to noise (SNR) and contrast-to-noise ratio (CNR) of hybrid gradient-echo echoplanar (GRE-EPI) first-pass myocardial perfusion imaging. Twenty one consecutive first-pass adenosine stress perfusion MR data sets interpreted positive for ischemia or infarction were processed by non-rigid Registration followed by KLT filtering. SNR and CNR were measured in abnormal and normal myocardium in unfiltered and KLT filtered images following nonrigid registration to compensate for respiratory and other motions. Image artifacts introduced by filtering in registered and nonregistered images were evaluated by two observers. There was a statistically sig- nificant increase in both SNR and CNR between normal and abnormal myocardium with KLT filtering (mean SNR increased by 62.18% ± 21.05% and mean CNR increased by 58.84% ± 18.06%; p = 0.01). Motion correction prior to KLT filtering reduced significantly the occurrence of filter induced artifacts (KLT only-artifacts in 42 out of 55 image series vs. registered plus KLT-artifacts in 3 out of 55 image series). In conclusion the combination of non-rigid registration and KLT filtering was shown to increase the SNR and CNR of GRE-EPI perfusion images. Subjective evaluation of image artifacts revealed that prior motion compensation significantly reduced the artifacts introduced by the KLT filtering process.
Maximal oxygen consumption (max) measured by cardiopulmonary exercise testing (CPX) is the gold standard for assessment of cardiorespiratory fitness. Likewise, cardiovascular magnetic resonance (CMR) is the gold standard for quantification of cardiac function. The combination of CPX and CMR may offer unique insights into cardiopulmonary pathophysiology; however, the MRI-compatible equipment needed to combine these tests has not been available to date. We sought to determine whether CPX testing in the MRI environment, using equipment modified for MRI yields results equivalent to those obtained in standard exercise physiology (EP) lab.
T2-Weighted (T2W) magnetic resonance imaging (MRI) pulse sequences have been used to detect edema in patients with acute myocardial infarction and differentiate acute from chronic infarction. T2W sequences have suffered from several problems including (i) signal intensity variability caused by phased array coils, (ii) high signal from slow moving ventricular chamber blood that can mimic and mask elevated T2 in sub-endocardial myocardium, (iii) motion artifacts, and (iv) the subjective nature of T2W image interpretation. In this work we demonstrate the advantages of a quantitative T2 mapping technique to accurately and reliably detect regions of edematous myocardial tissue without the limitations of qualitative T2W imaging.
T cells play a crucial role in atherosclerosis, with its infiltration preceding the formation of atheroma. However, how T-cell infiltration is regulated in atherosclerosis remains largely unknown. Here, this work demonstrates that dipeptidyl peptidase-4 (DPP4) is a novel regulator of T-cell motility in atherosclerosis. Single-cell ribonucleic acid (RNA) sequencing and flow cytometry show that CD4
Figure 1 A. Time course of exercise induced changes in the left calf muscles of a 30 year old male volunteer.Axial T1 (top row), T2 (middle row) and T2* (bottom row) maps acquired before exercise (Pre), immediately after exercise (Post 1), at ~20 minutes (Post 9) and at ~45 minutes (Post 18) are shown.B. Exercise-induced time course changes of mean T1 (a), mean T2 (b) and mean T2* values (c) of the four calf muscle groups in 24 volunteers before (Pre) and after exercise (Post_1 to 18 -~2:20 minute intervals).Graph in blue -TA, red -Sol, green -MG and purple -LG.
This study seeks to investigate changes in iron homeostasis and carotid arteries in women at risk of atherosclerosis, addressing a relatively unexplored hypothesis explaining why women have a 5-10 year lag in initial atherosclerotic events. Recent evidence points to hepcidin, the key regulator of macrophage iron uptake and release, as a potential mediator of risk. Furthermore, iron catalyzes the generation of free radicals that oxidize cholesterol stimulating atheroma formation. Magnetic resonance imaging (MRI) is ideally suited to study iron because of iron's local effects on magnetic susceptibility that can be quantified using a relaxation parameter called T2* ('T2-star'), as well as the ability to noninvasively characterize and quantify atherosclerotic plaque with MRI. This work outlines the rationale and study design to provide critical evidence related to the iron hypothesis, such that novel diagnostics and therapeutics to attenuate risk may be derived from a better understanding of iron's role in atherosclerosis.
To evaluate the role of early-life exposure to airborne fine particulate matter (diameter, <2.5 μm [PM(2.5)]) pollution on metabolic parameters, inflammation, and adiposity; and to investigate the involvement of oxidative stress pathways in the development of metabolic abnormalities.PM(2.5) inhalation exposure (6 h/d, 5 d/wk) was performed in C57BL/6 mice (wild type) and mice deficient in the cytosolic subunit of the nicotinamide adenine dinucleotide phosphate (NADPH) oxidase p47(phox) (p47(phox-/-)) beginning at the age of 3 weeks for a duration of 10 weeks. Both groups were simultaneously fed a normal diet or a high-fat diet for 10 weeks. PM(2.5)-exposed C57BL/6 mice fed a normal diet exhibited metabolic abnormalities after exposure to PM(2.5) or FA for 10 weeks. Consistent with insulin resistance, these abnormalities included enlarged subcutaneous and visceral fat contents, increased macrophage infiltration in visceral adipose tissue, and vascular dysfunction. Ex vivo-labeled and infused monocytes demonstrated increased adherence in the microcirculation of normal diet- or high-fat diet-fed PM(2.5)-exposed mice. p47(phox-/-) mice exhibited an improvement in parameters of insulin resistance, vascular function, and visceral inflammation in response to PM(2.5).Early-life exposure to high levels of PM(2.5) is a risk factor for subsequent development of insulin resistance, adiposity, and inflammation. Reactive oxygen species generation by NADPH oxidase appears to mediate this risk.
Although many methods already exist to map T 1 , T 2 and M 0 , these often involve special sequences not readily available on clinical scanners and/or may require long scan times. In contrast, the proposed method can run on most scanners, it offers flexible tradeoffs between scan time and image quality, and it generates spatially-aligned parameter maps. Validation was performed in gel phantoms with varying concentrations of contrast agents, and in vivo examples are presented from three neuroradiology patients. Compared to other quantitative mapping methods, the present method is meant to stand out in terms of its practicality and availability.
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