266 research outputs found
Free and smooth boundaries in 2-D finite-difference schemes for transient elastic waves
A method is proposed for accurately describing arbitrary-shaped free
boundaries in single-grid finite-difference schemes for elastodynamics, in a
time-domain velocity-stress framework. The basic idea is as follows: fictitious
values of the solution are built in vacuum, and injected into the numerical
integration scheme near boundaries. The most original feature of this method is
the way in which these fictitious values are calculated. They are based on
boundary conditions and compatibility conditions satisfied by the successive
spatial derivatives of the solution, up to a given order that depends on the
spatial accuracy of the integration scheme adopted. Since the work is mostly
done during the preprocessing step, the extra computational cost is negligible.
Stress-free conditions can be designed at any arbitrary order without any
numerical instability, as numerically checked. Using 10 grid nodes per minimal
S-wavelength with a propagation distance of 50 wavelengths yields highly
accurate results. With 5 grid nodes per minimal S-wavelength, the solution is
less accurate but still acceptable. A subcell resolution of the boundary inside
the Cartesian meshing is obtained, and the spurious diffractions induced by
staircase descriptions of boundaries are avoided. Contrary to what occurs with
the vacuum method, the quality of the numerical solution obtained with this
method is almost independent of the angle between the free boundary and the
Cartesian meshing.Comment: accepted and to be published in Geophys. J. In
Subendocardial contractile impairment in chronic ischemic myocardium: assessment by strain analysis of 3T tagged CMR
<p>Abstract</p> <p>Background</p> <p>The purpose of this study was to quantify myocardial strain on the subendocardial and epicardial layers of the left ventricle (LV) using tagged cardiovascular magnetic resonance (CMR) and to investigate the transmural degree of contractile impairment in the chronic ischemic myocardium.</p> <p>Methods</p> <p>3T tagged CMR was performed at rest in 12 patients with severe coronary artery disease who had been scheduled for coronary artery bypass grafting. Circumferential strain (C-strain) at end-systole on subendocardial and epicardial layers was measured using the short-axis tagged images of the LV and available software (Intag; Osirix). The myocardial segment was divided into stenotic and non-stenotic segments by invasive coronary angiography, and ischemic and non-ischemic segments by stress myocardial perfusion scintigraphy. The difference in C-strain between the two groups was analyzed using the Mann-Whitney U-test. The diagnostic capability of C-strain was analyzed using receiver operating characteristics analysis.</p> <p>Results</p> <p>The absolute subendocardial C-strain was significantly lower for stenotic (-7.5 ± 12.6%) than non-stenotic segment (-18.8 ± 10.2%, p < 0.0001). There was no difference in epicardial C-strain between the two groups. Use of cutoff thresholds for subendocardial C-strain differentiated stenotic segments from non-stenotic segments with a sensitivity of 77%, a specificity of 70%, and areas under the curve (AUC) of 0.76. The absolute subendocardial C-strain was significantly lower for ischemic (-6.7 ± 13.1%) than non-ischemic segments (-21.6 ± 7.0%, p < 0.0001). The absolute epicardial C-strain was also significantly lower for ischemic (-5.1 ± 7.8%) than non-ischemic segments (-9.6 ± 9.1%, p < 0.05). Use of cutoff thresholds for subendocardial C-strain differentiated ischemic segments from non-ischemic segments with sensitivities of 86%, specificities of 84%, and AUC of 0.86.</p> <p>Conclusions</p> <p>Analysis of tagged CMR can non-invasively demonstrate predominant impairment of subendocardial strain in the chronic ischemic myocardium at rest.</p
Extracellular volume quantification in isolated hypertension - changes at the detectable limits?
The funding source (British Heart Foundation and UK National Institute for Health Research) provided salaries for research training (FZ, TT, DS, SW), but had no role in study design, collection, analysis, interpretation, writing, or decisions with regard to publication. This work was undertaken at University College London Hospital, which received a proportion of funding from the UK Department of Health National Institute for Health Research Biomedical Research Centres funding scheme. We are grateful to Kingâs College London Laboratories for processing the collagen biomarker panel
Inhibition of Progenitor Dendritic Cell Maturation by Plasma from Patients with Peripartum Cardiomyopathy: Role in Pregnancy-associated Heart Disease
Dendritic cells (DCs) play dual roles in innate and adaptive immunity based
on their functional maturity, and both innate and adaptive immune responses have
been implicated in myocardial tissue remodeling associated with
cardiomyopathies. Peripartum cardiomyopathy (PPCM) is a rare disorder which
affects women within one month antepartum to five months postpartum. A high
occurrence of PPCM in central Haiti (1 in 300 live births) provided the unique
opportunity to study the relationship of immune activation and DC maturation
to the etiology of this disorder. Plasma samples from two groups (n = 12) of
age- and parity-matched Haitian women with or without evidence of PPCM were
tested for levels of biomarkers of cardiac tissue remodeling and immune
activation. Significantly elevated levels of GM-CSF, endothelin-1, proBNP and
CRP and decreased levels of TGF- were measured in PPCM subjects relative
to controls. Yet despite these findings, in vitro maturation of normal human
cord blood derived progenitor dendritic cells (CBDCs) was significantly
reduced (p < 0.001) in the presence of plasma from PPCM patients relative
to plasma from post-partum control subjects as determined by expression of
CD80, CD86, CD83, CCR7, MHC class II and the ability of these matured CBDCs
to induce allo-responses in PBMCs. These results represent the first findings
linking inhibition of DC maturation to the dysregulation of normal physiologic
cardiac
tissue remodeling during pregnancy and the pathogenesis of PPCM
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