156 research outputs found

    Temperature suppression of STM-induced desorption of hydrogen on Si(100) surfaces

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    The temperature dependence of hydrogen (H) desorption from Si(100) H-terminated surfaces by a scanning tunneling microscope (STM) is reported for negative sample bias. It is found that the STM induced H desorption rate (RR) decreases several orders of magnitude when the substrate temperature is increased from 300 K to 610 K. This is most noticeable at a bias voltage of -7 V where RR decreases by a factor of ~200 for a temperature change of 80 K, whilst it only decreases by a factor of ~3 at -5 V upon the same temperature change. The experimental data can be explained by desorption due to vibrational heating by inelastic scattering via a hole resonance. This theory predicts a weak suppression of desorption with increasing temperature due to a decreasing vibrational lifetime, and a strong bias dependent suppression due to a temperature dependent lifetime of the hole resonance.Comment: 5 pages, RevTeX, epsf files. Accepted for surface science letter

    the WAF method for non-homogeneous SWE with pollutant

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    This paper deals with the extension of the WAF method to discretize Shallow Water Equations with pollutants. We consider two different versions of the WAF method, by approximating the intermediate waves using the flux of HLL or the direct approach of HLLC solver. It is seen that both versions can be written under the same form with different definitions for the approximation of the velocity waves. We also propose an extension of the method to non-homogeneous systems. In the case of homogeneous systems it is seen that we can rewrite the third component of the numerical flux in terms of an intermediate wave speed approximation. We conclude that – in order to have the same relation for non-homogeneous systems – the approximation of the intermediate wave speed must be modified. The proposed extension of the WAF method preserves all stationary solutions, up to second order accuracy, and water at rest in an exact way, even with arbitrary pollutant concentration. Finally, we perform several numerical tests, by comparing it with HLLC solver, reference solutions and analytical solutions

    Subendocardial contractile impairment in chronic ischemic myocardium: assessment by strain analysis of 3T tagged CMR

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    <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

    Inhibition of Progenitor Dendritic Cell Maturation by Plasma from Patients with Peripartum Cardiomyopathy: Role in Pregnancy-associated Heart Disease

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    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

    Rapid Accumulation of CD14+CD11c+ Dendritic Cells in Gut Mucosa of Celiac Disease after in vivo Gluten Challenge

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    Of antigen-presenting cells (APCs) expressing HLA-DQ molecules in the celiac disease (CD) lesion, CD11c(+) dendritic cells (DCs) co-expressing the monocyte marker CD14 are increased, whereas other DC subsets (CD1c(+) or CD103(+)) and CD163(+)CD11c(-) macrophages are all decreased. It is unclear whether these changes result from chronic inflammation or whether they represent early events in the gluten response. We have addressed this in a model of in vivo gluten challenge.Treated HLA-DQ2(+) CD patients (n = 12) and HLA-DQ2(+) gluten-sensitive control subjects (n = 12) on a gluten-free diet (GFD) were orally challenged with gluten for three days. Duodenal biopsies obtained before and after gluten challenge were subjected to immunohistochemistry. Single cell digests of duodenal biopsies from healthy controls (n = 4), treated CD (n = 3) and untreated CD (n = 3) patients were analyzed by flow cytometry.In treated CD patients, the gluten challenge increased the density of CD14(+)CD11c(+) DCs, whereas the density of CD103(+)CD11c(+) DCs and CD163(+)CD11c(-) macrophages decreased, and the density of CD1c(+)CD11c(+) DCs remained unchanged. Most CD14(+)CD11c(+) DCs co-expressed CCR2. The density of neutrophils also increased in the challenged mucosa, but in most patients no architectural changes or increase of CD3(+) intraepithelial lymphocytes (IELs) were found. In control tissue no significant changes were observed.Rapid accumulation of CD14(+)CD11c(+) DCs is specific to CD and precedes changes in mucosal architecture, indicating that this DC subset may be directly involved in the immunopathology of the disease. The expression of CCR2 and CD14 on the accumulating CD11c(+) DCs indicates that these cells are newly recruited monocytes

    A discontinuous Galerkin method for poroelastic wave propagation : the two-dimensional case

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    In this paper, we consider a high-order discontinuous Galerkin (DG) method for modelling wave propagation in coupled poroelastic–elastic media. The upwind numerical flux is derived as an exact solution for the Riemann problem including the poroelastic–elastic interface. Attenuation mechanisms in both Biot's low- and high-frequency regimes are considered. The current implementation supports non-uniform basis orders which can be used to control the numerical accuracy element by element. In the numerical examples, we study the convergence properties of the proposed DG scheme and provide experiments where the numerical accuracy of the scheme under consideration is compared to analytic and other numerical solutions
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