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In the field of cardiovascular imaging, four-dimensional (4D) flow cardiovascular magnetic resonance (CMR) provides non-invasive assessment of blood flow. Dual velocity encoding (dual-VENC) strategies have emerged to obtain quantitative information on both low and high blood flow velocities simultaneously. However, these strategies often encounter difficulties in coping with large velocity ranges. This work presents a dual-VENC 4D flow CMR sequence that utilizes the coprime rule to define the VENC ratio. A dual-VENC 4D flow CMR sequence and reconstruction algorithm were developed and validated in vitro at two different field strengths, using a flow phantom generating realistic complex flow patterns. A digital twin of the phantom allowed comparison of the MRI measurements with computational fluid dynamics (CFD) simulations. Three patients with different cardiac pathologies were scanned in order to evaluate the in vivo feasibility of the proposed method. The results of the in vitro acquisitions demonstrated significant improvement in velocity-to-noise ratio (VNR) with respect to single-VENC acquisitions (110±3%) and conventional dual-VENC de-aliasing approach (75±3%). Furthermore, the effectiveness of aliasing correction was demonstrated even when both sets of images from the dual-VENC acquisition presented velocity aliasing artifacts. We observed a high degree of agreement between the measured and simulated velocity fields. The strength of this approach lies in the fact that, unlike the conventional de-aliasing method, no data is discarded. The final image is obtained by a weighted average of the VENClow and VENChigh datasets. Consequently, setting the value of the VENChigh to prevent aliasing is no longer necessary, and higher VNR gains are possible [Display omitted]

The aim was threefold: 1) expound the independent physiological parameters that drive FFR, 2) elucidate contradictory conclusions between fractional flow reserve (FFR) and coronary flow reserve (CFR), and 3) highlight the need of both FFR and CFR in clinical decision making. Simple explicit theoretical models were supported by coronary data analyzed retrospectively. FFR was expressed as a function of pressure loss coefficient, aortic pressure and hyperemic coronary microvascular resistance. The FFR-CFR relationship was also demonstrated mathematically and was shown to be exclusively dependent upon the coronary microvascular resistances. The equations were validated in a first series of 199 lesions whose pressures and distal velocities were monitored. A second dataset of 75 lesions with pre- and post-PCI measures of FFR and CFR was also analyzed to investigate the clinical impact of our hemodynamic reasoning. Hyperemic coronary microvascular resistance and pressure loss coefficient had comparable impacts (45% and 49%) on FFR. There was a good concordance (y = 0.96 x - 0.02, r2 = 0.97) between measured CFR and CFR predicted by FFR and coronary resistances. In patients with CFR < 2 and CFR/FFR ≥ 2, post-PCI CFR was significantly >2 (p < 0.001), whereas it was not (p = 0.94) in patients with CFR < 2 and CFR/FFR < 2. The FFR behavior and FFR-CFR relationship are predictable from basic hemodynamics. Conflicting conclusions between FFR and CFR are explained from coronary vascular resistances. As confirmed by our results, FFR and CFR are complementary; they could jointly contribute to better PCI guidance through the CFR-to-FFR ratio in patients with coronary artery disease.

We use Arabidopsis thaliana as a model to investigate coordination of cell proliferation and cell elongation in the three components that develop side by side in the seed. Two of these, the embryo and its nurturing annex, the endosperm, are placed under zygotic control and develop within the seed integument placed under maternal control. We show that integument cell proliferation and endosperm growth are largely independent from each other. By contrast, prevention of cell elongation in the integument by the mutation transparent testa glabra2 (ttg2) restricts endosperm and seed growth. Conversely, endosperm growth controlled by the HAIKU (IKU) genetic pathway modulates integument cell elongation. Combinations of TTG2 defective seed integument with reduction of endosperm size by iku mutations identify integument cell elongation and endosperm growth as the primary regulators of seed size. Our results strongly suggest that a cross talk between maternal and zygotic controls represents the primary regulator of the coordinated control of seed size in Arabidopsis.

The hereditary β-thalassemia major condition requires regular lifelong blood transfusions. Transfusion-related iron overloading has been associated with the onset of cardiovascular complications, including cardiac dysfunction and vascular anomalies. By using an untransfused murine model of β-thalassemia major, we tested the hypothesis that vascular endothelial dysfunction, alterations of arterial structure and of its mechanical properties would occur despite the absence of treatments. Vascular function and structure were evaluated ex vivo. Compared to the controls, endothelium-dependent vasodilation with acetylcholine was blunted in mesenteric resistance arteries of β-thalassemic mice while the endothelium-independent vasodilator (sodium nitroprusside) produced comparable vessel dilation, indicating endothelial cell impairment with preserved smooth muscle cell reactivity to nitric oxide (NO). While these findings suggest a decrease in NO bioavailability, Western blotting showed heightened expression of aortic endothelial NO synthase (eNOS) in β-thalassemia. Vascular remodeling of the common carotid arteries revealed increased medial elastin content. Under isobaric conditions, the carotid arteries of β-thalassemic mice exhibited decreased wall stress and softening due to structural changes of the vessel wall. A complex vasculopathy was identified in untransfused β-thalassemic mice characterized by altered carotid artery structure and endothelial dysfunction of resistance arterioles, likely attributable to reduced NO bioavailability despite enhanced vascular eNOS expression.

This study aimed to test the accuracy of a speckle tracking algorithm to assess myocardial deformation in a large range of heart rates and strain magnitudes compared to sonomicrometry. Using a tissue-mimicking phantom with cyclic radial deformation, radial strain derived from speckle tracking (RS-SpT) of the upper segment was assessed in short axis view by conventional echocardiography (Vivid q, GE) and post-processed with clinical software (EchoPAC, GE). RS-SpT was compared with radial strain measured simultaneously by sonomicrometers (RS-SN). Radial strain was assessed with increasing deformation rates (60 to 160 beats/min) and increasing pulsed volumes (50 to 100 ml/beat) to simulate physiological changes occurring during stress echocardiography. There was a significant correlation (R2 = 0.978, P <0.001) and a close agreement (bias ± 2SD, 0.39 ± 1.5%) between RS-SpT and RS-SN. For low strain values (<15%), speckle tracking showed a small but significant overestimation of radial strain compared to sonomicrometers. Two-way analysis of variance did not show any significant effect of the deformation rate. For RS-SpT, the feasibility was excellent and the intra- and inter-observer variability were low (the intraclass correlation coefficients were 0.96 and 0.97, respectively). Speckle tracking demonstrated a good correlation with sonomicrometry for the assessment of radial strain independently of the heart rate and strain magnitude in a physiological range of values. Though speckle tracking seems to be a reliable and reproducible technique to assess myocardial deformation variations during stress echocardiography, further studies are mandated to analyze the impact of angulated and artefactual out-of-plane motions and inter-vendor variability.

Background Left ventricular untwisting generates an early diastolic intraventricular pressure gradient (DIVPG) than can be quantified by echocardiography. We sought to confirm the quantitative relationship between peak untwisting rate and peak DIVPG in a large adult population. Methods From our echocardiographic database, we retrieved all the echocardiograms with a normal left ventricular ejection fraction, for whom color Doppler M-Mode interrogation of mitral inflow was available, and left ventricular untwisting rate was measurable using speckle tracking. Standard indices of left ventricular early diastolic function were assessed by Doppler (peaks E, e’ and Vp) and speckle tracking (peak strain rate Esr). Load dependency of DIVPG and untwisting rate was evaluated using a passive leg raising maneuver. Results We included 154 subjects, aged between 18 to 77 years old, 63% were male. Test-retest reliability for color Doppler-derived DIVPG measurements was good, the intraclass correlation coefficients were 0.97 [0.91–0.99] and 0.97 [0.67–0.99] for intra- and inter-observer reproducibility, respectively. Peak DIVPG was positively correlated with peak untwisting rate (r = 0.73, P  <  0.001). On multivariate analysis, peak DIVPG was the only diastolic parameter that was independently associated with untwisting rate. Age and gender were the clinical predictive factors for peak untwisting rate, whereas only age was independently associated with peak DIVPG. Untwisting rate and DIVPG were both load-dependent, without affecting their relationship. Conclusions Color Doppler-derived peak DIVPG was quantitatively and independently associated with peak untwisting rate. It thus provides a reliable flow-based index of early left ventricular diastolic function.

In flowering plants, maternal seed integument encloses the embryo and the endosperm, which are both derived from double fertilization. Although the development of these three components must be coordinated, we have limited knowledge of mechanisms involved in such coordination. The endosperm may play a central role in these mechanisms as epigenetic modifications of endosperm development, via imbalance of dosage between maternal and paternal genomes, affecting both the embryo and the integument. To identify targets of such epigenetic controls, we designed a genetic screen in Arabidopsis for mutants that phenocopy the effects of dosage imbalance in the endosperm. The two mutants haiku 1 and haiku 2 produce seed of reduced size that resemble seed with maternal excess in the maternal/paternal dosage. Homozygous haiku seed develop into plants indistinguishable from wild type. Each mutation is sporophytic recessive, and double-mutant analysis suggests that both mutations affect the same genetic pathway. The endosperm of haiku mutants shows a premature arrest of increase in size that causes precocious cellularization of the syncytial endosperm. Reduction of seed size in haiku results from coordinated reduction of endosperm size, embryo proliferation, and cell elongation of the maternally derived integument. We present further evidence for a control of integument development mediated by endosperm-derived signals.

The Horn and Schunck (HS) method, which amounts to the Jacobi iterative scheme in the interior of the image, was one of the first optical flow algorithms. In this article, we prove the convergence of the HS method, whenever the problem is well-posed. Our result is shown in the framework of a generalization of the HS method in dimension ≥ 1, with a broad definition of the discrete Laplacian. In this context, the condition for the convergence is that the intensity gradients are not all contained in a same hyperplane. Two other articles ([17] and [13]) claimed to solve this problem in the case = 2, but it appears that both of these proofs are erroneous. Moreover, we explain why some standard results on the convergence of the Jacobi method do not apply for the HS problem, unless = 1. It is also shown that the convergence of the HS scheme implies the convergence of the Gauss-Seidel and SOR schemes for the HS problem.

Different classes of small RNAs (sRNAs) refine the expression of numerous genes in higher eukaryotes by directing protein partners to complementary nucleic acids, where they mediate gene silencing. Plants encode a unique class of sRNAs, called trans-acting small interfering RNAs (tasiRNAs), which post-transcriptionally regulate protein-coding transcripts, as do microRNAs (miRNAs), and both sRNA classes control development through their targets. TasiRNA biogenesis requires multiple components of the siRNA pathway and also miRNAs. But while 21mer siRNAs originating from transgenes can mediate silencing across several cell layers, miRNA action seems spatially restricted to the producing or closely surrounding cells. We have previously described the isolation of a genetrap reporter line for TAS3a, the major locus producing AUXIN RESPONS FACTOR (ARF)-regulating tasiRNAs in the Arabidopsis shoot. Its activity is limited to the adaxial (upper) side of leaf primordia, thus spatially isolated from ARF-activities, which are located in the abaxial (lower) side. We show here by in situ hybridization and reporter fusions that the silencing activities of ARF-regulating tasiRNAs are indeed manifested non-cell autonomously to spatially control ARF activities. Endogenous tasiRNAs are thus mediators of a mobile developmental signal and might provide effective gene silencing at a distance beyond the reach of most miRNAs.

Abdominal aortic aneurysms (AAA) are localized, commonly-occurring dilations of the aorta. When equilibrium between blood pressure (loading) and wall mechanical resistance is lost, rupture ensues, and patient death follows, if not treated immediately. Experimental and numerical analyses of flow patterns in arteries show direct correlations between wall shear stress and wall mechano-adaptation with the development of zones prone to thrombus formation. For further insights into AAA flow topology/growth interaction, a workout of patient-specific computational flow dynamics (CFD) is proposed to compute finite-time Lyapunov exponents and extract Lagrangian-coherent structures (LCS). This computational model was first compared with 4-D phase-contrast magnetic resonance imaging (MRI) in 5 patients. To better understand the impact of flow topology and transport on AAA growth, hyperbolic, repelling LCS were computed in 1 patient during 8-year follow-up, including 9 volumetric morphologic AAA measures by computed tomography-angiography (CTA). LCS defined barriers to Lagrangian jet cores entering AAA. Domains enclosed between LCS and the aortic wall were considered to be stagnation zones. Their evolution was studied during AAA growth. Good correlation – 2-D cross-correlation coefficients of 0.65, 0.86 and 0.082 (min, max, SD) – was obtained between numerical simulations and 4-D MRI acquisitions in 6 specific cross-sections from 4 patients. In follow-up study, LCS divided AAA lumens into 3 dynamically-isolated zones: 2 stagnation volumes lying in dilated portions of the AAA, and circulating volume connecting the inlet to the outlet. The volume of each zone was tracked over time. Although circulating volume remained unchanged during 8-year follow-up, the AAA lumen and main stagnation zones grew significantly (8 cm3/year and 6 cm3/year, respectively). This study reveals that transient transport topology can be quantified in patient-specific AAA during disease progression by CTA, in parallel with lumen morphology. It is anticipated that analysis of the main AAA stagnation zones by patient-specific CFD on a yearly basis could help to predict AAA growth and rupture.