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Numerical simulations of pulsatile blood flow in an aortic coarctation require the use of turbulence modeling. This paper considers three models from the class of large eddy simulation (LES) models (Smagorinsky, Vreman, σ -model) and one model from the class of variational multiscale models (residual-based) within a finite element framework. The influence of these models on the estimation of clinically relevant biomarkers used to assess the degree of severity of the pathological condition (pressure difference, secondary flow degree, normalized flow displacement, wall shear stress) is investigated in detail. The simulations show that most methods are consistent in terms of severity indicators such as pressure difference and stenotic velocity. Moreover, using second-order velocity finite elements, different turbulence models might lead to considerably different results concerning other clinically relevant quantities such as wall shear stresses. These differences may be attributed to differences in numerical dissipation introduced by the turbulence models., (© 2023 The Authors. International Journal for Numerical Methods in Biomedical Engineering published by John Wiley & Sons Ltd.)

Purpose: Accurately estimating the arterial input function for dynamic contrast-enhanced MRI is challenging. An arterial input function is typically determined from signal magnitude changes related to a contrast agent, often leading to underestimation of peak concentrations. Alternatively, signal phase recovers the accurate peak concentration for straight vessels but suffers from high noise. A recent method proposed to fit the signal in the complex plane by combining the advantages of the previous 2 methods. The purpose of this work is to refine this complex-based method to determine the venous output function (VOF), an arterial input function surrogate, from the superior sagittal sinus., Methods: We propose a state-of-the-art complex-based method that includes direct compensation for blood inflow and signal phase correction accounting for the curvature of the superior sagittal sinus, generally assumed collinear with B 0 . We compared the magnitude-, phase-, and complex-based VOF determination methods against various simulated biases as well as for 29 brain metastases patients., Results: Angulation of the superior sagittal sinus relative to B 0 varied widely within patients, and its effect on the signal phase caused an underestimation of peak concentrations of up to 65%. Correction significantly increased the VOF peak concentration for the phase- and complex-based VOFs in the cohort. The phase-based method recovered accurate peak concentrations but lacked precision in the tail of the VOF. Our complex-based VOF completely recovered the effect of inflow and resulted in a high-peak concentration with limited noise., Conclusion: The new complex-based method resulted in high-quality VOF robust against superior sagittal sinus curvature and variations in patient positioning., (© 2021 International Society for Magnetic Resonance in Medicine.)

Purpose: In this study, we investigate the effects of pulsatile flow and inflow on dynamic susceptibility-contrast MRI intravascular arterial input function measurement in human brain arteries and measure how they are affected by first-order flow compensation., Methods: A dual-echo single-shot EPI sequence with alternating flow compensation gradients was used to acquire dynamic susceptibility-contrast images with electrocardiogram monitoring. The dynamic signal variations measured inside the middle cerebral and internal carotid arteries were associated to the pulsatile arterial blood velocities measured with a single-slice quantitative flow sequence throughout the cardiac cycle., Results: Major inverse correlations between intravascular signal and blood velocity were found for the standard single-shot EPI sequence. Flow compensation reduces these correlated variations that contribute to signal physiological noise. This causes a significant twofold increase of intravascular SNR in the middle cerebral and the internal carotid arteries (2.3 ± 0.9, P = 0.03) and (2.0 ± 0.9, P = 0.04), respectively; and reduced phase SD for the internal carotid arteries (0.72 ± 0.14, P = 0.004). The correction proposed in this work translates into a quantitative arterial input function with reduced noise in the internal carotid arteries., Conclusion: The physiological noise added by pulsatile flow and inflow for intravascular arterial input function measurement in the brain arteries is significantly reduced by flow compensation., (© 2019 International Society for Magnetic Resonance in Medicine.)

Background and Objectives: Many mathematical equations based on height have been developed to estimate the esophageal length (EL) in children. The aim of this study was to confirm whether the preexisting and most frequently used equation by Strobel et al is accurate in calculating the EL in our pediatric population. Our secondary goal was to evaluate whether a new formula could be developed using our nonsurgical and surgical populations' data for the correlation between patients' height and measured EL by esophageal manometry (EM)., Methods: From 2000 to 2009, 116 children between the ages of 3 and 18 years without previous esophageal surgery underwent EM (n = 31) at the Montreal Children's Hospital. During the same period, 55 EMs were performed on 34 children with a previous history of esophageal surgery. For both groups, we collected the following data: height, EL calculated by the Strobel formula, and EL measured by EM., Results: The Strobel equation was inaccurate in predicting the EL. The calculated EL was 3.0 ± 0.32 cm longer than the EM measurements (P < 0.001). The height (H) of nonsurgical children was found to be highly predictive of the lower esophageal sphincter location (L), and the derived linear regression equation is L = 0.216 (H) + 7.13 [r² = 0.85]., Conclusions: This study confirmed that the Strobel formula is not sufficiently accurate to predict EL in the pediatric population that is between 3 and 18 years old. A correlation exists between height and esophageal sphincter location position. If EM is unavailable, the use of a new mathematical equation like ours can be considered.

Objectives: Esophageal atresia with or without tracheo-esophageal fistula is a frequent malformation that occurs in about 1 of 3000 live births. It can be associated with other congenital malformations. The aim of this study was to measure the frequency of heterotopic pancreas (HP) in children with esophageal atresia (EA) and to evaluate possible linkage with other malformations., Materials and Methods: All patients with EA were prospectively followed since 2005 at Hôpital Sainte-Justine and since 2006 at the Montreal Children's Hospital. We compared 91 patients who underwent gastroscopy during that period with 182 control patients who submitted to gastroscopy for other indications. The presence or the absence of HP and its localization were noted in both groups. The following data were also collected on patients with EA: sex, gestational age, EA type, and other malformations., Results: Seventeen (18.7%) of the 91 patients with EA had gastric HP compared with 1 (0.5%) in the control group (OR 42, 95% confidence interval 7-249, P < 0.001). There were no differences between patients with or without HP regarding sex, prematurity, EA type, and the presence or absence of other congenital abnormalities., Conclusions: This study demonstrates, for the first time, that gastric HP is associated with EA irrespective of other malformations.

1. In the human airway epithelium, VIP/PACAP receptors are distributed in nerve fibers and in epithelial cells but their role in transepithelial ion transport have not been reported. Here, we show that human bronchial epithelial Calu-3 cells expressed the VPAC(1) receptor subtype which shares similar high affinity for VIP and PACAP-27. 2. The stoichiometric binding parameters characterizing the (125)I-VIP and (125)I-PACAP-27 binding to these receptors were determined. 3. We found that VIP (EC(50) approximately 7.6 nM) and PACAP-27 (EC(50) approximately 10 nM) stimulated glibenclamide-sensitive and DIDS-insensitive iodide efflux in Calu-3 cells. 4. The protein kinase A (PKA) inhibitor, H-89 and the protein kinase C (PKC) inhibitor, chelerythrine chloride prevented activation by both peptides demonstrating that PKA and PKC are part of the signaling pathway. This profile corresponds to the pharmacological signature of CFTR. 5. In the cystic fibrosis airway epithelial IB3-1 cell lacking functional CFTR but expressing VPAC(1) receptors, neither VIP, PACAP-27 nor forskolin stimulated chloride transport. 6. Ussing chamber experiments demonstrated stimulation of CFTR-dependent short-circuit currents by VIP or PACAP-27 applied to the basolateral but not to the apical side of Calu-3 cells monolayers. 7. This study shows the stimulation in human bronchial epithelial cells of CFTR-dependent chloride secretion following activation by VIP and PACAP-27 of basolateral VPAC(1) receptors.