Height and timing of growth spurt during puberty in young people living with vertically acquired HIV in Europe and Thailand.

OBJECTIVE: The aim of this study was to describe growth during puberty in young people with vertically acquired HIV. DESIGN: Pooled data from 12 paediatric HIV cohorts in Europe and Thailand. METHODS: One thousand and ninety-four children initiating a nonnucleoside reverse transcriptase inhibitor or boosted protease inhibitor based regimen aged 1-10 years were included. Super Imposition by Translation And Rotation (SITAR) models described growth from age 8 years using three parameters (average height, timing and shape of the growth spurt), dependent on age and height-for-age z-score (HAZ) (WHO references) at antiretroviral therapy (ART) initiation. Multivariate regression explored characteristics associated with these three parameters. RESULTS: At ART initiation, median age and HAZ was 6.4 [interquartile range (IQR): 2.8, 9.0] years and -1.2 (IQR: -2.3 to -0.2), respectively. Median follow-up was 9.1 (IQR: 6.9, 11.4) years. In girls, older age and lower HAZ at ART initiation were independently associated with a growth spurt which occurred 0.41 (95% confidence interval 0.20-0.62) years later in children starting ART age 6 to 10 years compared with 1 to 2 years and 1.50 (1.21-1.78) years later in those starting with HAZ less than -3 compared with HAZ at least -1. Later growth spurts in girls resulted in continued height growth into later adolescence. In boys starting ART with HAZ less than -1, growth spurts were later in children starting ART in the oldest age group, but for HAZ at least -1, there was no association with age. Girls and boys who initiated ART with HAZ at least -1 maintained a similar height to the WHO reference mean. CONCLUSION: Stunting at ART initiation was associated with later growth spurts in girls. Children with HAZ at least -1 at ART initiation grew in height at the level expected in HIV negative children of a comparable age

A hybrid spectral/finite-difference large-eddy simulator of turbulent processes in the upper ocean

A three-dimensional numerical model for large-eddy simulation (LES) of oceanic turbulent processes is described. The numerical formulation comprises a spectral discretization in the horizontal directions and a high-order compact finite-difference discretization in the vertical direction. Time-stepping is accomplished via a second-order accurate fractional-step scheme. LES subgrid-scale (SGS) closure is given by a traditional Smagorinsky eddy-viscosity parametrization for which the model coefficient is derived following similarity theory in the near-surface region. Alternatively, LES closure is given by the dynamic Smagorinsky parametrization for which the model coefficient is computed dynamically as a function of the flow. Validation studies are presented demonstrating the temporal and spatial accuracy of the formulation for laminar flows with analytical solutions. Further validation studies are described involving direct numerical simulation (DNS) and LES of turbulent channel flow and LES of decaying isotropic turbulence. Sample flow problems include surface Ekman layers and wind-driven shallow water flows both with and without Langmuir circulation (LC) generated by wave effects parameterized via the well-known Craik-Leibovich (C-L) vortex force. In the case of the surface Ekman layers, the inner layer (where viscous effects are important) is not resolved and instead is parameterized with the Smagorinsky models previously described. The validity of the dynamic Smagorinsky model (DSM) for parameterizing the surface inner layer is assessed and a modification to the surface stress boundary condition based on log-layer behavior is introduced improving the performance of the DSM. Furthermore, in Ekman layers with wave effects, the implicit LES grid filter leads to LC subgrid-scales requiring ad hoc modeling via an explicit spatial filtering of the C-L force in place of a suitable SGS parameterization. (C) 2009 Elsevier Ltd. All rights reserved

Oil Droplet Transport under Non-Breaking Waves: An Eulerian RANS Approach Combined with a Lagrangian Particle Dispersion Model

Oil droplet transport under a non-breaking deep water wave field is investigated herein using Computational Fluid dynamics (CFD). The Reynolds-averaged Navier–Stokes (RANS) equations were solved to simulate regular waves in the absence of wind stress, and the resulting water velocities agreed with Stokes theory for waves. The RANS velocity field was then used to predict the transport of buoyant particles representing oil droplets under the effect of non-locally generated turbulence. The RANS eddy viscosity exhibited an increase with depth until reaching a maximum at approximately a wave height below the mean water level. This was followed by a gradual decrease with depth. The impact of the turbulence was modeled using the local value of eddy diffusivity in a random walk framework with the added effects of the gradient of eddy diffusivity. The vertical gradient of eddy viscosity increased the residence time of droplets in the water column region of high diffusivity; neglecting the gradient of eddy diffusivity resulted in a deviation of the oil plume centroid by more than a half a wave height after 10 wave periods

Bio-Engineering of Pre-Vascularized Islet Organoids for the Treatment of Type 1 Diabetes

Lack of rapid revascularization and inflammatory attacks at the site of transplantation contribute to impaired islet engraftment and suboptimal metabolic control after clinical islet transplantation. In order to overcome these limitations and enhance engraftment and revascularization, we have generated and transplanted pre-vascularized insulin-secreting organoids composed of rat islet cells, human amniotic epithelial cells (hAECs), and human umbilical vein endothelial cells (HUVECs). Our study demonstrates that pre-vascularized islet organoids exhibit enhanced in vitro function compared to native islets, and, most importantly, better engraftment and improved vascularization in vivo in a murine model. This is mainly due to cross-talk between hAECs, HUVECs and islet cells, mediated by the upregulation of genes promoting angiogenesis (vegf-a) and β cell function (glp-1r, pdx1). The possibility of adding a selected source of endothelial cells for the neo-vascularization of insulin-scereting grafts may also allow implementation of β cell replacement therapies in more favourable transplantation sites than the liver