Jetstream 31 National Flying Laboratory: Lift and Drag Measurement and Modelling

Lift and drag flight test data is presented from the National Flying Laboratory Centre, Jetstream 31 aircraft. The aircraft has been modified as a flying classroom for completing flight test training courses, for engineering degree accreditation. The straight and level flight test data is compared to data from 10% and 17% scale wind tunnel models, a Reynolds Averaged Navier Stokes steady-state computational fluid dynamics model and an empirical model. Estimated standard errors in the flight test data are ±2.4%±2.4% in lift coefficient, ±2.7%±2.7% in drag coefficient. The flight test data also shows the aircraft to have a maximum lift to drag ratio of 10.5 at Mach 0.32, a zero lift drag coefficient of 0.0376 and an induced drag correction factor of 0.0607. When comparing the characteristics from the other models, the best overall comparison with the flight test data, in terms of lift coefficient, was with the empirical model. For the drag comparisons, all the models under predicted levels of drag by up to 43% when compared to the flight test data, with the best overall match between the flight test data and the 10% scale wind tunnel model. These discrepancies were attributed to various factors including zero lift drag Reynolds number effects, omission of a propeller system and surface excrescences on the models, as well as surface finish differences

Differential effects of selenium and knock-down of glutathione peroxidases on TNFα and flagellin inflammatory responses in gut epithelial cells

Selenium (Se) is essential for human health. Despite evidence that Se intake affects inflammatory responses, the mechanisms by which Se and the selenoproteins modulate inflammatory signalling, especially in the gut, are not yet defined. The aim of this work was to assess effects of altered Se supply and knock-down of individual selenoproteins on NF-κB activation in gut epithelial cells. Caco-2 cells were stably transfected with gene constructs expressing luciferase linked either to three upstream NF-κB response elements and a TATA box or only a TATA box. TNFα and flagellin activated NF-κB-dependent luciferase activity and increased IL-8 expression. Se depletion decreased expression of glutathione peroxidase1 (GPX1) and selenoproteins H and W and increased TNFα-stimulated luciferase activity, endogenous IL-8 expression and reactive oxygen species (ROS) production. These effects were not mimicked by independent knock-down of either GPX1, selenoprotein H or W; indeed, GPX1 knock-down lowered TNFα-induced NF-κB activation and did not affect ROS levels. GPX4 knock-down decreased NF-κB activation by flagellin but not by TNFα. We hypothesise that Se depletion alters the pattern of expression of multiple selenoproteins that in turn increases ROS and modulates NF-κB activation in epithelial cells, but that the effect of GPX1 knock-down is ROS-independent