Aero-Structural Design Optimization of Adaptive Shock Control Bumps

Shock control bumps (SCB) are a transonic flow control device that aim to reduce the overall drag due to a normal shock on a typical passenger jet at cruise. The concept of adaptive SCB which can be deployed for best use are investigated through an aero-structural design tool that produces optimal geometries. The optimizer uses a surface based performance metric to highlight the importance of the flow quality around the SCB as well as including a structural element that is required to provide the necessary flexibility to deform. The performance metric produces the target pressure distribution and successfully smears the shock. It is found that the structural constraint does not inhibit bump height and global airfoil performance is not significantly a↵ected, L/D varies < 0.6%. The aerodynamic pressure loading can be utilised to produce a new family of SCB geometries that are unachievable with mechanical actuation alone. The study shows that adaptive SCB that exploit the naturally occurring pressure field around an airfoil in a passive way are a feasible technology to mitigate the poor o↵-design performance of static SCB

Hypoxia induces pulmonary fibroblast proliferation through NFAT signaling

Abstract Idiopathic pulmonary fibrosis (IPF) is a chronic, progressive and typically fatal lung disease with a very low survival rate. Excess accumulation of fibroblasts, myofibroblasts and extracellular matrix creates hypoxic conditions within the lungs, causing asphyxiation. Hypoxia is, therefore, one of the prominent features of IPF. However, there have been few studies concerning the effects of hypoxia on pulmonary fibroblasts. In this study, we investigated the molecular mechanisms of hypoxia-induced lung fibroblast proliferation. Hypoxia increased the proliferation of normal human pulmonary fibroblasts and IPF fibroblasts after exposure for 3–6 days. Cell cycle analysis demonstrated that hypoxia promoted the G1/S phase transition. Hypoxia downregulated cyclin D1 and A2 levels, while it upregulated cyclin E1 protein levels. However, hypoxia had no effect on the protein expression levels of cyclin-dependent kinase 2, 4, and 6. Chemical inhibition of hypoxia-inducible factor (HIF)-2 reduced hypoxia-induced fibroblast proliferation. Moreover, silencing of Nuclear Factor Activated T cell (NFAT) c2 attenuated the hypoxia-mediated fibroblasts proliferation. Hypoxia also induced the nuclear translocation of NFATc2, as determined by immunofluorescence staining. NFAT reporter assays showed that hypoxia-induced NFAT signaling activation is dependent on HIF-2, but not HIF-1. Furthermore, the inhibition or silencing of HIF-2, but not HIF-1, reduced the hypoxia-mediated NFATc2 nuclear translocation. Our studies suggest that hypoxia induces the proliferation of human pulmonary fibroblasts through NFAT signaling and HIF-2