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This paper investigates the effects of Reynolds number on the wake characteristics of a notchback Ahmed body with effective backlight angle, βe = 17.8 deg. The Reynolds number based on the body height was varied from 5×10³ to 5×104 Prior to the Reynolds number investigation, a Reynolds-averaged Navier-Stokes (RANS) model assessment was performed using nine turbulence models consisting of one- and two-equation eddy-viscosity models and second moment closure models. The standard Spalart-Allmaras model was the only model that accurately predicted the asymmetric time-averaged wake topology, as reported in previous studies, for the βe = 17.8 deg notchback Ahmed body at Re = 5×104 The drag coefficient decreased with increasing Reynolds number, while the lift coefficient remained constant for Re >= 1×104 The wake structure exhibited three regimes: symmetric (Re ≤ 1×104), transitionally asymmetric (1×104 < Re > 3.5×104) states. The wake asymmetry was attributed to an imbalance in entrainment from the sides and asymmetric separation from the roof and the C-pillars of the body. The tilting and stretching terms in the vorticity transport equation were used to provide insight into the source of asymmetry in the vorticity field around the body. [ABSTRACT FROM AUTHOR]

As signalling organelles, cilia regulate their G protein-coupled receptor content by ectocytosis, a process requiring localised actin dynamics to alter membrane shape. Photoreceptor outer segments comprise an expanse of folded membranes (discs) at the tip of highly-specialised connecting cilia, into which photosensitive GPCRs are concentrated. Discs are shed and remade daily. Defects in this process, due to mutations, cause retinitis pigmentosa (RP). Whilst fundamental for vision, the mechanism of photoreceptor disc generation is poorly understood. Here, we show membrane deformation required for disc genesis is driven by dynamic actin changes in a process akin to ectocytosis. We show RPGR, a leading RP gene, regulates actin-binding protein activity central to this process. Actin dynamics, required for disc formation, are perturbed in Rpgr mouse models, leading to aborted membrane shedding as ectosome-like vesicles, photoreceptor death and visual loss. Actin manipulation partially rescues this, suggesting the pathway could be targeted therapeutically. These findings help define how actin-mediated dynamics control outer segment turnover., (© 2024. The Author(s).)