An experimental study was conducted to characterize the transient behavior of laminar flow separation on a NASA low-speed GA (W)-1 airfoil at the chord Reynolds number of 70,000. In addition to measuring the surface pressure distribution around the airfoil, a high-resolution particle image velocimetry (PIV) system was used to make detailed flow field measurements to quantify the evolution of unsteady flow structures around the airfoil at various angles of attack (AOAs). The surface pressure and PIV measurements clearly revealed that the laminar boundary layer would separate from the airfoil surface, as the adverse pressure gradient over the airfoil upper surface became severe at $AOA≥8.0deg$. The separated laminar boundary layer was found to rapidly transit to turbulence by generating unsteady Kelvin–Helmholtz vortex structures. After turbulence transition, the separated boundary layer was found to reattach to the airfoil surface as a turbulent boundary layer when the adverse pressure gradient was adequate at $AOA<12.0deg$, resulting in the formation of a laminar separation bubble on the airfoil. The turbulence transition process of the separated laminar boundary layer was found to be accompanied by a significant increase of Reynolds stress in the flow field. The reattached turbulent boundary layer was much more energetic, thus more capable of advancing against an adverse pressure gradient without flow separation, compared to the laminar boundary layer upstream of the laminar separation bubble. The laminar separation bubble formed on the airfoil upper surface was found to move upstream, approaching the airfoil leading edge as the AOA increased. While the total length of the laminar separation bubble was found to be almost unchanged ($∼20%$ of the airfoil chord length), the laminar portion of the separation bubble was found to be slightly stretched, and the turbulent portion became slightly shorter with the increasing AOA. After the formation of the separation bubble on the airfoil, the increase rate of the airfoil lift coefficient was found to considerably degrade, and the airfoil drag coefficient increased much faster with increasing AOA. The separation bubble was found to burst suddenly, causing airfoil stall, when the adverse pressure gradient became too significant at $AOA>12.0deg$.

This study aims to develop an experimentally validated computational fluid dynamics (CFD) model to estimate hemodynamic characteristics in cerebral aneurysms (CAs) using non-Newtonian blood analogues. Blood viscosities varying with shear rates were measured under four temperatures first, which serves as the reference for the generation of blood analogues. Using the blood analogue, particle image velocimetry (PIV) measurements were conducted to quantify flow characteristics in a CA model. Then, using the identical blood properties in the experiment, CFD simulations were executed to quantify the flow patterns, which were used to compare with the PIV counterpart. Additionally, hemodynamic characteristics in the simplified Newtonian and non-Newtonian models were quantified and compared using the experimentally validated CFD model. Results showed the proposed non-Newtonian viscosity model can predict blood shear-thinning properties accurately under varying temperatures and shear rates. Another developed viscosity model based on the blood analogue can well represent blood rheological properties. The comparisons in flow characteristics show good agreements between PIV and CFD, demonstrating the developed CFD model is qualified to investigate hemodynamic factors within CAs. Furthermore, results show the differences of absolute values were insignificant between Newtonian and non-Newtonian fluids in the distributions of wall shear stress (WSS) and oscillatory shear index (OSI) on arterial walls. However, not only does the simplified Newtonian model underestimate WSS and OSI in most regions of the aneurysmal sac, but it also makes mistakes in identifying the high OSI regions on the sac surface, which may mislead the hemodynamic assessment on the pathophysiology of CAs.