By using a Reynolds-averaged two-dimensional computation of a turbulent flow over an airfoil at post-stall angles of attack, we show that the massively separated and disordered unsteady flow can be effectively controlled by periodic blowing-suction near the leading edge with low-level power input. This unsteady forcing can modulate the evolution of the separated shear layer to promote the formation of concentrated lifting vortices, which in turn interact with trailing-edge vortices in a favourable manner and thereby alter the global deep-stall flow field. In a certain range of poststall angles of attack and forcing frequencies, the unforced random separated flow can become periodic or quasi-periodic, associated with a significant lift enhancement. This opens a promising possibility for flight beyond the static stall to a much higher angle of attack. The same local control also leads, in some situations, to a reduction of drag. On a part of the airfoil the pressure fluctuation is suppressed as well, which would be beneficial for high-α buffet control. The computations are in qualitative agreement with several recent post-stall flow control experiments. The physical mechanisms responsible for post-stall flow control, as observed from the numerical data, are explored in terms of nonlinear mode competition and resonance, as well as vortex dynamics. The leading-edge shear layer and vortex shedding from the trailing edge are two basic constituents of unsteady post-stall flow and its control. Since the former has a rich spectrum of response to various disturbances, in a quite wide range the natural frequency of both constituents can shift and lock-in to the forcing frequency or its harmonics. Thus, most of the separated flow becomes resonant, associated with much more organized flow patterns. During this nonlinear process the coalescence of small vortices from the disturbed leading-edge shear layer is enhanced, causing a stronger entrainment and hence a stronger lifting vortex. Meanwhile, the unfavourable trailing-edge vortex is pushed downstream. The wake pattern also has a corresponding change: the shed vortices of alternate signs tend to be aligned, forming a train of close vortex couples with stronger downwash, rather than a Kármán street.

BackgroundSpinal cord injury (SCI) is a devastating disease, which results in tissue loss and neurologic dysfunction. NLRP3 inflammasome plays an important role in the mechanism of diverse diseases. However, no studies have demonstrated the role of NLRP3 inflammasome and the effects of NLRP3 inflammasome inhibitors in a mouse model of SCI. We investigated whether inhibition of NLRP3 inflammasome activation by the pharmacologic inhibitor BAY 11-7082 or A438079 could exert neuroprotective effects in a mouse model of SCI.MethodsSCI was performed using an aneurysm clip with a closing force of 30 g at the level of the T6-T7 vertebra for 1 min. Motor recovery was evaluated by an open-field test. Neuronal death was assessed by terminal deoxynucleotidyl transferase dUTP nick end labeling and Nissl staining. Mitochondrial dysfunction was determined by quantitative real-time polymerase chain reaction (qPCR), western blot, and detection of mitochondrial membrane potential level. Microglia/macrophage activation and astrocytic response were evaluated by immunofluorescence labeling.ResultsInhibition of NLRP3 inflammasome activation by pharmacologic inhibitor BAY 11-7082 or A438079 reduced neuronal death, attenuated spinal cord anatomic damage, and promoted motor recovery. Furthermore, BAY 11-7082 or A438079 directly attenuated the levels of NLRP3 inflammasome and proinflammatory cytokines. Moreover, BAY 11-7082 or A438079 alleviated microglia/macrophage activation, neutrophils infiltration, and reactive gliosis, as well as mitochondrial dysfunction.ConclusionsCollectively, our results demonstrate that pharmacologic suppression of NLRP3 inflammasome activation controls neuroinflammation, attenuates mitochondrial dysfunction, alleviates the severity of spinal cord damage, and improves neurological recovery after SCI. These data strongly indicate that the NLRP3 inflammasome is a vital contributor to the secondary damage of SCI in mice.

This paper focuses on the theoretical treatment of the laminar, incompressible, and time-dependent flow of a viscous fluid in a porous channel with orthogonally moving walls. Assuming uniform injection or suction at the porous walls, two cases are considered for which the opposing walls undergo either uniform or nonuniform motions. For the first case, we follow Dauenhauer and Majdalani ͓Phys. Fluids 15, 1485 ͑2003͔͒ by taking the wall expansion ratio ␣ to be time invariant and then proceed to reduce the Navier-Stokes equations into a fourth order ordinary differential equation with four boundary conditions. Using the homotopy analysis method ͑HAM͒, an optimized analytical procedure is developed that enables us to obtain highly accurate series approximations for each of the multiple solutions associated with this problem. By exploring wide ranges of the control parameters, our procedure allows us to identify dual or triple solutions that correspond to those reported by Zaturska et al. ͓Fluid Dyn. Res. 4, 151 ͑1988͔͒. Specifically, two new profiles are captured that are complementary to the type I solutions explored by Dauenhauer and Majdalani. In comparison to the type I motion, the so-called types II and III profiles involve steeper flow turning streamline curvatures and internal flow recirculation. The second and more general case that we consider allows the wall expansion ratio to vary with time. Under this assumption, the Navier-Stokes equations are transformed into an exact nonlinear partial differential equation that is solved analytically using the HAM procedure. In the process, both algebraic and exponential models are considered to describe the evolution of ␣͑t͒ from an initial ␣ 0 to a final state ␣ 1. In either case, we find the time-dependent solutions to decay very rapidly to the extent of recovering the steady state behavior associated with the use of a constant wall expansion ratio. We then conclude that the time-dependent variation of the wall expansion ratio plays a secondary role that may be justifiably ignored.

This paper presents a general theory and physical interpretation of the interaction between a solid body and a Newtonian fluid flow in terms of the vorticity ω and the compression/expansion variable Π instead of primitive variables, i.e. velocity and pressure. Previous results are included as special simplified cases of the theory. The first part of this paper shows that the action of a solid wall on a fluid can be exclusively attributed to the creation of a vorticity-compressing ω–Π field directly from the wall, a process represented by respective boundary fluxes. The general formulae for these fluxes, applicable to any Newtonian flow over an arbitrarily curved surface, are derived from the force balance on the wall. This part of the study reconfirms and extends Lighthil's (1963) assertion on vorticity-creation physics, clarifies some currently controversial issues, and provides a sound basis for the formulation of initial boundary conditions for the ω-Π variables.The second part of this paper shows that the reaction of a Newtonian flow to a solid body can also be exclusively attributed to that of the ω-Π field created. In particular, the integrated force and moment formulae can be expressed solely in terms of the boundary vorticity flux. This implies an inherent unity of the action and reaction between a solid body and a ω-Π field.In both action and reaction phases the ω-Π coupling on the wall plays an essential role. Thus, once a solid wall is introduced into a flow, any theory that treats ω and Π separately will be physically incomplete.

Transition and turbulence production in a hypersonic boundary layer is investigated in the Mach 6 wind tunnel at Peking University, using Rayleigh-scattering visualization, fast-response pressure measurements, and particle image velocimetry. Detailed analysis of the experimental observations is provided. It is found that, although the second mode is primarily an acoustic wave, it causes the formation of high-frequency vortical waves. Moreover, the second mode interacts strongly with low-frequency waves, which leads to immediate transition to turbulence.freestream velocity, m∕s u = velocity vector, m∕s u = x component of the velocity, m∕s v = y component of the velocity, m∕s w = z component of the velocity, m∕s x = streamwise coordinate along the cone's surface, mm y = coordinate normal to the cone's surface, mm z = transverse coordinate normal to the x-y plane, mm= viscous normal stress, Pa ρ = density, kg∕m 3 τ f = flow time scale, s τ p = particle relaxation time, s Φ = viscous dissipation function per unit volume, kg∕m · s 3 ω = vorticity, 1∕s