94-GT-37 TURBULENCE MEASUREMENTS IN A HEATED, CONCAVE BOUNDARY LAYER UNDER HIGH FREE-STREAM TURBULENCE CONDITIONS 1111111EF41 1111111E1

Abstract Turbulence measurements for both momentum and heat transfer are taken in a low-velocity, turbulent boundary layer growing naturally over a concave wall. The experiments are conducted with negligible streamwise acceleration and a nominal free-stream turbulence intensity of -8%. Comparisons are made with data taken in an earlier study in the same test facility but with a 0.6% freestream turbulence intensity. Results show that elevated free-stream turbulence intensity enhances turbulence transport quantities like uv and 7t in most of the boundary layer. In contrast to the lowturbulence cases, high levels of transport of momentum are measured outside the boundary layer. Stable, Corder-like vortices, present in the flow under low-turbulence conditions, do not form when the freestream turbulence intensity is elevated. Turbulent Prandt1 numbers, Prt, within the log region of the boundary layer over the concave wall increase with streamwise distance to values as high as 1.2. Profiles of Pr' suggest that the increase in momentum transport with increased free-stream turbulence intensity precedes the increase in heat transport. Distributions of near-wall mixing length for momentum remain unchanged on the concave wall when free-stream turbulence intensity is elevated. Both for this level of free-stream turbulence and for the lower level, mixing length distributions increase linearly with distance from the wall following the standard slope. However when free-stream turbulence intensity is elevated, this linear region extends farther into the boundary layer, indicating the emerging importance of larger eddies in the wake of the boundary layer with the high-turbulence free-stream. Because these eddies are damped by the wall, the influence of the wall grows with eddy size

Turbulence Measurements in a Heated, Concave Boundary Layer Under High Free-Stream Turbulence Conditions

Turbulence measurements for both momentum and heat transfer are taken in a low-velocity, turbulent boundary layer growing naturally over a concave wall. The experiments are conducted with negligible streamwise acceleration and a nominal free-stream turbulence intensity of −8%. Comparisons are made with data taken in an earlier study in the same test facility but with a 0.6% free-stream turbulence intensity. Results show that elevated free-stream turbulence intensity enhances turbulence transport quantities like uv and vt in most of the boundary layer. In contrast to the low-turbulence cases, high levels of transport of momentum are measured outside the boundary layer. Stable, Görtler-like vortices, present in the flow under low-turbulence conditions, do not form when the free-stream turbulence intensity is elevated. Turbulent Prandtl numbers, Prt, within the log region of the boundary layer over the concave wall increase with streamwise distance to values as high as 1.2. Profiles of Prt suggest that the increase in momentum transport with increased free-stream turbulence intensity precedes the increase in heat transport. Distributions of near-wall mixing length for momentum remain unchanged on the concave wall when free-stream turbulence intensity is elevated. Both for this level of free-stream turbulence and for the lower level, mixing length distributions increase linearly with distance from the wall following the standard slope. However when free-stream turbulence intensity is elevated, this linear region extends farther into the boundary layer, indicating the emerging importance of larger eddies in the wake of the boundary layer with the high-turbulence free-stream. Because these eddies are damped by the wall, the influence of the wall grows with eddy size.</jats:p

Halting of caspase activity protects tau from MC1-conformational change and aggregation

Intracellular neurofibrillary tangles (NFTs) are the hallmark of Alzheimer’s disease and other tauopathies in which tau, a microtubule-associated protein, loses its ability to stabilize microtubules. Several post-translational modifications including phosphorylation and truncation increase tau’s propensity to aggregate thus forming NFTs; however, the mechanisms underlying tau conformational change and aggregation still remain to be defined. Caspase activation and subsequent proteolytic cleavage of tau is thought to be a potential trigger of this disease-related pathological conformation. The aim of this work was to investigate the link between caspase activation and a disease-related conformational change of tau in a neuroblastoma cell-based model of spontaneous tau aggregation. We demonstrated that caspase induction initiates proteolytic cleavage of tau and generation of conformationally altered and aggregated tau recognized by the MC1 conformational antibody. Most importantly, these events were shown to be attenuated with caspase inhibitors. This implies that therapeutics aimed at inhibiting caspase-mediated tau cleavage may prove beneficial in slowing cleavage and aggregation, thus potentially halting tau pathology and disease progression

Halting of caspase activity protects tau from MC1-conformational change and aggregation

Intracellular neurofibrillary tangles (NFTs) are the hallmark of Alzheimer’s disease and other tauopathies in which tau, a microtubule-associated protein, loses its ability to stabilize microtubules. Several post-translational modifications including phosphorylation and truncation increase tau’s propensity to aggregate thus forming NFTs; however, the mechanisms underlying tau conformational change and aggregation still remain to be defined. Caspase activation and subsequent proteolytic cleavage of tau is thought to be a potential trigger of this disease-related pathological conformation. The aim of this work was to investigate the link between caspase activation and a disease-related conformational change of tau in a neuroblastoma cell-based model of spontaneous tau aggregation. We demonstrated that caspase induction initiates proteolytic cleavage of tau and generation of conformationally altered and aggregated tau recognized by the MC1 conformational antibody. Most importantly, these events were shown to be attenuated with caspase inhibitors. This implies that therapeutics aimed at inhibiting caspase-mediated tau cleavage may prove beneficial in slowing cleavage and aggregation, thus potentially halting tau pathology and disease progression

Halting of caspase activity protects tau from MC1-conformational change and aggregation

Intracellular neurofibrillary tangles (NFTs) are the hallmark of Alzheimer’s disease and other tauopathies in which tau, a microtubule-associated protein, loses its ability to stabilize microtubules. Several post-translational modifications including phosphorylation and truncation increase tau’s propensity to aggregate thus forming NFTs; however, the mechanisms underlying tau conformational change and aggregation still remain to be defined. Caspase activation and subsequent proteolytic cleavage of tau is thought to be a potential trigger of this disease-related pathological conformation. The aim of this work was to investigate the link between caspase activation and a disease-related conformational change of tau in a neuroblastoma cell-based model of spontaneous tau aggregation. We demonstrated that caspase induction initiates proteolytic cleavage of tau and generation of conformationally altered and aggregated tau recognized by the MC1 conformational antibody. Most importantly, these events were shown to be attenuated with caspase inhibitors. This implies that therapeutics aimed at inhibiting caspase-mediated tau cleavage may prove beneficial in slowing cleavage and aggregation, thus potentially halting tau pathology and disease progression