On the flow along swept leading edges

Flight tests on the Handley Page suction wing showed that turbulence, generated at the wing root, can propagate along the leading edge and cause the whole flow to be turbulent. The flow on the attachment line of a swept wing was studied in a low speed wind tunnel with particular reference to the problem of turbulent contamination. The critical Reynolds number, R9L, of the attachment line boundary layer for the spanwise spread of turbulence was found to be about 100 for sweep angles in the range 40°- 60°. A device was developed to act as a barrier to the turbulent root flow 30 that a clean laminar flow could exist outboard. This device was shown to be effective up to an Re of at least 170. With the aid of this bump experiments were Possible on L laminar boundary layer at Reynolds numbers above the lower critical value. A spark was used to introduce spots of turbulence into the attachment line boundary layer and the propagation speeds of the leading and trailing edges were measured. The spots expanded, the leading edge moving faster than the trailing edge, at high Reynolds numbers, and contracted at low values. The behaviour of Tollmien-Schlichting waves was also investigated by exciting the flow with sound emanating from a small hole on the attachment line. Measurements of the perturbation phase and amplitude were made downstream of the source and although accurate values of wave length and propagation speed could be found no difficulties were experienced in evaluating the amplification ratio. Nevertheless, all small disturbances decayed at a sufficient distance from the source hole up to the highest Reynolds number tested of 170

Transition in incompressible boundary layers with two-dimensional excrescences

An experimental investigation of the transition process in boundary layers subjected to forward- or aft-facing two-dimensional step excrescences is described. The objective of the work was to characterize the variation of transition Reynolds numbers with measurable roughness and boundary layer parameters, with the specific goal of specifying new tolerance criteria for laminar flow airfoils, alongside a fundamental investigation of linear boundary layer stability mechanisms. Results from an ongoing program of increasing complexity on effects of pressure gradient on excrescence-induced transition are presented. Preliminary N-factor calculations are used to determine the effects of boundary layer stability and attempt to isolate the effect of the disturbance due to the excrescence

Experimental investigation of the vorticity amplification on a swept wing with a blunt leading edge

A high level of turbulence is generated in the region upstream of the leading edge of a wing. The phenomenon has been investigated on two-dimensional wings and the existence of coherent structures at the stagnation point has been observed. The present paper deals with the flow upstream of the leading edge of a swept wing. A swept wing with a blunt leading edge has been used as a model in order to have a relatively thick boundary layer on the attachment line. The experiment has been carried out in a low turbulence wind tunnel and the freestream turbulence has been changed through a metallic string positioned ahead of the model. Two different configurations for the same string have been studied and compared to the clean case

A method of reducing the drag of transport wings

The paper describes research work that has been carried out to reduce the viscous drag of transport aircraft wings by controlling the turbulent contamination on the attachment line. Laminar leading edges will reduce the boundary layer thickness downstream and thus reduce drag. This scenario was postulated by M. Gaster in a paper presented to the AIAA Seattle conference in 2008. The effect of maintaining a laminar attachment line on the overall flow on a wing has been modeled and drag reductions calculated. These values are compared with wind tunnel measurements of viscous drag of a wing with both laminar and turbulent attachment lines

Fatty Acid Incubation of Myotubes From Humans With Type 2 Diabetes Leads to Enhanced Release of β-Oxidation Products Because of Impaired Fatty Acid Oxidation: Effects of Tetradecylthioacetic Acid and Eicosapentaenoic Acid

OBJECTIVE—Increased availability of fatty acids is important for accumulation of intracellular lipids and development of insulin resistance in human myotubes. It is unknown whether different types of fatty acids like eicosapentaenoic acid (EPA) or tetradecylthioacetic acid (TTA) influence these processes

FA1 Induces Pro-Inflammatory and Anti-Adipogenic Pathways/Markers in Human Myotubes Established from Lean, Obese, and Type 2 Diabetic Subjects but Not Insulin Resistance

Aims: Delta like 1/fetal antigen 1 (Dlk1/FA1) is a protein secreted by hormone producing cells in adult human and mice that is known to inhibit adipogenesis. Recent studies demonstrated the role of Dlk1/FA1 in inducing insulin resistance in mice. To investigate the involvement of circulating Dlk1/FA1 in insulin resistance and type 2 diabetes in human subjects, we studied the effects of chronic FA1 on the intermediary metabolism in myotubes established from lean, obese, and type 2 diabetic (T2D) subjects. Methods: Myotube cultures were established from lean and obese control subjects, and obese T2D subjects and treated with soluble FA1 for 4 days supplemented with/without palmitate (PA). Lipid- and glucose metabolism were studied with labeled precursors while quantitative expression of genes was analyzed using real-time PCR. Results: Diabetic myotubes express significantly reduced insulin stimulated glucose metabolism compared to lean myotubes and a significantly decreased basal PA oxidation. Chronic FA1 exposure did not affect the intermediary metabolism in myotubes. Insulin sensitivity of glucose and lipid metabolism was not affected by chronic FA1 exposure in myotubes established from lean, obese, and T2D subjects. Instead, chronic FA1 exposure induced pro-inflammatory cytokines expression (IL-6 and CCL2) in association with reducing adipogenic markers (ADD1, AP2, CD36, and PPARg2) in myotubes. Consistent with this observation, addition of FA1 to cultured myotubes was show to significantly inhibit their differentiation into adipocyte. Conclusion: Our results exclude direct effects of FA1 on glucose and lipid metabolism in cultured myotubes established from lean, obese, and T2D subjects. Therefore, the pathogenesis of FA1-induced IR might mainly be mediated via the FA1-induced stimulation of pro-inflammatory cytokines, which on turn inhibit adipogenesis in human myotubes

Insulin Resistance Is Not Conserved in Myotubes Established from Women with PCOS

Polycystic ovary syndrome (PCOS) is the most common endocrine disorder among premenopausal women, who often develop insulin resistance. We tested the hypothesis that insulin resistance in skeletal muscle of patients with polycystic ovary syndrome (PCOS) is an intrinsic defect, by investigating the metabolic characteristics and gene expression of in vitro differentiated myotubes established from well characterized PCOS subjects.Using radiotracer techniques, RT-PCR and enzyme kinetic analysis we examined myotubes established from PCOS subjects with or without pioglitazone treatment, versus healthy control subjects who had been extensively metabolically characterized in vivo. Results. Myotubes established from PCOS and matched control subjects comprehensively expressed all insulin-sensitive biomarkers; glucose uptake and oxidation, glycogen synthesis and lipid uptake. There were no significant differences between groups either at baseline or during acute insulin stimulation, although in vivo skeletal muscle was insulin resistant. In particular, we found no evidence for defects in insulin-stimulated glycogen synthase activity between groups. Myotubes established from PCOS patients with or without pioglitazone treatment also showed no significant differences between groups, neither at baseline nor during acute insulin stimulation, although in vivo pioglitazone treatment significantly improved insulin sensitivity. Consistently, the myotube cultures failed to show differences in mRNA levels of genes previously demonstrated to differ in PCOS patients with or without pioglitazone treatment (PLEK, SLC22A16, and TTBK).These results suggest that the mechanisms governing insulin resistance in skeletal muscle of PCOS patients in vivo are not primary, but rather adaptive.ClinicalTrials.gov NCT00145340

The Evolution of Modulated Wavetrains Into Turbulent Spots

Experiment are being carried out to study the process by which th almost periodic disturbance waves generated naturally by the freestream evolve into turbulence. The boundary layer on a flat plate has been used for this study. The novelty of the approach is in the form of artificial excitation that is used. In this work the flow is excited artificially by deterministic white noise. The weak T-S wave created develops down stream, becomes nonlinear and blows up locally onto a highly distorted flow. These large local distortions of the mean flow allow very high frequency disturbances to grow and form into small turbulent spots. The spots arise from the excitation, and if the same noise sequence is repeated a spot will form at the same position and time instant relative to the excitation

Growth mechanisms of perturbations in boundary layers over a compliant wall

The temporal modal and nonmodal growth of three-dimensional perturbations in the boundary-layer flow over an infinite compliant flat wall is considered. Using a wall-normal velocity/wall-normal vorticity formalism, the dynamic boundary condition at the compliant wall admits a linear dependence on the eigenvalue parameter, as compared to a quadratic one in the canonical formulation of the problem. This greatly simplifies the accurate calculation of the continuous spectrum by means of a spectral method, thereby yielding a very effective filtering of the pseudospectra as well as a clear identification of instability regions. The regime of global instability is found to be matching the regime of the favorable phase of the forcing by the flow on the compliant wall so as to enhance the amplitude of the wall. An energy-budget analysis for the least-decaying hydroelastic (static-divergence, traveling-wave-flutter and near-stationary transitional) and Tollmien--Schlichting modes in the parameter space reveals the primary routes of energy flow. Moreover, the flow exhibits a slower transient growth for the maximum growth rate of a superposition of streamwise-independent modes due to a complex dependence of the wall-boundary condition with the Reynolds number. The initial and optimal perturbations are compared with the boundary-layer flow over a solid wall; differences and similarities are discussed. Unlike the solid-wall case, viscosity plays a pivotal role in the transient growth. A slowdown of the maximum growth rate with the Reynolds number is uncovered and found to originate in the transition of the fluid-solid interaction from a two-way to a one-way coupling. Finally, a term-by-term energy budget analysis is performed to identify the key contributors to the transient growth mechanism

Increased FAT/CD36 Cycling and Lipid Accumulation in Myotubes Derived from Obese Type 2 Diabetic Patients

BACKGROUND: Permanent fatty acid translocase (FAT/)CD36 relocation has previously been shown to be related to abnormal lipid accumulation in the skeletal muscle of type 2 diabetic patients, however mechanisms responsible for the regulation of FAT/CD36 expression and localization are not well characterized in human skeletal muscle. METHODOLOGY/PRINCIPAL FINDINGS: Primary muscle cells derived from obese type 2 diabetic patients (OBT2D) and from healthy subjects (Control) were used to examine the regulation of FAT/CD36. We showed that compared to Control myotubes, FAT/CD36 was continuously cycling between intracellular compartments and the cell surface in OBT2D myotubes, independently of lipid raft association, leading to increased cell surface FAT/CD36 localization and lipid accumulation. Moreover, we showed that FAT/CD36 cycling and lipid accumulation were specific to myotubes and were not observed in reserve cells. However, in Control myotubes, the induction of FAT/CD36 membrane translocation by the activation of (AMP)-activated protein kinase (AMPK) pathway did not increase lipid accumulation. This result can be explained by the fact that pharmacological activation of AMPK leads to increased mitochondrial beta-oxidation in Control cells. CONCLUSION/SIGNIFICANCE: Lipid accumulation in myotubes derived from obese type 2 diabetic patients arises from abnormal FAT/CD36 cycling while lipid accumulation in Control cells results from an equilibrium between lipid uptake and oxidation. As such, inhibiting FAT/CD36 cycling in the skeletal muscle of obese type 2 diabetic patients should be sufficient to diminish lipid accumulation