Supersonic Jet Excitation using Flapping Injection

Supersonic jet noise reduction is important for high speed military aircraft. Lower acoustic levels would reduce structural fatigue leading to longer lifetime of the jet aircraft. It is not solely structural aspects which are of importance, health issues of the pilot and the airfield per- sonnel are also very important, as high acoustic levels may result in severe hearing damage. It remains a major challenge to reduce the overall noise levels of the aircraft, where the supersonic exhaust is the main noise source for near ground operation. Fluidic injection into the supersonic jet at the nozzle exhaust has been shown as a promising method for noise reduction. It has been shown to speed up the mix- ing process of the main jet, hence reducing the kinetic energy level of the jet and the power of the total acoustic radiation. Furthermore, the interaction mechanism between the fluidic injection and the shock structure in the jet exhaust plays a crucial role in the total noise radia- tion. In this study, LES is used to investigate the change in flow struc- tures of a supersonic (M=1.56) jet from a converging-diverging nozzle. Six fluidic actuators, evenly distributed around the nozzle exit, inject air in a radial direction towards the main flow axis with a total mass flow ratio of 3%. Steady injection is compared with flapping injection. With flapping injection turned on, the injection angle of each injector is varied sinusoidally in the nozzle exit plane and the variation is the same for all injectors. This fluid dynamics video is submitted to the APS DFD Gallery of Fluid Motion 2013 at the 66 the Annual Meeting of the American Physical Society, Division of Fluid Dynamics (24-26 November, Pittsburgh, PA, USA).Comment: 3 pages, 2 linked animations/video

Transforming the shock pattern of supersonic jets using fluidic injection

Double shock diamonds establish in the exhaust of modular convergent-divergent nozzles. These consist of two shock structures; one originating from the nozzle throat and another from its exit. Analyzing the shock pattern developing for different fluidic injection operating conditions, it is shown that fluidic injection allows the rearrangement of the shock structures relative to each other. Overlapping the two structures caused large pressure oscillations in the exhaust and high amplitudes of shock associated noise, whereas staggering the shock structures mitigated these effects. The screech tone frequency did not change for all injection operating configurations, although the shock diamonds had been shifted drastically with respect to each other. Hence, the screech phenomenon is dominated by the primary shock spacing originating from the nozzle throat

Clinical trial: lubiprostone in patients with constipation-associated irritable bowel syndrome – results of two randomized, placebo-controlled studies

Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/75355/1/j.1365-2036.2008.03881.x.pd

Large Eddy Simulation of Highly Compressible Jets with Tripped Boundary Layers

In high-speed aircraft, supersonic jets used for propulsion can lead to very intense aerodynamically generated acoustic noise. Thus, there is a need to study the aerodynamic and aeroacoustic properties of highly compressible jets. In previous studies, several simulations of supersonic jets have been conducted. Unfortunately, the turbulence intensity at the nozzle exit was dependent on the internal geometry of the nozzle and could not be tuned. This is a pity given that, as shown experimentally and numerically for subsonic and supersonic jets, the boundary layer state of the jet affects the jet flow and noise. In this study, a boundary-layer tripping method permitting to obtain an initially turbulent supersonic jet is studied. The influence of the tripped jet boundary layers on the flow and acoustic fields of the jet is analyzed. The impact of nozzle-exit turbulence levels on the noise radiation and notably on the acoustic components specific to supersonic jets (screech noise, broadband shock-associated noise, mixing noise and Mach wave radiation) is discussed

Lubiprostone ameliorates the cystic fibrosis mouse intestinal phenotype

<p>Abstract</p> <p>Background</p> <p>Cystic fibrosis (CF) is caused by mutations in the <it>CFTR </it>gene that impair the function of CFTR, a cAMP-regulated anion channel. In the small intestine loss of CFTR function creates a dehydrated, acidic luminal environment which is believed to cause an accumulation of mucus, a phenotype characteristic of CF. CF mice have small intestinal bacterial overgrowth, an altered innate immune response, and impaired intestinal transit. We investigated whether lubiprostone, which can activate the CLC2 Cl^-channel, would improve the intestinal phenotype in CF mice.</p> <p>Methods</p> <p><it>Cftr^tm1UNC</it>(CF) and wildtype (WT) littermate mice on the C57BL/6J background were used. Lubiprostone (10 μg/kg-day) was administered by gavage for two weeks. Mucus accumulation was estimated from crypt lumen widths in periodic acid-Schiff base, Alcian blue stained sections. Luminal bacterial load was measured by qPCR for the bacterial 16<it>S </it>gene. Gastric emptying and small intestinal transit in fasted mice were assessed using gavaged rhodamine dextran. Gene expression was evaluated by Affymetrix Mouse430 2.0 microarray and qRT-PCR.</p> <p>Results</p> <p>Crypt width in control CF mice was 700% that of WT mice (<it>P </it>< 0.001). Lubiprostone did not affect WT crypt width but, unexpectedly, increased CF crypt width 22% (<it>P </it>= 0.001). Lubiprostone increased bacterial load in WT mice to 490% of WT control levels (<it>P </it>= 0.008). Conversely, lubiprostone decreased bacterial overgrowth in CF mice by 60% (<it>P </it>= 0.005). Lubiprostone increased gastric emptying at 20 min postgavage in both WT (<it>P </it>< 0.001) and CF mice (<it>P </it>< 0.001). Lubiprostone enhanced small intestinal transit in WT mice (<it>P </it>= 0.024) but not in CF mice (<it>P </it>= 0.377). Among other innate immune markers, expression of mast cell genes was elevated 4-to 40-fold in the CF intestine as compared to WT, and lubiprostone treatment of CF mice decreased expression to WT control levels.</p> <p>Conclusions</p> <p>These results indicate that lubiprostone has some benefits for the CF intestinal phenotype, especially on bacterial overgrowth and the innate immune response. The unexpected observation of increased mucus accumulation in the crypts of lubiprostone-treated CF mice suggests the possibility that lubiprostone increases mucus secretion.</p

Lubiprostone Stimulates Duodenal Bicarbonate Secretion in Rats

Lubiprostone, a bicyclic fatty acid, is used for the treatment of chronic constipation. No published study has addressed the effect of lubiprostone on intestinal ion secretion in vivo. The aim of this study was to test the hypothesis that lubiprostone augments duodenal HCO3 − secretion (DBS). Rat proximal duodenal loops were perfused with pH 7.0 Krebs, control vehicle (medium-chain triglycerides), or lubiprostone (0.1–10 μM). We measured DBS with flow-through pH and CO2 electrodes, perfusate [Cl−] with a Cl− electrode, and water flux using a non-absorbable ferrocyanide marker. Some rats were pretreated with a potent, selective CFTR antagonist, CFTRinh-172 (1 mg/kg, ip), 1 h before experiments. Perfusion of lubiprostone concentration dependently increased DBS, whereas net Cl− output and net water output were only increased at 0.1 μM, compared with vehicle. CFTRinh-172 reduced lubiprostone (10 μM)-induced DBS increase, whereas net Cl− output was also unchanged. Nevertheless, CFTRinh-172 reduced basal net water output, which was reversed by lubiprostone. Furthermore, lubiprostone-induced DBS was inhibited by EP4 receptor antagonist, not by an EP1/2 receptor antagonist or by indomethacin pretreatment. In this first study of the effect of lubiprostone on intestinal ion secretion in vivo, lubiprostone stimulated CFTR-dependent DBS without changing net Cl− secretion. This effect supports the hypothesis that Cl− secreted by CFTR is recycled across the apical membrane by anion exchangers. Recovery of water output during CFTR inhibition suggests that lubiprostone may improve the intestinal phenotype in CF patients. Furthermore, increased DBS suggests that lubiprostone may protect the duodenum from acid-induced injury via EP4 receptor activation