Semiempirical airframe noise prediction model and evaluation with flight data

A semiempirical maximum overall sound pressure level (OASPL) airframe noise model was derived. Noise radiated from aircraft wings was modeled on the trailing edge diffractes quadrupole sound theory. The acoustic dipole sound theory was used to model noise from the landing gear. The model was correlated with maximum OASPL flyover noise measurements obtained for three jet aircraft. One third octave band sound pressure level flyover data was correlated and interpreted

Landing approach airframe noise measurements and analysis

Flyover measurements of the airframe noise produced by the AeroCommander, JetStar, CV-990, and B-747 airplanes are presented for various landing approach configurations. Empirical and semiempirical techniques are presented to correlate the measured airframe noise with airplane design and aerodynamic parameters. Airframe noise for the jet-powered airplanes in the clean configuration (flaps and gear retracted) was found to be adequately represented by a function of airplane weight and the fifth power of airspeed. Results show the airframe noise for all four aircraft in the landing configuration (flaps extended and gear down) also varied with the fifth power of airspeed, but this noise level could not be represented by the addition of a constant to the equation for clean-configuration airframe noise

Measured noise reductions resulting from modified approach procedures for business jet aircraft

Five business jet airplanes were flown to determine the noise reductions that result from the use of modified approach procedures. The airplanes tested were a Gulfstream 2, JetStar, Hawker Siddeley 125-400, Sabreliner-60 and LearJet-24. Noise measurements were made 3, 5, and 7 nautical miles from the touchdown point. In addition to a standard 3 deg glide slope approach, a 4 deg glide slope approach, a 3 deg glide slope approach in a low-drag configuration, and a two-segment approach were flown. It was found that the 4 deg approach was about 4 EPNdB quieter than the standard 3 deg approach. Noise reductions for the low-drag 3 deg approach varied widely among the airplanes tested, with an average of 8.5 EPNdB on a fleet-weighted basis. The two-segment approach resulted in noise reductions of 7 to 8 EPNdB at 3 and 5 nautical miles from touchdown, but only 3 EPNdB at 7 nautical miles from touchdown when the airplanes were still in level flight prior to glide slope intercept. Pilot ratings showed progressively increasing workload for the 4 deg, low-drag 3 deg, and two-segment approaches

Role of TRAIL and the pro-apoptotic Bcl-2 homolog Bim in acetaminophen-induced liver damage

Acetaminophen (N-acetyl-para-aminophenol (APAP), paracetamol) is a commonly used analgesic and antipyretic agent. Although considered safe at therapeutic doses, accidental or intentional overdose causes acute liver failure characterized by centrilobular hepatic necrosis with high morbidity and mortality. Although many molecular aspects of APAP-induced cell death have been described, no conclusive mechanism has been proposed. We recently identified TNF-related apoptosis-inducing ligand (TRAIL) and c-Jun kinase (JNK)-dependent activation of the pro-apoptotic Bcl-2 homolog Bim as an important apoptosis amplification pathway in hepatocytes. In this study, we, thus, investigated the role of TRAIL, c-JNK and Bim in APAP-induced liver damage. Our results demonstrate that TRAIL strongly synergizes with APAP in inducing cell death in hepatocyte-like cells lines and primary hepatocyte. Furthermore, we found that APAP strongly induces the expression of Bim in a c-JNK-dependent manner. Consequently, TRAIL- or Bim-deficient mice were substantially protected from APAP-induced liver damage. This study identifies the TRAIL-JNK-Bim axis as a novel target in the treatment of APAP-induced liver damage and substantiates its general role in hepatocyte death

Could sound be used as a strategy for reducing symptoms of perceived motion sickness?

<p>Abstract</p> <p>Background</p> <p>Working while exposed to motions, physically and psychologically affects a person. Traditionally, motion sickness symptom reduction has implied use of medication, which can lead to detrimental effects on performance. Non-pharmaceutical strategies, in turn, often require cognitive and perceptual attention. Hence, for people working in high demand environments where it is impossible to reallocate focus of attention, other strategies are called upon. The aim of the study was to investigate possible impact of a mitigation strategy on perceived motion sickness and psychophysiological responses, based on an artificial sound horizon compared with a non-positioned sound source.</p> <p>Methods</p> <p>Twenty-three healthy subjects were seated on a motion platform in an artificial sound horizon or in non-positioned sound, in random order with one week interval between the trials. Perceived motion sickness (Mal), maximum duration of exposure (ST), skin conductance, blood volume pulse, temperature, respiration rate, eye movements and heart rate were measured continuously throughout the trials.</p> <p>Results</p> <p>Mal scores increased over time in both sound conditions, but the artificial sound horizon, applied as a mitigation strategy for perceived motion sickness, showed no significant effect on Mal scores or ST. The number of fixations increased with time in the non-positioned sound condition. Moreover, fixation time was longer in the non-positioned sound condition compared with sound horizon, indicating that the subjects used more time to fixate and, hence, assumingly made fewer saccades.</p> <p>Conclusion</p> <p>A subliminally presented artificial sound horizon did not significantly affect perceived motion sickness, psychophysiological variables or the time the subjects endured the motion sickness triggering stimuli. The number of fixations and fixation times increased over time in the non-positioned sound condition.</p

Acrolein Induces Endoplasmic Reticulum Stress and Causes Airspace Enlargement

BACKGROUND: Given the relative abundance and toxic potential of acrolein in inhaled cigarette smoke, it is surprising how little is known about the pulmonary and systemic effects of acrolein. Here we test the hypothesis whether systemic administration of acrolein could cause endoplasmic reticulum (ER) stress, and lung cell apoptosis, leading to the enlargement of the alveolar air spaces in rats. METHODS: Acute and chronic effects of intraperitoneally administered acrolein were tested. Mean alveolar airspace area was measured by using light microscopy and imaging system software. TUNEL staining and immunohistochemistry (IHC) for active caspase 3 and Western blot analysis for active caspase 3, and caspase 12 were performed to detect apoptosis. The ER-stress related gene expression in the lungs was determined by Quantitative real-time PCR analysis. Acrolein-protein adducts in the lung tissue were detected by IHC. RESULTS: Acute administration of acrolein caused a significant elevation of activated caspase 3, upregulation of VEGF expression and induced ER stress proteins in the lung tissue. The chronic administration of acrolein in rats led to emphysematous lung tissue remodeling. TUNEL staining and IHC for cleaved caspase 3 showed a large number of apoptotic septal cells in the acrolein-treated rat lungs. Chronic acrolein administration cause the endoplasmic reticulum stress response manifested by significant upregulation of ATF4, CHOP and GADd34 expression. In smokers with COPD there was a considerable accumulation of acrolein-protein adducts in the inflammatory, airway and vascular cells. CONCLUSIONS: Systemic administration of acrolein causes endoplasmic reticulum stress response, lung cell apoptosis, and chronic administration leads to the enlargement of the alveolar air spaces and emphysema in rats. The substantial accumulation of acrolein-protein adducts in the lungs of COPD patients suggest a role of acrolein in the pathogenesis of emphysema