1/3-Octave Analysis of Core/Combustor-Noise Measurements for the DGEN Aeropropulsion Research Turbofan with Application to Noise Prediction

This work continues the analysis of data obtained during a 2017 NASA DGEN Aeropropulsion Research Turbofan (DART) core/combustor-noise baseline test in the NASA GRC Aero-Acoustic Propulsion Laboratory (AAPL). The DART is a cost-efficient testbed for the study of core-noise physics and mitigation. Acoustic data were simultaneously acquired using the AAPL overhead microphone array in the engine aft-quadrant farfield, a single midfield microphone, and two infinite-tube-probe sensors for unsteady pressures at the core-nozzle exit. The data are here examined on an 1/3-octave basis as a first step in extending and improving core-noise prediction capability

An Analytical Assessment of NASA's N+1 Subsonic Fixed Wing Project Noise Goal

The Subsonic Fixed Wing Project of NASA's Fundamental Aeronautics Program has adopted a noise reduction goal for new, subsonic, single-aisle, civil aircraft expected to replace current 737 and A320 airplanes. These so-called 'N+1' aircraft - designated in NASA vernacular as such since they will follow the current, in-service, 'N' airplanes - are hoped to achieve certification noise goal levels of 32 cumulative EPNdB under current Stage 4 noise regulations. A notional, N+1, single-aisle, twinjet transport with ultrahigh bypass ratio turbofan engines is analyzed in this study using NASA software and methods. Several advanced noise-reduction technologies are analytically applied to the propulsion system and airframe. Certification noise levels are predicted and compared with the NASA goal

A Process for Assessing NASA's Capability in Aircraft Noise Prediction Technology

An acoustic assessment is being conducted by NASA that has been designed to assess the current state of the art in NASA s capability to predict aircraft related noise and to establish baselines for gauging future progress in the field. The process for determining NASA s current capabilities includes quantifying the differences between noise predictions and measurements of noise from experimental tests. The computed noise predictions are being obtained from semi-empirical, analytical, statistical, and numerical codes. In addition, errors and uncertainties are being identified and quantified both in the predictions and in the measured data to further enhance the credibility of the assessment. The content of this paper contains preliminary results, since the assessment project has not been fully completed, based on the contributions of many researchers and shows a select sample of the types of results obtained regarding the prediction of aircraft noise at both the system and component levels. The system level results are for engines and aircraft. The component level results are for fan broadband noise, for jet noise from a variety of nozzles, and for airframe noise from flaps and landing gear parts. There are also sample results for sound attenuation in lined ducts with flow and the behavior of acoustic lining in ducts

GWAS analysis of handgrip and lower body strength in older adults in the CHARGE consortium

Decline in muscle strength with aging is an important predictor of health trajectory in the elderly. Several factors, including genetics, are proposed contributors to variability in muscle strength. To identify genetic contributors to muscle strength, a meta-analysis of genomewide association studies of handgrip was conducted. Grip strength was measured using a handheld dynamometer in 27 581 individuals of European descent over 65 years of age from 14 cohort studies. Genomewide association analysis was conducted on ~2.7 million imputed and genotyped variants (SNPs). Replication of the most significant findings was conducted using data from 6393 individuals from three cohorts. GWAS of lower body strength was also characterized in a subset of cohorts. Two genomewide significant (P-value< 5 × 10−8) and 39 suggestive (P-value< 5 × 10−5) associations were observed from meta-analysis of the discovery cohorts. After meta-analysis with replication cohorts, genomewide significant association was observed for rs752045 on chromosome 8 (β = 0.47, SE = 0.08, P-value = 5.20 × 10−10). This SNP is mapped to an intergenic region and is located within an accessible chromatin region (DNase hypersensitivity site) in skeletal muscle myotubes differentiated from the human skeletal muscle myoblasts cell line. This locus alters a binding motif of the CCAAT/enhancer-binding protein-β (CEBPB) that is implicated in muscle repair mechanisms. GWAS of lower body strength did not yield significant results. A common genetic variant in a chromosomal region that regulates myotube differentiation and muscle repair may contribute to variability in grip strength in the elderly. Further studies are needed to uncover the mechanisms that link this genetic variant with muscle strength

The relationship between coronary calcification and the natural history of coronary artery disease

OBJECTIVES The aim of the current study was to explore the impact of plaque calcification in terms of absolute calcified plaque volume (CPV) and in the context of its percentage of the total plaque volume at a lesion and patient level on the progression of coronary artery disease.BACKGROUND Coronary artery calcification is an established marker of risk of future cardiovascular events. Despite this, plaque calcification is also considered a marker of plaque stability, and it increases in response to medical therapy.METHODS This analysis included 925 patients with 2,568 lesions from the PARADIGM (Progression of Atherosclerotic Plaque Determined by Computed Tomographic Angiography Imaging) registry, in which patients underwent clinically indicated serial coronary computed tomography angiography. Plaque calcification was examined by using CPV and percent CPV (PCPV), calculated as (CPV/plaque volume) x 100 at a per-plaque and per-patient level (summation of all individual plaques).RESULTS CPV was strongly correlated with plaque volume (r = 0.780; p < 0.001) at baseline and with plaque progression (r = 0.297; p < 0.001); however, this association was reversed after accounting for plaque volume at baseline (r = -0146; p < 0.001). In contrast, PCPV was an independent predictor of a reduction in plaque volume (r = -0.11; p < 0.001) in univariable and multivariable linear regression analyses. Patient-level analysis showed that high CPV was associated with incident major adverse cardiac events (hazard ratio: 3.01: 95% confidence interval: 1.58 to 5.72), whereas high PCPV was inversely associated with major adverse cardiac events (hazard ratio: 0.529; 95% confidence interval: 0.229 to 0.968) in multivariable analysis.CONCLUSIONS Calcified plaque is a marker for risk of adverse events and disease progression due to its strong association with the total plaque burden. When considered as a percentage of the total plaque volume, increasing PCPV is a marker of plaque stability and reduced risk at both a lesion and patient level. (C) 2021 by the American College of Cardiology Foundation.Cardiolog

A meta-analysis of genome-wide association studies identifies multiple longevity genes

Human longevity is heritable, but genome-wide association (GWA) studies have had limited success. Here, we perform two meta-analyses of GWA studies of a rigorous longevity phenotype definition including 11,262/3484 cases surviving at or beyond the age corresponding to the 90th/99th survival percentile, respectively, and 25,483 controls whose age at death or at last contact was at or below the age corresponding to the 60th survival percentile. Consistent with previous reports, rs429358 (apolipoprotein E (ApoE) ε4) is associated with lower odds of surviving to the 90th and 99th percentile age, while rs7412 (ApoE ε2) shows the opposite. Moreover, rs7676745, located near GPR78, associates with lower odds of surviving to the 90th percentile age. Gene-level association analysis reveals a role for tissue-specific expression of multiple genes in longevity. Finally, genetic correlation of the longevity GWA results with that of several disease-related phenotypes points to a shared genetic architecture between health and longevity