Design integration and noise studies for jet STOL aircraft. Task 7C: Augmentor wing cruise blowing valveless system. Volume 1: Static testing of augmentor noise and performance

Static performance and acoustic tests were conducted on a two-dimensional one-third-scale augmentor flap model that simulated a cruise blowing augmentor system designed for a scale augmentor flap model that simulated a cruise blowing augmentor, which offers a degree of 150-passenger STOL airplane. The cruise blowing augmentor, which offers a degree of simplicity by requiring no fan air diverter valves, was simulated by fitting existing lobe suppressor nozzles with new nozzle fairings. Flow turning performance of the cruise blowing augmentor was measured through a large range of flap deflection angles. The noise suppression characteristics of a multilayer acoustic lining installed in the augmentor were also measured

Static noise tests on augmentor wing jet STOL research aircraft (C8A Buffalo)

Results are presented for full scale ground static acoustic tests of over-area conical nozzles and a lobe nozzle installed on the Augmentor Wing Jet STOL Research Aircraft, a modified C8A Buffalo. The noise levels and spectrums of the test nozzles are compared against those of the standard conical nozzle now in use on the aircraft. Acoustic evaluations at 152 m (500 ft), 304 m (1000 ft), and 1216 m (4000 ft) are made at various engine power settings with the emphasis on approach and takeoff power. Appendix A contains the test log and propulsion calculations. Appendix B gives the original test plan, which was closely adhered to during the test. Appendix C describes the acoustic data recording and reduction systems, with calibration details

Noise and static performance characteristics of a STOL aircraft jet flap

Static noise and performance tests were conducted on a 1/4-scale jet flap model with a multilobe nozzle of array area ratio of 2.7. The model nozzle and flap tested were a two-dimensional section of a distributed blowing system similar to previously investigated augmentor wing systems without the upper shroud and intake door. Noise data were measured with the nozzle alone and also during attached flow conditions with the flap at two turning angles representing takeoff and approach conditions. The noise data are scaled to a 200,000-lb TOGW four-engine airplane and are presented in terms of perceived noise level and one-third octave band sound pressure level. Comparisons are made with the noise levels produced by an augmentor wing airplane fitted with a three-element acoustically lined augmentor flap. The static performance is presented in terms of thrust recovery and effective turning angle

Test of acoustic tone source and propulsion performance of C8A Buffalo suppressor nozzle

Results are presented for a static acoustic and propulsion performance ground test conducted at the Boeing hot nozzle facility on the C8A Buffalo noise suppressor nozzle. Various methods to remove a nozzle-associated 2000-Hz tone are evaluated. Results of testing this rectangular-array lobed nozzle for propulsion performance and acoustic directivity are reported. Recommendations for future nozzle modifications and further testing are included. Appendix A contains the test plan. Appendix B presents the test log. Appendix C contains plots of the one-third octave sound pressure levels recorded during the test. Appendix D describes the acoustic data recording and reduction systems. The performance data is tabulated in Appendix E

A Geophysical Atlas for Interpretation of Satellite-derived Data

A compilation of maps of global geophysical and geological data plotted on a common scale and projection is presented. The maps include satellite gravity, magnetic, seismic, volcanic, tectonic activity, and mantle velocity anomaly data. The Bibliographic references for all maps are included

Antiinflammatory Therapy with Canakinumab for Atherosclerotic Disease

Background: Experimental and clinical data suggest that reducing inflammation without affecting lipid levels may reduce the risk of cardiovascular disease. Yet, the inflammatory hypothesis of atherothrombosis has remained unproved. Methods: We conducted a randomized, double-blind trial of canakinumab, a therapeutic monoclonal antibody targeting interleukin-1β, involving 10,061 patients with previous myocardial infarction and a high-sensitivity C-reactive protein level of 2 mg or more per liter. The trial compared three doses of canakinumab (50 mg, 150 mg, and 300 mg, administered subcutaneously every 3 months) with placebo. The primary efficacy end point was nonfatal myocardial infarction, nonfatal stroke, or cardiovascular death. RESULTS: At 48 months, the median reduction from baseline in the high-sensitivity C-reactive protein level was 26 percentage points greater in the group that received the 50-mg dose of canakinumab, 37 percentage points greater in the 150-mg group, and 41 percentage points greater in the 300-mg group than in the placebo group. Canakinumab did not reduce lipid levels from baseline. At a median follow-up of 3.7 years, the incidence rate for the primary end point was 4.50 events per 100 person-years in the placebo group, 4.11 events per 100 person-years in the 50-mg group, 3.86 events per 100 person-years in the 150-mg group, and 3.90 events per 100 person-years in the 300-mg group. The hazard ratios as compared with placebo were as follows: in the 50-mg group, 0.93 (95% confidence interval [CI], 0.80 to 1.07; P = 0.30); in the 150-mg group, 0.85 (95% CI, 0.74 to 0.98; P = 0.021); and in the 300-mg group, 0.86 (95% CI, 0.75 to 0.99; P = 0.031). The 150-mg dose, but not the other doses, met the prespecified multiplicity-adjusted threshold for statistical significance for the primary end point and the secondary end point that additionally included hospitalization for unstable angina that led to urgent revascularization (hazard ratio vs. placebo, 0.83; 95% CI, 0.73 to 0.95; P = 0.005). Canakinumab was associated with a higher incidence of fatal infection than was placebo. There was no significant difference in all-cause mortality (hazard ratio for all canakinumab doses vs. placebo, 0.94; 95% CI, 0.83 to 1.06; P = 0.31). Conclusions: Antiinflammatory therapy targeting the interleukin-1β innate immunity pathway with canakinumab at a dose of 150 mg every 3 months led to a significantly lower rate of recurrent cardiovascular events than placebo, independent of lipid-level lowering. (Funded by Novartis; CANTOS ClinicalTrials.gov number, NCT01327846.

Whole-genome sequencing reveals host factors underlying critical COVID-19

Critical COVID-19 is caused by immune-mediated inflammatory lung injury. Host genetic variation influences the development of illness requiring critical care1 or hospitalization2–4 after infection with SARS-CoV-2. The GenOMICC (Genetics of Mortality in Critical Care) study enables the comparison of genomes from individuals who are critically ill with those of population controls to find underlying disease mechanisms. Here we use whole-genome sequencing in 7,491 critically ill individuals compared with 48,400 controls to discover and replicate 23 independent variants that significantly predispose to critical COVID-19. We identify 16 new independent associations, including variants within genes that are involved in interferon signalling (IL10RB and PLSCR1), leucocyte differentiation (BCL11A) and blood-type antigen secretor status (FUT2). Using transcriptome-wide association and colocalization to infer the effect of gene expression on disease severity, we find evidence that implicates multiple genes—including reduced expression of a membrane flippase (ATP11A), and increased expression of a mucin (MUC1)—in critical disease. Mendelian randomization provides evidence in support of causal roles for myeloid cell adhesion molecules (SELE, ICAM5 and CD209) and the coagulation factor F8, all of which are potentially druggable targets. Our results are broadly consistent with a multi-component model of COVID-19 pathophysiology, in which at least two distinct mechanisms can predispose to life-threatening disease: failure to control viral replication; or an enhanced tendency towards pulmonary inflammation and intravascular coagulation. We show that comparison between cases of critical illness and population controls is highly efficient for the detection of therapeutically relevant mechanisms of disease

Whole-genome sequencing reveals host factors underlying critical COVID-19

Critical COVID-19 is caused by immune-mediated inflammatory lung injury. Host genetic variation influences the development of illness requiring critical care1 or hospitalization2,3,4 after infection with SARS-CoV-2. The GenOMICC (Genetics of Mortality in Critical Care) study enables the comparison of genomes from individuals who are critically ill with those of population controls to find underlying disease mechanisms. Here we use whole-genome sequencing in 7,491 critically ill individuals compared with 48,400 controls to discover and replicate 23 independent variants that significantly predispose to critical COVID-19. We identify 16 new independent associations, including variants within genes that are involved in interferon signalling (IL10RB and PLSCR1), leucocyte differentiation (BCL11A) and blood-type antigen secretor status (FUT2). Using transcriptome-wide association and colocalization to infer the effect of gene expression on disease severity, we find evidence that implicates multiple genes—including reduced expression of a membrane flippase (ATP11A), and increased expression of a mucin (MUC1)—in critical disease. Mendelian randomization provides evidence in support of causal roles for myeloid cell adhesion molecules (SELE, ICAM5 and CD209) and the coagulation factor F8, all of which are potentially druggable targets. Our results are broadly consistent with a multi-component model of COVID-19 pathophysiology, in which at least two distinct mechanisms can predispose to life-threatening disease: failure to control viral replication; or an enhanced tendency towards pulmonary inflammation and intravascular coagulation. We show that comparison between cases of critical illness and population controls is highly efficient for the detection of therapeutically relevant mechanisms of disease