Performance Characteristics of an Axial-flow Transonic Compressor Operating up to Tip Relative Inlet Mach Number of 1.34

Performance data are presented for a transonic axial-flow compressor rotor designed to operate at a tip speed of 1300 ft/sec with maximum relative tip Mach number of 1.37. The compressor had an inlet diameter of 16 inches, a hub-tip diameter ratio of 0.5 and design specific weight flow of 31.1 (lb/sec/(sq ft frontal area). Experimental values of relative total-pressure-loss coefficient were considerably higher than the assumed values. This disparity, hub choking, and application of the simple radial-equilibrium concept are discussed. The data of this report are used to extend previously presented correlation plots of compressor design parameters to higher Mach numbers

Performance of Compressor of XJ-41-V Turbojet Engine VI - Analysis of Compressor Flow Choking

An extended analysis was made of the previously reported performance investigation of the original compressor from the XJ-41-v turbojet engine and a similar compressor revised a to obtain a 33-percent increase in the geometric passage area at the vaned-collector entrance. This analysis was based on the concept of the vaned-collector entrance as the throat section of a nozzle. Because of nonuniform air distribution at the vaned-collector entrance, approximately 90 percent of the available flow area was utilized in the original compressor and 94percent in the revised com$ressor. The increase in maximum weight flow obtained with the revised compressor was disproportionate to the increased effective critical throat area because. the air density at the revised vaned-collector entrance for maximum flow was lower than that obtained in the original compressor. This reduction in density resulted from the large pressure losses near the impeller inlet of the revised compressor, which is indicative of impending flow choking in the impeller, The.calculated maximum corrected weight-flow capacity of a compressor consisting of the revised vaneless diffuser and vaned collector with a theoretical impeller that combined peak impeller pressure ratio and peak impeller efficiency at the . maximum flow point would be 112 pounds per second for an equivalent impeller speed of 11,500 rpm

Performance of Compressor of XJ-41-V Turbojet Engine

An investigation of the XJ-41-V turbojet-engine compressor was conducted to determine the performance of the compressor and to obtain fundamental information on the aerodynamic problems associated with large centrifugal-type compressors. The results of the research conducted on the original compressor indicated the compressor would not meet the desired engine-design air-flow requirements because of an air-flow restriction in the vaned collector. The compressor air-flow choking point occurred near the entrance to the vaned-collector passage and was instigated by a poor mass-flow distribution at the vane entrance and from relatively large negative angles of attack of the air stream along the entrance edges of the vanes at the outer passage wall and large positive angles of attack at the inner passage wall. As a result of the analysis, a design change of the vaned collector entrance is recommended for improving the maximum flow capacity of the compressor

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

A922 Sequential measurement of 1 hour creatinine clearance (1-CRCL) in critically ill patients at risk of acute kidney injury (AKI)

Meeting abstrac

Dimethyl fumarate in patients admitted to hospital with COVID-19 (RECOVERY): a randomised, controlled, open-label, platform trial

Dimethyl fumarate (DMF) inhibits inflammasome-mediated inflammation and has been proposed as a treatment for patients hospitalised with COVID-19. This randomised, controlled, open-label platform trial (Randomised Evaluation of COVID-19 Therapy [RECOVERY]), is assessing multiple treatments in patients hospitalised for COVID-19 (NCT04381936, ISRCTN50189673). In this assessment of DMF performed at 27 UK hospitals, adults were randomly allocated (1:1) to either usual standard of care alone or usual standard of care plus DMF. The primary outcome was clinical status on day 5 measured on a seven-point ordinal scale. Secondary outcomes were time to sustained improvement in clinical status, time to discharge, day 5 peripheral blood oxygenation, day 5 C-reactive protein, and improvement in day 10 clinical status. Between 2 March 2021 and 18 November 2021, 713 patients were enroled in the DMF evaluation, of whom 356 were randomly allocated to receive usual care plus DMF, and 357 to usual care alone. 95% of patients received corticosteroids as part of routine care. There was no evidence of a beneficial effect of DMF on clinical status at day 5 (common odds ratio of unfavourable outcome 1.12; 95% CI 0.86-1.47; p = 0.40). There was no significant effect of DMF on any secondary outcome

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

Dimethyl fumarate in patients admitted to hospital with COVID-19 (RECOVERY): a randomised, controlled, open-label, platform trial

Dimethyl fumarate (DMF) inhibits inflammasome-mediated inflammation and has been proposed as a treatment for patients hospitalised with COVID-19. This randomised, controlled, open-label platform trial (Randomised Evaluation of COVID-19 Therapy [RECOVERY]), is assessing multiple treatments in patients hospitalised for COVID-19 (NCT04381936, ISRCTN50189673). In this assessment of DMF performed at 27 UK hospitals, adults were randomly allocated (1:1) to either usual standard of care alone or usual standard of care plus DMF. The primary outcome was clinical status on day 5 measured on a seven-point ordinal scale. Secondary outcomes were time to sustained improvement in clinical status, time to discharge, day 5 peripheral blood oxygenation, day 5 C-reactive protein, and improvement in day 10 clinical status. Between 2 March 2021 and 18 November 2021, 713 patients were enroled in the DMF evaluation, of whom 356 were randomly allocated to receive usual care plus DMF, and 357 to usual care alone. 95% of patients received corticosteroids as part of routine care. There was no evidence of a beneficial effect of DMF on clinical status at day 5 (common odds ratio of unfavourable outcome 1.12; 95% CI 0.86-1.47; p = 0.40). There was no significant effect of DMF on any secondary outcome