Exhaust Nozzle for a Multitube Detonative Combustion Engine

An improved type of exhaust nozzle has been invented to help optimize the performances of multitube detonative combustion engines. The invention is applicable to both air-breathing and rocket engines used to propel some aircraft and spacecraft, respectively. In a detonative combustion engine, thrust is generated through the expulsion of combustion products from a detonation process in which combustion takes place in a reaction zone coupled to a shock wave. The combustion releases energy to sustain the shock wave, while the shock wave enhances the combustion in the reaction zone. The coupled shockwave/reaction zone, commonly referred to as a detonation, propagates through the reactants at very high speed . typically of the order of several thousands of feet per second (of the order of 1 km/s). The very high speed of the detonation forces combustion to occur very rapidly, thereby contributing to high thermodynamic efficiency. A detonative combustion engine of the type to which the present invention applies includes multiple parallel cylindrical combustion tubes, each closed at the front end and open at the rear end. Each tube is filled with a fuel/oxidizer mixture, and then a detonation wave is initiated at the closed end. The wave propagates rapidly through the fuel/oxidizer mixture, producing very high pressure due to the rapid combustion. The high pressure acting on the closed end of the tube contributes to forward thrust. When the detonation wave reaches the open end of the tube, it produces a blast wave, behind which the high-pressure combustion products are expelled from the tube. The process of filling each combustion tube with a detonable fuel/oxidizer mixture and then producing a detonation repeated rapidly to obtain repeated pulses of thrust. Moreover, the multiple combustion tubes are filled and fired in a repeating sequence. Hence, the pressure at the outlet of each combustion tube varies cyclically. A nozzle of the present invention channels the expansion of the pulsed combustion gases from the multiple combustion tubes into a common exhaust stream, in such a manner as to enhance performance in two ways: (1) It reduces the cyclic variations of pressure at the outlets of the combustion tubes so as to keep the pressure approximately constant near the optimum level needed for filling the tubes, regardless of atmospheric pressure at the altitude of operation; and (2) It maximizes the transfer of momentum from the exhaust gas to the engine, thereby maximizing thrust. The figure depicts a typical engine equipped with a nozzle according to the invention. The nozzle includes an interface section comprising multiple intake ports that couple the outlets of the combustion tubes to a common plenum. Proceeding from its upstream to its downstream end, the interface section tapers to a larger cross-sectional area for flow. This taper fosters expansion of the exhaust gases flowing from the outlets of the combustion tubes and contributes to the desired equalization of exhaust combustion pressure. The cross-sectional area for flow in the common plenum is greater than, or at least equal to, the combined cross-sectional flow areas of the combustor tubes. In the common plenum, the exhaust streams from the individual combustion tubes mix to form a single compound subsonic exhaust stream. Downstream of the common plenum is the throat that tapers to a smaller flow cross section. In this throat, the exhaust gases become compressed to form a compound sonic gas stream. Downstream of the throat is an expansion section, which typically has a bell or a conical shape. (The expansion section can be truncated or even eliminated in the case of an air-breathing engine.) After entering the expansion section, the exhaust gases expand rapidly from compound sonic to compound supersonic speeds and are then vented to the environment. The basic invention admits of numerous variations. For example, the combustion tubes can be arranged around the central axin a symmetrical or asymmetrical pattern other than the one shown in the figure. For another example, the flow cross-sectional area(s) of one or more of the intake ports in the interface section, of the common plenum, the throat, and/or the expansion section can be varied, either symmetrically or asymmetrically, to adjust dynamics of the exhaust stream or to direct the thrust vector away from the central axis

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

Altres ajuts: Department of Health and Social Care (DHSC); Illumina; LifeArc; Medical Research Council (MRC); UKRI; Sepsis Research (the Fiona Elizabeth Agnew Trust); the Intensive Care Society, Wellcome Trust Senior Research Fellowship (223164/Z/21/Z); BBSRC Institute Program Support Grant to the Roslin Institute (BBS/E/D/20002172, BBS/E/D/10002070, BBS/E/D/30002275); UKRI grants (MC_PC_20004, MC_PC_19025, MC_PC_1905, MRNO2995X/1); UK Research and Innovation (MC_PC_20029); the Wellcome PhD training fellowship for clinicians (204979/Z/16/Z); the Edinburgh Clinical Academic Track (ECAT) programme; the National Institute for Health Research, the Wellcome Trust; the MRC; Cancer Research UK; the DHSC; NHS England; the Smilow family; the National Center for Advancing Translational Sciences of the National Institutes of Health (CTSA award number UL1TR001878); the Perelman School of Medicine at the University of Pennsylvania; National Institute on Aging (NIA U01AG009740); the National Institute on Aging (RC2 AG036495, RC4 AG039029); the Common Fund of the Office of the Director of the National Institutes of Health; NCI; NHGRI; NHLBI; NIDA; NIMH; NINDS.Critical COVID-19 is caused by immune-mediated inflammatory lung injury. Host genetic variation influences the development of illness requiring critical care or hospitalization 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