Experimental performance of the regenerator for the Chrysler upgraded automotive gas turbine engine

Automobile gas turbine engine regenerator performance was studied in a regenerator test facility that provided a satisfactory simulation of the actual engine operating environment but with independent control of airflow and gas flow. Velocity and temperature distributions were measured immediately downstream of both the core high-pressure-side outlet and the core low-pressure-side outlet. For the original engine housing, the regenerator temperature effectiveness was 1 to 2 percent higher than the design value, and the heat transfer effectiveness was 2 to 4 percent lower than the design value over the range of test conditions simulating 50 to 100 percent of gas generator speed. Recalculating the design values to account for seal leakage decreased the design heat transfer effectiveness to values consistent with those measured herein. A baffle installed in the engine housing high-pressure-side inlet provided more uniform velocities out of the regenerator but did not improve the effectiveness. A housing designed to provide more uniform axial flow to the regenerator was also tested. Although temperature uniformity was improved, the effectiveness values were not improved. Neither did 50-percent flow blockage (90 degree segment) applied to the high-pressure-side inlet change the effectiveness significantly

Performance of a Brayton power system with a space type radiator

Test results of an experimental investigation to measure Brayton engine performance while operating at the sink temperatures of a typical low earth orbit are presented. The results indicate that the radiator area was slightly oversized. The steady state and transient responses of the power system to the sink temperatures in orbit were measured. During the orbital operation, the engine did not reach the steady state operation of either sun or shade conditions. The alternator power variation during orbit was + or - 4 percent from its mean value of 9.3 kilowatts

Changes in SARS-CoV-2 Spike versus Nucleoprotein Antibody Responses Impact the Estimates of Infections in Population-Based Seroprevalence Studies.

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2)-specific antibody responses to the spike (S) protein monomer, S protein native trimeric form, or the nucleocapsid (N) proteins were evaluated in cohorts of individuals with acute infection (n = 93) and in individuals enrolled in a postinfection seroprevalence population study (n = 578) in Switzerland. Commercial assays specific for the S1 monomer, for the N protein, or within a newly developed Luminex assay using the S protein trimer were found to be equally sensitive in antibody detection in the acute-infection-phase samples. Interestingly, compared to anti-S antibody responses, those against the N protein appear to wane in the postinfection cohort. Seroprevalence in a "positive patient contacts" group (n = 177) was underestimated by N protein assays by 10.9 to 32.2%, while the "randomly selected" general population group (n = 311) was reduced by up to 45% relative to the S protein assays. The overall reduction in seroprevalence targeting only anti-N antibodies for the total cohort ranged from 9.4 to 31%. Of note, the use of the S protein in its native trimer form was significantly more sensitive compared to monomeric S proteins. These results indicate that the assessment of anti-S IgG antibody responses against the native trimeric S protein should be implemented to estimate SARS-CoV-2 infections in population-based seroprevalence studies.IMPORTANCE In the present study, we have determined SARS-CoV-2-specific antibody responses in sera of acute and postinfection phase subjects. Our results indicate that antibody responses against viral S and N proteins were equally sensitive in the acute phase of infection, but that responses against N appear to wane in the postinfection phase where those against the S protein persist over time. The most sensitive serological assay in both acute and postinfection phases used the native S protein trimer as the binding antigen, which has significantly greater conformational epitopes for antibody binding compared to the S1 monomer protein used in other assays. We believe these results are extremely important in order to generate correct estimates of SARS-CoV-2 infections in the general population. Furthermore, the assessment of antibody responses against the trimeric S protein will be critical to evaluate the durability of the antibody response and for the characterization of a vaccine-induced antibody response

Design of a bed load and driftwood filtering dam, analysis of the phenomena and hydraulic design

Flood protection often calls on to the realization of retention works for bed load as well as wood and debris flow. Certain relatively recent arrangements did not perform according to their intended function, what shows the complexity of the design and the implementation of such works. Adaptations were necessary to reach the security objectives. The design of a retention dam for solid materials and floating driftwood requires the consideration of numerous hydraulic and material transport processes. The analyses and design validation can be made with two approaches: physical modelling by the construction of a reduced scale model and the test realization or numerical simulation, by means of software packages such as GESMAT (1D) or TOPOFLOW (2D). The present work consists in implementing both approaches, in estimating and in comparing the answers which could be given for a bed load and debris flow filtering dam on a river with a slope of the order of 10%. Thanks to water level gauges and visual observations during tests on the physical model, the progression of the obstructions by driftwood and bed load is well understood, and the effectiveness of these obstructions proven. The tested work plays at first a role of filtering and retention and secondly a role of side overflow towards a zone with low damage potential, when the capacity of the in-stream retention space is reached. The performed numerical simulations, essentially in 1D, reproduce well the phenomena of bed load aggradation. Moreover, the potential obstruction by floating wood is considered and influences the behavior of the structure. By putting in parallel physical and numerical models, it was possible thanks to the results from the physical scale model to refine the numerical simulation tools taking into consideration additional components and behavior-type rules. These further established rules can now be used for other cases where physical modelling is not foreseen

A cost-effective heuristic to schedule local and remote memory in cluster computers

Cluster computers represent a cost-effective alternative solution to supercomputers. In these systems, it is common to constrain the memory address space of a given processor to the local motherboard. Constraining the system in this way is much cheaper than using a full-fledged shared memory implementation among motherboards. However, memory usage among motherboards can be unfairly balanced. On the other hand, remote memory access (RMA) hardware provides fast interconnects among the motherboards of a cluster. RMA devices can be used to access remote RAM memory from a local motherboard. This work focuses on this capability in order to achieve a better global use of the total RAM memory in the system. More precisely, the address space of local applications is extended to remote motherboards and is used to access remote RAM memory. This paper presents an ideal memory scheduling algorithm and proposes a cost-effective heuristic to allocate local and remote memory among local applications. Compared to the devised ideal algorithm, the heuristic obtains the same (or closely resembling) results while largely reducing the computational cost. In addition, we analyze the impact on the performance of stand alone applications varying the memory distribution among regions (local, local to board, and remote). Then, this study is extended to any number of concurrent applications. Experimental results show that a QoS parameter is needed in order to avoid unacceptable performance degradation. © 2011 Springer Science+Business Media, LLC.This work was supported by Spanish CICYT under Grant TIN2009-14475-C04-01 and by Consolider-Ingenio under Grant CSD2006-00046.Serrano Gómez, M.; Sahuquillo Borrás, J.; Petit Martí, SV.; Hassan Mohamed, H.; Duato Marín, JF. (2012). A cost-effective heuristic to schedule local and remote memory in cluster computers. Journal of Supercomputing. 59(3):1533-1551. https://doi.org/10.1007/s11227-011-0566-8S15331551593IBM journal of Research and Development staff (2008) Overview of the IBM blue gene/P project. IBM J Res Dev 52(1/2):199–220Blocksome M, Archer C, Inglett T, McCarthy P, Mundy M, Ratterman J, Sidelnik A, Smith B, Almási G, Castaños J, Lieber D, Moreira J, Krishnamoorthy S, Tipparaju V, Nieplocha J (2006) Design and implementation of a one-sided communication interface for the IBM eServer Blue Gene® supercomputer. In: Proceedings of the 2006 ACM/IEEE conference on supercomputing, SC ’06, Tampa, FL, USA, November 2006, pp 54–54Kumar S, Dózsa G, Almasi G, Heidelberger P, Chen D, Giampapa M, Blocksome M, Faraj A, Parker J, Ratterman J, Smith BE, Archer C (2008) The deep computing messaging framework: generalized scalable message passing on the blue gene/P supercomputer. In: Proceedings of the 22nd annual international conference on supercomputing, Island of Kos, Greece, June 2008, pp 94–103Tipparaju V, Kot A, Nieplocha J, Bruggencate MT, Chrisochoides N (2007) Evaluation of remote memory access communication on the cray XT3. In: Proceedings of the 21th international parallel and distributed processing symposium, Long Beach, California, USA, March 2007, pp 1–7Nussle M, Scherer M, Bruning U (2009) A resource optimized remote-memory-access architecture for low-latency communication. In: International conference on parallel processing, Sept 2009, pp 220–227http://www.hypertransport.org/Serrano M, Sahuquillo J, Hassan H, Petit S, Duato J (2010) A scheduling heuristic to handle local and remote memory in cluster computers. In: Proceedings of the 12th IEEE international conference on high performance computing, Melbourne, Australia, Sept 2010, pp 35–42Keltcher CN, McGrath KJ, Ahmed A, Conway P (2003) The AMD opteron processor for multiprocessor servers. IEEE MICRO 23(2):66–76Duato J, Silla F, Yalamanchili S (2009) Extending hypertransport protocol for improved scalability. In: First international workshop on hypertransport research and applications.Litz H, Fröening H, Nuessle M, Brüening U (2007) A hypertransport network interface controller for ultra-low latency message transfers. HyperTransport Consortium White Paperhttps://www.simics.net/http://www.cs.wisc.edu/gems/http://www.cs.virginia.edu/stream/Woo SC, Ohara M, Torrie E, Singh JP, Gupta A (1995) The SPLASH-2 programs: Characterization and methodological considerations. In: Proceedings of the 22nd annual international symposium on computer architecture, New York, NY, USA, 1995, pp 24–36Levitin A (2003) Introduction to the design and analysis of algorithms. Addison Wesley, ReadingOleszkiewicz J, Xiao L, Liu Y (2004) Parallel network RAM: Effectively utilizing global cluster memory for large data-intensive parallel programs. In: Proceedings of 33rd international conference on parallel processing, Montreal, Quebec, Canada, pp 353–360Liang S, Noronha R, Panda DK (2005) Swapping to remote memory over infiniband: An approach using a high performance network block device. In: Proceedings of the 2005 IEEE international conference on cluster computing, Boston, Massachusetts, USA, pp 1–10Oguchi M, Kitsuregawa M (2000) Using available remote memory dynamically for parallel data mining application on ATM-connected PC cluster. In: Proceedings of the 14th international parallel & distributed processing symposium, Cancun, Mexico, pp 411–420Werstein P, Jia X, Huang Z (2007) A remote memory swapping system for cluster computers. In: Proceedings of the eighth international conference on parallel and distributed computing, applications and technologies, Adelaide, Australia, pp 75–81Midorikawa H, Kurokawa M, Himeno R, Sato M (2008) DLM: A distributed large memory system using remote memory swapping over cluster nodes. In: Proceedings of the 2008 IEEE international conference on cluster computing, Tsukuba, Japan, October 2008, pp 268–27

SARS-CoV-2 susceptibility and COVID-19 disease severity are associated with genetic variants affecting gene expression in a variety of tissues

Variability in SARS-CoV-2 susceptibility and COVID-19 disease severity between individuals is partly due to genetic factors. Here, we identify 4 genomic loci with suggestive associations for SARS-CoV-2 susceptibility and 19 for COVID-19 disease severity. Four of these 23 loci likely have an ethnicity-specific component. Genome-wide association study (GWAS) signals in 11 loci colocalize with expression quantitative trait loci (eQTLs) associated with the expression of 20 genes in 62 tissues/cell types (range: 1:43 tissues/gene), including lung, brain, heart, muscle, and skin as well as the digestive system and immune system. We perform genetic fine mapping to compute 99% credible SNP sets, which identify 10 GWAS loci that have eight or fewer SNPs in the credible set, including three loci with one single likely causal SNP. Our study suggests that the diverse symptoms and disease severity of COVID-19 observed between individuals is associated with variants across the genome, affecting gene expression levels in a wide variety of tissue types

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

SARS-CoV-2 susceptibility and COVID-19 disease severity are associated with genetic variants affecting gene expression in a variety of tissues

Variability in SARS-CoV-2 susceptibility and COVID-19 disease severity between individuals is partly due to genetic factors. Here, we identify 4 genomic loci with suggestive associations for SARS-CoV-2 susceptibility and 19 for COVID-19 disease severity. Four of these 23 loci likely have an ethnicity-specific component. Genome-wide association study (GWAS) signals in 11 loci colocalize with expression quantitative trait loci (eQTLs) associated with the expression of 20 genes in 62 tissues/cell types (range: 1:43 tissues/gene), including lung, brain, heart, muscle, and skin as well as the digestive system and immune system. We perform genetic fine mapping to compute 99% credible SNP sets, which identify 10 GWAS loci that have eight or fewer SNPs in the credible set, including three loci with one single likely causal SNP. Our study suggests that the diverse symptoms and disease severity of COVID-19 observed between individuals is associated with variants across the genome, affecting gene expression levels in a wide variety of tissue types

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