Booster propulsion/vehicle impact study, 2

This is the final report in a study examining the impact of launch vehicles for various boost propulsion design options. These options included: differing boost phase engines using different combinations of fuels and coolants to include RP-1, methane, propane (subcooled and normal boiling point), and hydrogen; variable and high mixture ratio hydrogen engines; translating nozzles on boost phase engines; and cross feeding propellants from the booster to second stage. Vehicles examined included a fully reusable two stage cargo vehicle and a single stage to orbit vehicle. The use of subcooled propane as a fuel generated vehicles with the lowest total vehicle dry mass. Engines with hydrogen cooling generated only slight mass reductions from the reference, all-hydrogen vehicle. Cross feeding propellants generated the most significant mass reductions from the reference two stage vehicle. The use of high mixture ratio or variable mixture ratio hydrogen engines in the boost phase of flight resulted in vehicles with total dry mass 20 percent greater than the reference hydrogen vehicle. Translating nozzles for boost phase engines generated a heavier vehicle. Also examined were the design impacts on the vehicle and ground support subsystems when subcooled propane is used as a fuel. The most significant cost difference between facilities to handle normal boiling point versus subcooled propane is 5 million dollars. Vehicle cost differences were negligible. A significant technical challenge exists for properly conditioning the vehicle propellant on the ground and in flight when subcooled propane is used as fuel

Strutjet-powered reusable launch vehicles

Martin Marietta and Aerojet are co-investigating the feasibility and viability of reusable launch vehicle designs. We are assessing two vehicle concepts, each delivering 8000 lb to a geosynchronous transfer orbit (GTO). Both accomplish this task as a two-state system. The major difference between the two concepts is staging. The first concept, the two-stage-to-orbit (TSTO) system, stages at about 16 kft/sec, allowing immediate return of the first stage to the launch site using its airbreathing propulsion system for a powered cruise flight. The second concept, the single-stage-to-orit (SSTO) system, accomplishes stage separation in a stable low earth orbit (LEO)

Defining a rat blood pressure quantitative trait locus to a <81.8 kb congenic segment: comprehensive sequencing and renal transcriptome analysis

Evidence from multiple linkage and genome-wide association studies suggest that human chromosome 2 (HSA2) contains alleles that influence blood pressure (BP). Homologous to a large segment of HSA2 is rat chromosome 9 (RNO9), to which a BP quantitative trait locus (QTL) was previously mapped. The objective of the current study was to further resolve this BP QTL. Eleven congenic strains with introgressed segments spanning <81.8 kb to <1.33 Mb were developed by introgressing genomic segments of RNO9 from the Dahl salt-resistant (R) rat onto the genome of the Dahl salt-sensitive (S) rat and tested for BP. The congenic strain with the shortest introgressed segment spanning <81.8 kb significantly lowered BP of the hypertensive S rat by 25 mmHg and significantly increased its mean survival by 45 days. In contrast, two other congenic strains had increased BP compared with the S. We focused on the <81.8 kb congenic strain, which represents the shortest genomic segment to which a BP QTL has been mapped to date in any species. Sequencing of this entire region in both S and R rats detected 563 variants. The region did not contain any known or predicted rat protein coding genes. Furthermore, a whole genome renal transcriptome analysis between S and the <81.8 kb S.R congenic strain revealed alterations in several critical genes implicated in renal homeostasis. Taken together, our results provide the basis for future studies to examine the relationship between the candidate variants within the QTL region and the renal differentially expressed genes as potential causal mechanisms for BP regulation