Contingency power for small turboshaft engines using water injection into turbine cooling air

Because of one engine inoperative requirements, together with hot-gas reingestion and hot day, high altitude takeoff situations, power augmentation for multiengine rotorcraft has always been of critical interest. However, power augmentation using overtemperature at the turbine inlet will shorten turbine life unless a method of limiting thermal and mechanical stresses is found. A possible solution involves allowing the turbine inlet temperature to rise to augment power while injecting water into the turbine cooling air to limit hot-section metal temperatures. An experimental water injection device was installed in an engine and successfully tested. Although concern for unprotected subcomponents in the engine hot section prevented demonstration of the technique's maximum potential, it was still possible to demonstrate increases in power while maintaining nearly constant turbine rotor blade temperature

Advances in Engine Test Capabilities at the NASA Glenn Research Center's Propulsion Systems Laboratory

The Propulsion Systems Laboratory at the National Aeronautics and Space Administration (NASA) Glenn Research Center is one of the premier U.S. facilities for research on advanced aeropropulsion systems. The facility can simulate a wide range of altitude and Mach number conditions while supplying the aeropropulsion system with all the support services necessary to operate at those conditions. Test data are recorded on a combination of steady-state and highspeed data-acquisition systems. Recently a number of upgrades were made to the facility to meet demanding new requirements for the latest aeropropulsion concepts and to improve operational efficiency. Improvements were made to data-acquisition systems, facility and engine-control systems, test-condition simulation systems, video capture and display capabilities, and personnel training procedures. This paper discusses the facility s capabilities, recent upgrades, and planned future improvements

SNAPSHOT USA 2019 : a coordinated national camera trap survey of the United States

This article is protected by copyright. All rights reserved.With the accelerating pace of global change, it is imperative that we obtain rapid inventories of the status and distribution of wildlife for ecological inferences and conservation planning. To address this challenge, we launched the SNAPSHOT USA project, a collaborative survey of terrestrial wildlife populations using camera traps across the United States. For our first annual survey, we compiled data across all 50 states during a 14-week period (17 August - 24 November of 2019). We sampled wildlife at 1509 camera trap sites from 110 camera trap arrays covering 12 different ecoregions across four development zones. This effort resulted in 166,036 unique detections of 83 species of mammals and 17 species of birds. All images were processed through the Smithsonian's eMammal camera trap data repository and included an expert review phase to ensure taxonomic accuracy of data, resulting in each picture being reviewed at least twice. The results represent a timely and standardized camera trap survey of the USA. All of the 2019 survey data are made available herein. We are currently repeating surveys in fall 2020, opening up the opportunity to other institutions and cooperators to expand coverage of all the urban-wild gradients and ecophysiographic regions of the country. Future data will be available as the database is updated at eMammal.si.edu/snapshot-usa, as well as future data paper submissions. These data will be useful for local and macroecological research including the examination of community assembly, effects of environmental and anthropogenic landscape variables, effects of fragmentation and extinction debt dynamics, as well as species-specific population dynamics and conservation action plans. There are no copyright restrictions; please cite this paper when using the data for publication.Publisher PDFPeer reviewe

Flexwall Hydraulic Hose Replacement in the NASA Glenn 10- by 10-Foot Supersonic Propulsion Wind Tunnel

The space-time conservation-element and solution-element method is employed to numerically study the near-field screech-tone noise of a typical underexpanded circular jet issuing from a sonic nozzle. Both axisymmetric and fully three-dimensional computations are carried out. The self-sustained feedback loop is properly simulated. The computed shock-cell structure, acoustic wave length, screech-tone frequency, and sound-pressure levels are in good agreement with existing experimental results

Genetic and acute CPEB1 depletion ameliorate fragile X pathophysiology

Fragile X syndrome (FXS), the most common cause of inherited mental retardation and autism, is caused by transcriptional silencing of FMR1, which encodes the translational repressor fragile X mental retardation protein (FMRP). FMRP and cytoplasmic polyadenylation element-binding protein (CPEB), an activator of translation, are present in neuronal dendrites, are predicted to bind many of the same mRNAs and may mediate a translational homeostasis that, when imbalanced, results in FXS. Consistent with this possibility, Fmr1(-/y); Cpeb1(-/-) double-knockout mice displayed amelioration of biochemical, morphological, electrophysiological and behavioral phenotypes associated with FXS. Acute depletion of CPEB1 in the hippocampus of adult Fmr1(-/y) mice rescued working memory deficits, demonstrating reversal of this FXS phenotype. Finally, we find that FMRP and CPEB1 balance translation at the level of polypeptide elongation. Our results suggest that disruption of translational homeostasis is causal for FXS and that the maintenance of this homeostasis by FMRP and CPEB1 is necessary for normal neurologic function

Increased Expression of the PI3K Enhancer PIKE Mediates Deficits in Synaptic Plasticity and Behavior in Fragile X Syndrome

The PI3K enhancer PIKE links PI3K catalytic subunits to group 1 metabotropic glutamate receptors (mGlu1/5) and activates PI3K signaling. The roles of PIKE in synaptic plasticity and the etiology of mental disorders are unknown. Here, we show that increased PIKE expression is a key mediator of impaired mGlu1/5-dependent neuronal plasticity in mouse and fly models of the inherited intellectual disability fragile X syndrome (FXS). Normalizing elevated PIKE protein levels in FXS mice reversed deficits in molecular and cellular plasticity and improved behavior. Notably, PIKE reduction rescued PI3K-dependent and -independent neuronal defects in FXS. We further show that PI3K signaling is increased in a fly model of FXS and that genetic reduction of the Drosophila ortholog of PIKE, CenG1A rescued excessive PI3K signaling, mushroom body defects, and impaired short-term memory in these flies. Our results demonstrate a crucial role of increased PIKE expression in exaggerated mGlu1/5 signaling causing neuronal defects in FXS