137 research outputs found

    Wind Tunnel Testing of a 120th Scale Large Civil Tilt-Rotor Model in Airplane and Helicopter Modes

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    In April 2012 and October 2013, NASA and the U.S. Army jointly conducted a wind tunnel test program examining two notional large tilt rotor designs: NASA's Large Civil Tilt Rotor and the Army's High Efficiency Tilt Rotor. The approximately 6%-scale airframe models (unpowered) were tested without rotors in the U.S. Army 7- by 10-foot wind tunnel at NASA Ames Research Center. Measurements of all six forces and moments acting on the airframe were taken using the wind tunnel scale system. In addition to force and moment measurements, flow visualization using tufts, infrared thermography and oil flow were used to identify flow trajectories, boundary layer transition and areas of flow separation. The purpose of this test was to collect data for the validation of computational fluid dynamics tools, for the development of flight dynamics simulation models, and to validate performance predictions made during conceptual design. This paper focuses on the results for the Large Civil Tilt Rotor model in an airplane mode configuration up to 200 knots of wind tunnel speed. Results are presented with the full airframe model with various wing tip and nacelle configurations, and for a wing-only case also with various wing tip and nacelle configurations. Key results show that the addition of a wing extension outboard of the nacelles produces a significant increase in the lift-to-drag ratio, and interestingly decreases the drag compared to the case where the wing extension is not present. The drag decrease is likely due to complex aerodynamic interactions between the nacelle and wing extension that results in a significant drag benefit

    Second-Generation Large Civil Tiltrotor 7- by 10-Foot Wind Tunnel Test Data Report

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    An approximately 6-percent scale model of the NASA Second-Generation Large Civil Tiltrotor (LCTR2) Aircraft was tested in the U.S. Army 7- by 10-Foot Wind Tunnel at NASA Ames Research Center January 4 to April 19, 2012, and September 18 to November 1, 2013. The full model was tested, along with modified versions in order to determine the effects of the wing tip extensions and nacelles; the wing was also tested separately in the various configurations. In both cases, the wing and nacelles used were adopted from the U.S. Army High Efficiency Tilt Rotor (HETR) aircraft, in order to limit the cost of the experiment. The full airframe was tested in high-speed cruise and low-speed hover flight conditions, while the wing was tested only in cruise conditions, with Reynolds numbers ranging from 0 to 1.4 million. In all cases, the external scale system of the wind tunnel was used to collect data. Both models were mounted to the scale using two support struts attached underneath the wing; the full airframe model also used a third strut attached at the tail. The collected data provides insight into the performance of the preliminary design of the LCTR2 and will be used for computational fluid dynamics (CFD) validation and the development of flight dynamics simulation models

    Ion‐scale structure in Mercury’s magnetopause reconnection diffusion region

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    The strength and time dependence of the electric field in a magnetopause diffusion region relate to the rate of magnetic reconnection between the solar wind and a planetary magnetic field. Here we use ~150 ms measurements of energetic electrons from the Mercury Surface, Space Environment, GEochemistry, and Ranging (MESSENGER) spacecraft observed over Mercury’s dayside polar cap boundary (PCB) to infer such small‐scale changes in magnetic topology and reconnection rates. We provide the first direct measurement of open magnetic topology in flux transfer events at Mercury, structures thought to account for a significant portion of the open magnetic flux transport throughout the magnetosphere. In addition, variations in PCB latitude likely correspond to intermittent bursts of ~0.3–3 mV/m reconnection electric fields separated by ~5–10 s, resulting in average and peak normalized dayside reconnection rates of ~0.02 and ~0.2, respectively. These data demonstrate that structure in the magnetopause diffusion region at Mercury occurs at the smallest ion scales relevant to reconnection physics.Key PointsEnergetic electrons at Mercury map magnetic topology at ~150 msFirst direct observation of flux transfer event open‐field topology at MercuryModulations of the reconnection rate at Mercury occur at ion kinetic scalesPeer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/133575/1/grl54476_am.pdfhttp://deepblue.lib.umich.edu/bitstream/2027.42/133575/2/grl54476.pd

    'Ain't it a Ripping Night': Alcoholism and the Legacies of Empire in Salman Rushdie's Midnight's Children.

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    In the era of decolonisation that followed the Second World War, various authors sought to engage with India and the Empire’s past anew throughout their novels, identifying medicine and illness as key parts of Imperial authority and colonial experience. Salman Rushdie’s approach to the Raj in Midnight’s Children (1981) focused on the broad sweep of colonial life, juxtaposing the political and the personal. This article argues that Rushdie explores the history of colonial India by employing alcohol and alcoholism as lenses through which to explore the cultural, political and medical legacies of Empire. Through analysis of Midnight’s Children as well as a range of medical sources related to alcohol and inebriation, it will illustrate how drinking is central to Rushdie’s approach to secular and religious identities in newly independent India, as well as a means of satirising and undermining the supposed benefit that Empire presented to India and Indians

    The 2021 Eurpean Alliance of Associations for Rheumatology/American College of Rheumatology points to consider for diagnosis and management of autoinflammatory type i interferonopathies: CANDLE/PRAAS, SAVI and AGS

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    Objective: Autoinflammatory type I interferonopathies, chronic atypical neutrophilic dermatosis with lipodystrophy and elevated temperature/proteasome-associated autoinflammatory syndrome (CANDLE/PRAAS), stimulator of interferon genes (STING)-associated vasculopathy with onset in infancy (SAVI) and Aicardi-Goutières syndrome (AGS) are rare and clinically complex immunodysregulatory diseases. With emerging knowledge of genetic causes and targeted treatments, a Task Force was charged with the development of \u27points to consider\u27 to improve diagnosis, treatment and long-term monitoring of patients with these rare diseases. Methods: Members of a Task Force consisting of rheumatologists, neurologists, an immunologist, geneticists, patient advocates and an allied healthcare professional formulated research questions for a systematic literature review. Then, based on literature, Delphi questionnaires and consensus methodology, \u27points to consider\u27 to guide patient management were developed. Results: The Task Force devised consensus and evidence-based guidance of 4 overarching principles and 17 points to consider regarding the diagnosis, treatment and long-term monitoring of patients with the autoinflammatory interferonopathies, CANDLE/PRAAS, SAVI and AGS. Conclusion: These points to consider represent state-of-the-art knowledge to guide diagnostic evaluation, treatment and management of patients with CANDLE/PRAAS, SAVI and AGS and aim to standardise and improve care, quality of life and disease outcomes

    The Conservation Status of Marine Bony Shorefishes of the Greater Caribbean

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    The greater Caribbean biogeographic region covered in this report (representing 38 countries and territories) encompasses an outstanding marine bony shorefish richness of approximately 1,360 species, with many (53%) being endemic. This report provides an overview of the conservation status of greater Caribbean shorefishes, with detailed information available through the IUCN Red List, and gives recommendations

    The 2021 EULAR and ACR points to consider for diagnosis and management of autoinflammatory type I interferonopathies: CANDLE/PRAAS, SAVI and AGS

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    Objective: Autoinflammatory type I interferonopathies, chronic atypical neutrophilic dermatosis with lipodystrophy and elevated temperature/proteasome-associated autoinflammatory syndrome (CANDLE/PRAAS), stimulator of interferon genes (STING)-associated vasculopathy with onset in infancy (SAVI) and Aicardi-Goutières syndrome (AGS) are rare and clinically complex immunodysregulatory diseases. With emerging knowledge of genetic causes and targeted treatments, a Task Force was charged with the development of 'points to consider' to improve diagnosis, treatment and long-term monitoring of patients with these rare diseases. Methods: Members of a Task Force consisting of rheumatologists, neurologists, an immunologist, geneticists, patient advocates and an allied healthcare professional formulated research questions for a systematic literature review. Then, based on literature, Delphi questionnaires and consensus methodology, 'points to consider' to guide patient management were developed. Results: The Task Force devised consensus and evidence-based guidance of 4 overarching principles and 17 points to consider regarding the diagnosis, treatment and long-term monitoring of patients with the autoinflammatory interferonopathies, CANDLE/PRAAS, SAVI and AGS. Conclusion: These points to consider represent state-of-the-art knowledge to guide diagnostic evaluation, treatment and management of patients with CANDLE/PRAAS, SAVI and AGS and aim to standardise and improve care, quality of life and disease outcomes

    The 2021 EULAR and ACR points to consider for diagnosis and management of autoinflammatory type I interferonopathies: CANDLE/PRAAS, SAVI and AGS

    Get PDF
    Objective: Autoinflammatory type I interferonopathies, chronic atypical neutrophilic dermatosis with lipodystrophy and elevated temperature/proteasome-associated autoinflammatory syndrome (CANDLE/PRAAS), stimulator of interferon genes (STING)-associated vasculopathy with onset in infancy (SAVI) and Aicardi-Goutières syndrome (AGS) are rare and clinically complex immunodysregulatory diseases. With emerging knowledge of genetic causes and targeted treatments, a Task Force was charged with the development of 'points to consider' to improve diagnosis, treatment and long-term monitoring of patients with these rare diseases. Methods: Members of a Task Force consisting of rheumatologists, neurologists, an immunologist, geneticists, patient advocates and an allied healthcare professional formulated research questions for a systematic literature review. Then, based on literature, Delphi questionnaires and consensus methodology, 'points to consider' to guide patient management were developed. Results: The Task Force devised consensus and evidence-based guidance of 4 overarching principles and 17 points to consider regarding the diagnosis, treatment and long-term monitoring of patients with the autoinflammatory interferonopathies, CANDLE/PRAAS, SAVI and AGS. Conclusion: These points to consider represent state-of-the-art knowledge to guide diagnostic evaluation, treatment and management of patients with CANDLE/PRAAS, SAVI and AGS and aim to standardise and improve care, quality of life and disease outcomes

    A large scale hearing loss screen reveals an extensive unexplored genetic landscape for auditory dysfunction

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    The developmental and physiological complexity of the auditory system is likely reflected in the underlying set of genes involved in auditory function. In humans, over 150 non-syndromic loci have been identified, and there are more than 400 human genetic syndromes with a hearing loss component. Over 100 non-syndromic hearing loss genes have been identified in mouse and human, but we remain ignorant of the full extent of the genetic landscape involved in auditory dysfunction. As part of the International Mouse Phenotyping Consortium, we undertook a hearing loss screen in a cohort of 3006 mouse knockout strains. In total, we identify 67 candidate hearing loss genes. We detect known hearing loss genes, but the vast majority, 52, of the candidate genes were novel. Our analysis reveals a large and unexplored genetic landscape involved with auditory function

    Genetically-controlled Vesicle-Associated Membrane Protein 1 expression may contribute to Alzheimer’s pathophysiology and susceptibility

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    Background Alzheimer’s disease is a neurodegenerative disorder in which extracellular deposition of β-amyloid (Aβ) oligomers causes synaptic injury resulting in early memory loss, altered homeostasis, accumulation of hyperphosphorylated tau and cell death. Since proteins in the SNAP (Soluble N-ethylmaleimide-sensitive factor Attachment Protein) REceptors (SNARE) complex are essential for neuronal Aβ release at pre-synaptic terminals, we hypothesized that genetically controlled SNARE expression could alter neuronal Aß release at the synapse and hence play an early role in Alzheimer’s pathophysiology. Results Here we report 5 polymorphisms in Vesicle-Associated Membrane Protein 1 (VAMP1), a gene encoding a member of the SNARE complex, associated with bidirectionally altered cerebellar VAMP1 transcript levels (all p < 0.05). At the functional level, we demonstrated that control of VAMP1 expression by heterogeneous knockdown in mice resulted in up to 74% reduction in neuronal Aβ exocytosis (p < 0.001). We performed a case-control association study of the 5 VAMP1 expression regulating polymorphisms in 4,667 Alzheimer’s disease patients and 6,175 controls to determine their contribution to Alzheimer’s disease risk. We found that polymorphisms associated with increased brain VAMP1 transcript levels conferred higher risk for Alzheimer’s disease than those associated with lower VAMP1 transcript levels (p = 0.03). Moreover, we also report a modest protective association for a common VAMP1 polymorphism with Alzheimer’s disease risk (OR = 0.88, p = 0.03). This polymorphism was associated with decreased VAMP1 transcript levels (p = 0.02) and was functionally active in a dual luciferase reporter gene assay (p < 0.01). Conclusions Genetically regulated VAMP1 expression in the brain may modify both Alzheimer’s disease risk and may contribute to Alzheimer’s pathophysiology
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