57 research outputs found

    Wall-resolved large eddy simulation for aeroengine aeroacoustic investigation

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    The work presented here forms part of a larger project on Large-Eddy Simulation (LES) of aeroengine aeroacoustic interactions. In this paper, we concentrate on LES of near-field flow over an isolated NACA0012 aerofoil at zero angle-of-attack and a chord based Reynolds number of Rec = 2 × 105. A wall-resolved compressible Numerical Large Eddy Simulation (NLES) approach is employed to resolve streak-like structures in the near-wall flow regions. The calculated unsteady pressure/velocity field will be imported into an analyticallybased scheme for far-field trailing-edge noise prediction later. The boundary-layer mean and root-mean-square (rms) velocity profiles, the surface pressure fluctuation over the aerofoil, and the wake flow development are compared with experimental data and previous computational simulations in our research group. It is found that the results from the wall-resolved compressible NLES are very encouraging as they correlate well with test data. The main features of the wall-resolved compressible NLES, as well as the advantages of such compressible NLES over previous incompressible LES performed in our research group, are also discussed. This paper will be presented at the ISABE 2017 Conference, 5-8 September 2017, Manchester, UK

    Toward Future Installations: Mutual Interactions of Short Intakes With Modern High Bypass Fans

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    In this paper, we investigate the coupled interaction between a new short intake design with a modern fan in a high-bypass ratio civil engine, specifically under the off-design condition of high incidence. The interaction is expected to be much more significant than that on a conventional intake. The performance of both the intake-alone and rotor-alone configurations are examined under isolation. Subsequently, a comprehensive understanding on the two-way interaction between intake and fan is presented. This includes the effect of fan on intake angles of attack (AoA) tolerance (FoI) and the effect of circumferential and radial flow distortion induced by the intake on the fan performance (IoF). In the FoI scenario, the rotor effectively redistributes the mass flow at the fan-face. The AoA tolerance of the short-intake design has increased by ≈4 deg when compared with the intake-alone configuration. Dynamic nature of distortion due to shock unsteadiness has been quantified. ST plots and power spectral density (PSD) of pressure fluctuations show the existence of a spectral gap between the shock unsteadiness and blade passing, with almost an order of magnitude difference in the corresponding frequencies. In the IoF scenario, both the “large” (O(360 deg)) and “small” scale distortion (O(10–60 deg)) induced by the intake results in a non-uniform inflow to the rotor. Sector analysis reveals a substantial variation in the local operating condition of the fan as opposed to its steady characteristic. Streamline curvature, upwash, and wake thickening are identified to be the three key factors affecting the fan performance. These underlying mechanisms are discussed in detail to provide further insights into the physical understanding of the fan-intake interaction. In addition to the shock-induced separation on the intake lip, the current study shows that shorter intakes are much more prone to the upwash effect at higher AoA. Insufficient flow straightening along the engine axis is reconfirmed to be one of the limiting factors for the short-intake design

    A Self-Similar Sine-Cosine Fractal Architecture for Multiport Interferometers

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    Multiport interferometers based on integrated beamsplitter meshes have recently captured interest as a platform for many emerging technologies. In this paper, we present a novel architecture for multiport interferometers based on the Sine-Cosine fractal decomposition of a unitary matrix. Our architecture is unique in that it is self-similar, enabling the construction of modular multi-chiplet devices. Due to this modularity, our design enjoys improved resilience to hardware imperfections as compared to conventional multiport interferometers. Additionally, the structure of our circuit enables systematic truncation, which is key in reducing the hardware footprint of the chip as well as compute time in training optical neural networks, while maintaining full connectivity. Numerical simulations show that truncation of these meshes gives robust performance even under large fabrication errors. This design is a step forward in the construction of large-scale programmable photonics, removing a major hurdle in scaling up to practical machine learning and quantum computing applications.Comment: 8 pages, 5 figure

    GNAO1 encephalopathy: broadening the phenotype and evaluating treatment and outcome

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    OBJECTIVE: To describe better the motor phenotype, molecular genetic features, and clinical course of GNAO1-related disease. METHODS: We reviewed clinical information, video recordings, and neuroimaging of a newly identified cohort of 7 patients with de novo missense and splice site GNAO1 mutations, detected by next-generation sequencing techniques. RESULTS: Patients first presented in early childhood (median age of presentation 10 months, range 0-48 months), with a wide range of clinical symptoms ranging from severe motor and cognitive impairment with marked choreoathetosis, self-injurious behavior, and epileptic encephalopathy to a milder phenotype, featuring moderate developmental delay associated with complex stereotypies, mainly facial dyskinesia and mild epilepsy. Hyperkinetic movements were often exacerbated by specific triggers, such as voluntary movement, intercurrent illnesses, emotion, and high ambient temperature, leading to hospital admissions. Most patients were resistant to drug intervention, although tetrabenazine was effective in partially controlling dyskinesia for 2/7 patients. Emergency deep brain stimulation (DBS) was life saving in 1 patient, resulting in immediate clinical benefit with complete cessation of violent hyperkinetic movements. Five patients had well-controlled epilepsy and 1 had drug-resistant seizures. Structural brain abnormalities, including mild cerebral atrophy and corpus callosum dysgenesis, were evident in 5 patients. One patient had a diffuse astrocytoma (WHO grade II), surgically removed at age 16. CONCLUSIONS: Our findings support the causative role of GNAO1 mutations in an expanded spectrum of early-onset epilepsy and movement disorders, frequently exacerbated by specific triggers and at times associated with self-injurious behavior. Tetrabenazine and DBS were the most useful treatments for dyskinesia

    Testing Data Acquisition Systems for Use in Monitoring Building Energy Conservation Systems

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    Dedicated microprocessor-based data acquisition systems are beginning to be used to monitor the energy savings from building energy conservation retrofits. These systems capture data from important monitoring points and store the values for periodic transfer to a central location. While there are many data loggers available that appear suited to this task, choosing between them is complicated by a large number of manufacturers, a lack of standard communications protocols, and most significantly, no standardized tests for reporting their capabilities. This paper addresses the last point with a battery of tests that were developed and applied to data loggers from nine manufacturers

    Cerebral hypomyelination associated with biallelic variants of FIG4

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    The lipid phosphatase gene FIG4 is responsible for Yunisâ Varón syndrome and Charcotâ Marieâ Tooth disease Type 4J, a peripheral neuropathy. We now describe four families with FIG4 variants and prominent abnormalities of central nervous system (CNS) white matter (leukoencephalopathy), with onset in early childhood, ranging from severe hypomyelination to mild undermyelination, in addition to peripheral neuropathy. Affected individuals inherited biallelic FIG4 variants from heterozygous parents. Cultured fibroblasts exhibit enlarged vacuoles characteristic of FIG4 dysfunction. Two unrelated families segregate the same Gâ >â A variant in the +1 position of intron 21 in the homozygous state in one family and compound heterozygous in the other. This mutation in the splice donor site of exon 21 results in readâ through from exon 20 into intron 20 and truncation of the final 115 Câ terminal amino acids of FIG4, with retention of partial function. The observed CNS white matter disorder in these families is consistent with the myelination defects in the FIG4 null mouse and the known role of FIG4 in oligodendrocyte maturation. The families described here the expanded clinical spectrum of FIG4 deficiency to include leukoencephalopathy.Peer Reviewedhttps://deepblue.lib.umich.edu/bitstream/2027.42/149294/1/humu23720-sup-0001-Supp_Mat_Lenk_2018.pdfhttps://deepblue.lib.umich.edu/bitstream/2027.42/149294/2/humu23720.pdfhttps://deepblue.lib.umich.edu/bitstream/2027.42/149294/3/humu23720_am.pd

    Genetic and phenotypic spectrum associated with IFIH1 gain-of-function

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    IFIH1 gain‐of‐function has been reported as a cause of a type I interferonopathy encompassing a spectrum of autoinflammatory phenotypes including Aicardi–Goutières syndrome and Singleton Merten syndrome. Ascertaining patients through a European and North American collaboration, we set out to describe the molecular, clinical and interferon status of a cohort of individuals with pathogenic heterozygous mutations in IFIH1. We identified 74 individuals from 51 families segregating a total of 27 likely pathogenic mutations in IFIH1. Ten adult individuals, 13.5% of all mutation carriers, were clinically asymptomatic (with seven of these aged over 50 years). All mutations were associated with enhanced type I interferon signaling, including six variants (22%) which were predicted as benign according to multiple in silico pathogenicity programs. The identified mutations cluster close to the ATP binding region of the protein. These data confirm variable expression and nonpenetrance as important characteristics of the IFIH1 genotype, a consistent association with enhanced type I interferon signaling, and a common mutational mechanism involving increased RNA binding affinity or decreased efficiency of ATP hydrolysis and filament disassembly rate
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