190 research outputs found

    Experimental Results for a Flapped Natural-laminar-flow Airfoil with High Lift/drag Ratio

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    Experimental results have been obtained for a flapped natural-laminar-flow airfoil, NLF(1)-0414F, in the Langley Low-Turbulence Pressure Tunnel. The tests were conducted over a Mach number range from 0.05 to 0.40 and a chord Reynolds number range from about 3.0 x 10(6) to 22.0 x 10(6). The airfoil was designed for 0.70 chord laminar flow on both surfaces at a lift coefficient of 0.40, a Reynolds number of 10.0 x 10(6), and a Mach number of 0.40. A 0.125 chord simple flap was incorporated in the design to increase the low-drag, lift-coefficient range. Results were also obtained for a 0.20 chord split-flap deflected 60 deg

    Computational Analysis of a Wing Designed for the X-57 Distributed Electric Propulsion Aircraft

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    A computational study of the wing for the distributed electric propulsion X-57 Maxwell airplane configuration at cruise and takeoff/landing conditions was completed. Two unstructured-mesh, Navier-Stokes computational fluid dynamics methods, FUN3D and USM3D, were used to predict the wing performance. The goal of the X-57 wing and distributed electric propulsion system design was to meet or exceed the required lift coefficient 3.95 for a stall speed of 58 knots, with a cruise speed of 150 knots at an altitude of 8,000 ft. The X-57 Maxwell airplane was designed with a small, high aspect ratio cruise wing that was designed for a high cruise lift coefficient (0.75) at angle of attack of 0deg. The cruise propulsors at the wingtip rotate counter to the wingtip vortex and reduce induced drag by 7.5 percent at an angle of attack of 0.6deg. The unblown maximum lift coefficient of the high-lift wing (with the 30deg flap setting) is 2.439. The stall speed goal performance metric was confirmed with a blown wing computed effective lift coefficient of 4.202. The lift augmentation from the high-lift, distributed electric propulsion system is 1.7. The predicted cruise wing drag coefficient of 0.02191 is 0.00076 above the drag allotted for the wing in the original estimate. However, the predicted drag overage for the wing would only use 10.1 percent of the original estimated drag margin, which is 0.00749

    Computational Component Build-Up for the X-57 Distributed Electric Propulsion Aircraft

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    A computational study of the wing for the distributed electric propulsion X-57 Maxwell airplane configuration at cruise and takeoff/landing conditions was completed. Three unstructured-mesh, Navier-Stokes computational fluid dynamics methods, FUN3D, USM3D and Kestrel, were used to predict the performance buildup of components to the full X-57 configuration. The goal of the X-57 wing and distributed electric propulsion system design was to meet or exceed the required lift coefficient of 3.95 for a stall speed of 58 knots. The X-57 Maxwell airplane was designed with a small, high aspect ratio cruise wing that was designed for a high cruise lift coefficient of 0.75 at a cruise speed of 150 knots and altitude of 8,000 ft, with an angle of attack of approximately 0deg. The computational data indicates that the X-57 full aircraft drag would meet the cruise drag goal with a 25 count drag margin. The cruise configuration maximum lift coefficient is 2.07 and without including the stabilator is 1.86 at an angle of attack of 14 deg, predicted with the USM3D flow solver using the Spalart-Allmaras turbulence model. The maximum lift coefficient for the high-lift wing (with the 30deg flap deflection) without the stabilator contribution is 2.60 at an angle of attack of 13 deg. For high-lift blowing conditions with 13.7 hp/prop, the maximum lift coefficient excluding the stabilator is 4.426 at (alpha) = 13 deg. Therefore, the lift augmentation from the high-lift propellers is 1.7 and the total lift augmentation from the high-lift system (30 deg flap deflection and the high-lift blowing) is 2.38. The drag for the high-lift wing with 30 deg flap deflection is much higher than the cruise wing configuration, but the high-lift system is used only during a small portion of the flight envelope. The pitching moment is relatively constant for both blown and unblown conditions when the stabilator is excluded. Modeling the full geometry has indicated some adverse effects from the fuselage on the wing and stabilator. At high angles of attack, the solutions with the USM3D flow solver using the Spalart-Allmaras turbulence model indicates large flow separation on the wing upper surface between the two high-lift nacelles near the fuselage, and also a reduction in sectional lift on the stabilator in the first 50 percent of the stabilator semispan. However, the large flow separation near the fuselage is mostly eliminated in the solutions predicted with two codes, USM3D and Kestrel, using Hybrid Reynolds-averaged Navier Stokes/Large Eddy Simulation turbulence models

    Cerebral Collateral Circulation in Carotid Artery Disease

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    Carotid artery disease is common and increases the risk of stroke. However, there is wide variability on the severity of clinical manifestations of carotid disease, ranging from asymptomatic to fatal stroke. The collateral circulation has been recognized as an important aspect of cerebral circulation affecting the risk of stroke as well as other features of stroke presentation, such as stroke patterns in patients with carotid artery disease. The cerebral circulation attempts to maintain constant cerebral perfusion despite changes in systemic conditions, due to its ability to autoregulate blood flow. In case that one of the major cerebral arteries is compromised by occlusive disease, the cerebral collateral circulation plays an important role in preserving cerebral perfusion through enhanced recruitment of blood flow. With the advent of techniques that allow rapid evaluation of cerebral perfusion, the collateral circulation of the brain and its effectiveness may also be evaluated, allowing for prompt assessment of patients with acute stroke due to involvement of the carotid artery, and risk stratification of patients with carotid stenosis in chronic stages. Understanding the cerebral collateral circulation provides a basis for the future development of new diagnostic tools, risk stratification, predictive models and new therapeutic modalities. In the present review we discuss basic aspects of the cerebral collateral circulation, diagnostic methods to assess collateral circulation, and implications in occlusive carotid artery disease

    Maternal microchimerism in cord blood and risk of childhood-onset type 1 diabetes

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    Background Maternal microchimerism (MMc), the transmission of small quantities of maternal cells to the fetus, is relatively common and persistent. MMc has been detected with increased frequency in the circulation and pancreas of type 1 diabetes (T1D) patients. We investigated for the first time whether MMc levels at birth predict future T1D risk. We also tested whether cord blood MMc predicted MMc in samples taken at T1D diagnosis. Methods Participants in the Norwegian Mother and Child Cohort study were human leukocyte antigen (HLA) class II typed to determine non‐inherited, non‐shared maternal alleles (NIMA). Droplet digital (dd) polymerase chain reaction (PCR) assays specific for common HLA class II NIMA (HLADQB1*03:01, *04:02, and *06:02/03) were developed and validated. MMc was estimated as maternal DNA quantity in the fetal circulation, by NIMA specific ddPCR, measured in cord blood DNA from 71 children who later developed T1D and 126 controls within the cohort. Results We found detectable quantities of MMc in 34/71 future T1D cases (48%) and 53/126 controls (42%) (adjusted odds ratio [aOR] 1.27, 95% confidence interval (CI) 0.68‐2.36), and no significant difference in ranks of MMc quantities between cases and controls (Mann‐Whitney P = .46). There was a possible association in the NIMA HLA‐DQB1*03:01 subgroup with later T1D (aOR 3.89, 95%CI 1.05‐14.4). MMc in cord blood was not significantly associated with MMc at T1D diagnosis. Conclusions Our findings did not support the hypothesis that the degree of MMc in cord blood predict T1D risk. The potential subgroup association with T1D risk should be replicated in a larger cohort

    Bifactor Structure of the Schizotypal Personality Questionnaire Across the Schizotypy Spectrum

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    Despite widespread use in schizophrenia-spectrum research, uncertainty remains around an empirically supported and theoretically meaningful factor structure of the Schizotypal Personality Questionnaire (SPQ). Current identified structures are limited by reliance on exclusively nonclinical samples. The current study compared factor structures of the SPQ in a sample of 335 nonpsychiatric individuals, 292 schizotypy-spectrum individuals (schizophrenia, schizoaffective disorder, or schizotypal personality disorder), and the combined group (N = 627). Unidimensional, correlated, and hierarchical models were assessed in addition to a bifactor model, wherein subscales load simultaneously onto a general factor and a specific factor. The best-fitting model across samples was a two-specific factor bifactor model, consistent with the nine symptom dimensions of schizotypy as primarily a direct manifestation of a unitary construct. Such findings, for the first time demonstrated in a clinical sample, have broad implications for transdiagnostic approaches, including reifying schizotypy as a construct underlying diverse manifestations of phenomenology across a wide range of severity

    Prenatal iron exposure and childhood type 1 diabetes

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    Acknowledgements: We are grateful to all the participating families in Norway who take part in this on-going cohort study. We thank Dr. Maria Vistnes at Diakonhjemmet Hospital, Oslo, Norway for help with cytokine assays, PM Ueland and Ø Midttun at BEVITAL, Bergen, Norway, for neopterin and KTR assay, and Kathleen Gillespie at Bristol University, UK for confirmatory HLA genotyping. The Norwegian Mother and Child Cohort Study is supported by the Norwegian Ministry of Health and Care Services and the Ministry of Education and Research, NIH/NIEHS (contract no N01-ES-75558), NIH/NINDS (grant no. 1 UO1 NS 047537-01 and grant no. 2 UO1 NS 047537-06A1). The sub-study was funded by a research grant from the Research Council of Norway. The Norwegian Childhood Diabetes Registry is financed by the South-Eastern Norway Regional Health Authority. Dr London was supported by the Intramural Research Program of the NIH, National Institute of Environmental Health Sciences. Dr Størdal was supported by an unrestricted grant from Oak Foundation, Geneva, Switzerland.Peer reviewedPublisher PD
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