369 research outputs found

    Sound Radiated by a Supercritical Airfoil Operating in the Incompressible Regime

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    Measurements of far-field sound radiated by two and three-dimensional supercritical airfoils (ONERA OAT 15A) placed in a low Mach number flow were performed in an anechoic open-jet facility. The chord-based Reynolds numbers were between 156,000 and 468,000, while the Mach numbers ranged between 0.04 and 0.13. For the three-dimensional airfoil, two different aspect ratios (span-to-chord ratio) of 1.0 and 1.5 were considered. For comparison, the sound radiated by a symmetric NACA 0012 and cambered NACA 2412 airfoil was also measured under the same conditions. The noise from the two-dimensional airfoil was found to scale on the fifth power of Mach number. The noise generated by the cross-flow across the tip was the dominant noise source for the three-dimensional airfoils, particularly under high-lift conditions where it exceeds the noise from the mid-span portion across the considered frequency range. The tip noise spectra for the supercritical airfoils exhibit a prominent peak that scales with the free-stream velocity, but its frequency is a weak function of the lift on the airfoil and the aspect ratio. No such peak was observed for the NACA profiles even for higher lift conditions. The beamformed source maps for NACA profiles reveal an intense high-frequency noise source near the tip leading-edge which is much weaker for the supercritical airfoil due to differences in the curvature of the profiles. The tip noise spectra for the supercritical airfoil can be scaled on the fourth power of Mach number and the length-scale associated with the spectral peak. The tip noise peak magnitude and frequencies were found to be nearly independent of the airfoil aspect ratio; however, a reduction in AR was found to shift the tip noise source region further inboard. Stereo particle image velocimetry (PIV) measurements performed in a cross-plane behind the three-dimensional airfoils show that this is because a reduction in AR also shifts vortex core towards the mid-span. The PIV results were also used to quantify the meander of the tip vortex and it is shown that the amplitude of vortex meandering is independent of the angle of attack and the aspect ratio with a value between 0.5 – 0.6% of the chord-length for all cases considered

    Determination of the breakpoint and molecular diagnosis of a common Ξ±-thalassaemia-1 deletion in the Indian population

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    The previously described South African type α-thalassaemia-1 mutation was identified in Indian HbH patients using a polymerase chain reaction (PCR) strategy. A multiplex PCR assay was devised to detect heterozygotes and homozygotes. This α-thalassaemia-1 mutation was found to be the commonest determinant causing HbH disease in this population. In one family this mutation was found in combination with a novel splice donor mutation α2 IVS I-1 (G→A). Characterization of the breakpoint junction sequence revealed, in addition to a 23 kb deletion, that there was an addition of ~160 bp bridging the breakpoints. Similar to other deletions in the α-globin gene cluster, there is an Alu repeat-mediated mechanism for the origin of the deletion

    Molecular genetics of hereditary prothrombin deficiency in Indian patients: identification of a novel Ala362→Thr (Prothrombin Vellore 1) mutation

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    Prothrombin deficiency is a rare (1:200 000) autosomal recessive disorder caused by diverse mutations in prothrombin gene. We have studied the molecular basis of this disorder in four unrelated Indian patients. The diagnosis was based on prolonged prothrombin (PT) and activated partial thromboplastin times and low factor II coagulant activity (FII: C) measured using a PT based assay. FII: C levels ranged between 4.7% and 17.5%. Mutations were identified in all the four patients. Five different causative mutations including four (80%) missense and an in-frame deletion (20%) were identified. One of them was a novel, Ala362→Thr aminoacid change affecting 'B' chain of α-thrombin. This mutation was present in a compound heterozygous state with a previously reported Arg-1→Gln missense change affecting pro-peptide cleavage site. Ala362→Thr occurred at a codon, evolutionarily conserved in all the 24 different prothrombins or its related serine proteases studied. Molecular modeling of this mutation was found to cause a conformational change around the region involving a catalytic triad residue His363 and a cysteine residue at codon 364. The FII: C level in this patient was 17.5%. Three other previously reported mutations were also detected in the homozygous state: Arg271→Cys in Kringle-2 region, a Glu309?Lys in 'A' chain of α-thrombin and an in-frame deletion of 3 bp (AAG) leading to Del Lys301/302 in 'A' chain of α-thrombin. This is the first report of the molecular basis of prothrombin deficiency in Indian patients and we suggest the eponym 'Prothrombin Vellore 1' for Ala362→Thr mutation

    Six novel mutations including triple heterozygosity for Phe31Ser, 514delT and 516T→G factor X gene mutations are responsible for congenital factor X deficiency in patients of Nepali and Indian origin

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    Factor X (FX) deficiency is a rare (1 : 100000) autosomal recessive disorder caused by heterogeneous mutations in FX gene. We have studied the molecular basis this disease in six Indian and one Nepali patients. Diagnosis was confirmed by measuring the FX coagulant activity (FX: C) using a PT based assay. Six of them had a FX: C of < 1% and one patient had 24% coagulant activity. Mutations were identified in all the seven patients. These included eight (88.8%) missense and one frame-shift (11.2%) mutations of which six were novel. Three of the novel mutations, a Phe31Ser affecting 'Gla' domain and 514delT and 516T?G mutations affecting Cys132 in 'connecting region' were identified in a triple compound heterozygous state in a Nepali patient presenting with a severe phenotype. Two other novel mutations, Gly133Arg, may affect the disulphide bridge between Cys132-Cys302 in the connecting region while Gly223Arg may perturb the catalytic triad (His236, Asp282 and Ser379). The other novel mutation, Ser354Arg, involves the replacement of a small-buried residue by a large basic aminoacid and is likely to have steric or electrostatic effects in the pocket involving Lys351-Arg347-Lys414 that contributes to the core epitope of FXa for binding to FVa. Three previously reported mutations, Thr318Met; Gly323Ser; Gly366Ser were also identified. This is the first report of the molecular basis of FX deficiency in patients from the Indian subcontinent

    Recovery of wall-shear stress to equilibrium flow conditions after a rough-to-smooth step change in turbulent boundary layers

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    This paper examines the recovery of the wall-shear stress of a turbulent boundary layer that has undergone a sudden transition from a rough to a smooth surface. Early work of Antonia and Luxton (J. Fluid Mech., vol. 53, 1972, pp. 737–757) questioned the reliability of standard smooth-wall methods for measuring wall-shear stress in such conditions, and subsequent studies show significant disagreement depending on the approach used to determine the wall-shear stress downstream. Here we address this by utilising a collection of experimental databases at ReΟ„β‰ˆ4100 that have access to both β€˜direct’ and β€˜indirect’ measures of the wall-shear stress to understand the recovery to equilibrium conditions of the new surface. Our results reveal that the viscous region ( z+≲4 ) recovers almost immediately to an equilibrium state with the new wall conditions; however, the buffer region and beyond takes several boundary layer thicknesses before recovering to equilibrium conditions, which is longer than previously thought. A unique direct numerical simulation database of a wall-bounded flow with a rough-to-smooth wall transition is employed to confirm these findings. In doing so, we present evidence that any estimate of the wall-shear stress from the mean velocity profile in the buffer region or further away from the wall tends to underestimate its magnitude in the near vicinity of the rough-to-smooth transition, and this is likely to be partly responsible for the large scatter of recovery lengths to equilibrium conditions reported in the literature. Our results also reveal that smaller energetic scales in the near-wall region recover to an equilibrium state associated with the new wall conditions within one boundary layer thickness downstream of the transition, while larger energetic scales exhibit an over-energised state for several boundary layer thicknesses downstream of the transition. Based on these observations, an alternative approach to estimating the wall-shear stress from the premultiplied energy spectrum is proposed

    Genetically encoded intrabody sensors report the interaction and trafficking of Ξ²-arrestin 1 upon activation of G protein-coupled receptors

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    Agonist stimulation of G protein-coupled receptors (GPCRs) typically leads to phosphorylation of GPCRs and binding to multifunctional proteins called Ξ²-arrestins (Ξ²arrs). The GPCR-Ξ²arr interaction critically contributes to GPCR desensitization, endocytosis, and downstream signaling, and GPCR-Ξ²arr complex formation can be used as a generic readout of GPCR and Ξ²arr activation. Although several methods are currently available to monitor GPCR-Ξ²arr interactions, additional sensors to visualize them may expand the toolbox and complement existing methods. We have previously described antibody fragments (FABs) that recognize activated Ξ²arr1 upon its interaction with the vasopressin V2 receptor C-terminal phosphopeptide (V2Rpp). Here, we demonstrate that these FABs efficiently report the formation of a GPCR-Ξ²arr1 complex for a broad set of chimeric GPCRs harboring the V2R C terminus. We adapted these FABs to an intrabody format by converting them to single-chain variable fragments (ScFvs) and used them to monitor the localization and trafficking of Ξ²arr1 in live cells. We observed that upon agonist simulation of cells expressing chimeric GPCRs, these intrabodies first translocate to the cell surface, followed by trafficking into intracellular vesicles. The translocation pattern of intrabodies mirrored that of Ξ²arr1, and the intrabodies co-localized with Ξ²arr1 at the cell surface and in intracellular vesicles. Interestingly, we discovered that intrabody sensors can also report Ξ²arr1 recruitment and trafficking for several unmodified GPCRs. Our characterization of intrabody sensors for Ξ²arr1 recruitment and trafficking expands currently available approaches to visualize GPCR-Ξ²arr1 binding, which may help decipher additional aspects of GPCR signaling and regulation

    Erosion of Trust in the Medical Profession in India : Time for Doctors to Act

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    In India, over the last decade, a series of stewardship failures in the health system, particularly in the medical profession, have led to a massive erosion of trust in these institutions. In many low- and middle-income countries (LMICs), the situation is similar and has reached crisis proportions; this crisis requires urgent attention. This paper draws on the insights from the recent developments in India, to argue that a purely control-based regulatory response to this crisis in the medical profession, as is being currently envisaged by the Parliament and the Supreme Court of India, runs the risk of undermining the trusting interpersonal relations between doctors and their patients. A more balanced approach which takes into account the differences between system and interpersonal forms of trust and distrust is warranted. Such an approach should on one hand strongly regulate the institutions mandated with the stewardship and qualities of care functions, and simultaneously on the other hand, initiate measures to nurture the trusting interpersonal relations between doctors and patients. The paper concludes by calling for doctors, and those mandated with the stewardship of the profession, to individually and collectively, critically self-reflect upon the state of their profession, its priorities and its future direction

    Design and fabrication of an automated temperature programmed reaction system to evaluate 3-way catalysts Ce 1-x-y (La/Y) x Pt y O 2-Ξ΄ Ξ΄

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    Abstract. A completely automated temperature-programmed reaction (TPR) system for carrying out gas-solid catalytic reactions under atmospheric flow conditions is fabricated to study CO and hydrocarbon oxidation, and NO reduction. The system consists of an all-stainless steel UHV system, quadrupole mass spectrometer SX200 (VG Scientific), a tubular furnace and micro-reactor, a temperature controller, a versatile gas handling system, and a data acquisition and analysis system. The performance of the system has been tested under standard experimental conditions for CO oxidation over well-characterized Ce 1-x-y Pt x (La/Y) y O 2-Ξ΄ catalysts. Testing of 3-way catalysis with CO, NO and C 2 H 2 to convert to CO 2 , N 2 and H 2 O is done with this catalyst which shows complete removal of pollutants below 325Β°C. Fixed oxide-ion defects in Pt substituted Ce 1-y (La/Y) y O 2-y/2 show higher catalytic activity than Pt ion-substituted CeO 2

    ΠœΠ΅Ρ‚ΠΎΠ΄ΠΈΡ‡Π΅ΡΠΊΠ°Ρ Ρ€Π°Π±ΠΎΡ‚Π° Π² дошкольной ΠΎΠ±Ρ€Π°Π·ΠΎΠ²Π°Ρ‚Π΅Π»ΡŒΠ½ΠΎΠΉ ΠΎΡ€Π³Π°Π½ΠΈΠ·Π°Ρ†ΠΈΠΈ ΠΊΠ°ΠΊ условиС ΠΏΠΎΠ²Ρ‹ΡˆΠ΅Π½ΠΈΡ ΠΈΠ½Ρ„ΠΎΡ€ΠΌΠ°Ρ†ΠΈΠΎΠ½Π½ΠΎ-ΠΊΠΎΠΌΠΌΡƒΠ½ΠΈΠΊΠ°Ρ†ΠΈΠΎΠ½Π½ΠΎΠΉ компСтСнтности ΠΏΠ΅Π΄Π°Π³ΠΎΠ³ΠΎΠ²

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    Π’Π΅ΠΌΠ° Ρ€Π°Π±ΠΎΡ‚Ρ‹ Π°ΠΊΡ‚ΡƒΠ°Π»ΡŒΠ½Π°. Π’ Π’ΠšΠ  прСдставлСны условия, ΡΠΏΠΎΡΠΎΠ±ΡΡ‚Π²ΡƒΡŽΡ‰ΠΈΠ΅ Ρ€Π°Π·Π²ΠΈΡ‚ΠΈΡŽ ΠΊΠΎΠΌΠΏΠΎΠ½Π΅Π½Ρ‚ΠΎΠ² ИКК ΠΏΠ΅Π΄Π°Π³ΠΎΠ³ΠΎΠ². Π Π°Π±ΠΎΡ‚Π° ΠΈΠΌΠ΅Π΅Ρ‚ ΠΏΡ€Π°ΠΊΡ‚ΠΈΡ‡Π΅ΡΠΊΡƒΡŽ значимост
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