Inertia diaphragm pressure transducer Patent

Design and development of inertia diaphragm pressure transduce

Evaluation of mean and turbulent velocity measurements in subsonic accelerated boundary layers

Exploratory measurements of the mean and turbulent flow in the wall boundary layer of a 15.5- by 10.2-cm channel were obtained as part of an instrumentation development program for measurements in compressible flow. Mean surface and flow-field surveys were obtained at channel Mach numbers ranging from 0.2 to 0.9. The mean velocity distributions were obtained with total pressure probes and a laser velocimeter. At a channel Mach number of 0.2, several types of hot-wire probes were used to obtain both velocity fluctuations and Reynolds shear-stress results

An experimental documentation of trailing-edge flows at high Reynolds number

Experiments documenting attached trailing-edge and near-wake flows at high Reynolds numbers are described. A long, airfoil-like model was tested at subsonic and low transonic Mach numbers, and both symmetrical and asymmetrical flows with pressure gradients upstream of the trailing edge were investigated. Model surface pressures and detailed mean and turbulence flow qualities were measured in the vicinity of the trailing edge and in the near-wake. The data obtained are of sufficient quality and detail to be useful as test cases in assessing turbulence models and calculation methods

An experimental and computational investigation of the flow field about a transonic airfoil in supercritical flow with turbulent boundary-layer separation

A combined experimental and computational research program is described for testing and guiding turbulence modeling within regions of separation induced by shock waves incident in turbulent boundary layers. Specifically, studies are made of the separated flow the rear portion of an 18%-thick circular-arc airfoil at zero angle of attack in high Reynolds number supercritical flow. The measurements include distributions of surface static pressure and local skin friction. The instruments employed include highfrequency response pressure cells and a large array of surface hot-wire skin-friction gages. Computations at the experimental flow conditions are made using time-dependent solutions of ensemble-averaged Navier-Stokes equations, plus additional equations for the turbulence modeling

Turbulence Modeling for Unsteady Transonic Flows

Conditionally sampled, ensemble-averaged velocity measurements, made with a laser velocimeter, were taken in the flowfield over the rear half of an 18% thick circular arc airfoil at zero incidence tested at M = 0.76 and at a Reynolds number based on chord of 11 x 10(exp 6). Data for one cycle of periodic unsteady flow having a reduced frequency f of 0.49 are analyzed. A series of compression waves, which develop in the early stages of the cycle, strengthen and coalesce into a strong shock wave that moves toward the airfoil leading edge. A thick shear layer forms downstream of the shock wave. The kinetic energy and shear stresses increase dramatically, reach a maximum when dissipation and diffusion of the turbulence exceed production, and then decrease substantially. The response lime of the turbulence to the changes brought about by the shock-wave passage upstream depends on the shock-wave strength and position in the boundary layer. The cycle completes itself when the shock wave passes the midchord, weakens, and the shear layer collapses. Remarkably good comparisons are found with computations that employ the time-dependent Reynolds averaged form of the Navier-Stokes equations using an algebraic eddy viscosity model, developed for steady flows

Hypoxanthine-guanine phosophoribosyltransferase (HPRT) deficiency: Lesch-Nyhan syndrome

Deficiency of hypoxanthine-guanine phosphoribosyltransferase (HPRT) activity is an inborn error of purine metabolism associated with uric acid overproduction and a continuum spectrum of neurological manifestations depending on the degree of the enzymatic deficiency. The prevalence is estimated at 1/380,000 live births in Canada, and 1/235,000 live births in Spain. Uric acid overproduction is present inall HPRT-deficient patients and is associated with lithiasis and gout. Neurological manifestations include severe action dystonia, choreoathetosis, ballismus, cognitive and attention deficit, and self-injurious behaviour. The most severe forms are known as Lesch-Nyhan syndrome (patients are normal at birth and diagnosis can be accomplished when psychomotor delay becomes apparent). Partial HPRT-deficient patients present these symptoms with a different intensity, and in the least severe forms symptoms may be unapparent. Megaloblastic anaemia is also associated with the disease. Inheritance of HPRT deficiency is X-linked recessive, thus males are generally affected and heterozygous female are carriers (usually asymptomatic). Human HPRT is encoded by a single structural gene on the long arm of the X chromosome at Xq26. To date, more than 300 disease-associated mutations in the HPRT1 gene have been identified. The diagnosis is based on clinical and biochemical findings (hyperuricemia and hyperuricosuria associated with psychomotor delay), and enzymatic (HPRT activity determination in haemolysate, intact erythrocytes or fibroblasts) and molecular tests. Molecular diagnosis allows faster and more accurate carrier and prenatal diagnosis. Prenatal diagnosis can be performed with amniotic cells obtained by amniocentesis at about 15–18 weeks' gestation, or chorionic villus cells obtained at about 10–12 weeks' gestation. Uric acid overproduction can be managed by allopurinol treatment. Doses must be carefully adjusted to avoid xanthine lithiasis. The lack of precise understanding of the neurological dysfunction has precluded development of useful therapies. Spasticity, when present, and dystonia can be managed with benzodiazepines and gamma-aminobutyric acid inhibitors such as baclofen. Physical rehabilitation, including management of dysarthria and dysphagia, special devices to enable hand control, appropriate walking aids, and a programme of posture management to prevent deformities are recommended. Self-injurious behaviour must be managed by a combination of physical restraints, behavioural and pharmaceutical treatments

Altered purine and pyrimidine metabolism in erythrocytes with purine nucleoside phosphorylase deficiency

Purine and pyrimidine metabolism was compared in erythrocytes from three patients from two families with purine nucleoside phosphorylase deficiency and T-cell immunodeficiency, one heterozygote subject for this enzyme deficiency, one patient with a complete deficiency of hypoxanthine-guanine phosphoribosyltransferase, and two normal subjects. The erythrocytes from the heterozygote subject were indistinguishable from the normal erythrocytes. The purine nucleoside phosphorylase deficient erythrocytes had a block in the conversion of inosine to hypoxanthine. The erythrocytes with 0.07% of normal purine nucleoside phosphorylase activity resembled erythrocytes with hypoxanthine-guanine phosphoribosyltransferase deficiency by having an elevated intracellular concentration of PP-ribose-P, increased synthesis of PP-ribose-P, and an elevated rate of carbon dioxide release from orotic acid during its conversion to UMP. Two hypotheses to account for the associated immunodeficiency—that the enzyme deficiency leads to a block of PP-ribose-P synthesis or inhibition of pyrimidine synthesis—could not be supported by observations in erythrocytes from both enzyme-deficient families.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/44134/1/10528_2004_Article_BF00484238.pd