Integral Equation Solution of the Full Potential Equation for Three-Dimensional, Steady, Transonic Wing Flows

An integral equation method for solving the full potential equation has been developed for three dimensional transonic vortex-wing flows. This method is capable of capturing shocks using the Murman-Cole type of finite difference scheme and is capable of predicting accurate and force-free wake shape as well. Reading the full potential equation as Poisson\u27s equation, the solution for the velocity field has been expressed in terms of an integral equation using Green\u27s theorem. The solution consists of a surface integral of vorticity distribution on the wing and its free-vortex sheets and a volume integral of source distribution within a computational region around the flow domain under consideration. The solution is obtained through two iteration loops: the outer loop iterates the vorticity distribution and wake shape, while the inner loop iterates the field compressibility. A computer program has been constructed for implementation of this methodology and has been used to solve a flow around a rectangular flat wing with a trailing wake. The program can be modified without difficulties to solve flow problems with complex configurations. The wing and its free-vortex sheets are modeled using a bilinear vortex panel distribution, while the field compressibility of the flow domain under consideration is modeled using a constant, distributed, source strength over each of the discretized rectangular-parallelopiped volume cells. The technique of pre-calculated and stored induced velocity for field compressibility calculations has greatly reduced the computational time. The successive grid refinement has also effectively and reliably reduced the computational domain and greatly improved the accuracy as well. The numerical results show that this method is computationally stable and efficient and also show its great potential in solving unsteady transonic flow problems. The study conducted in this dissertation also sheds some light in the vectorization of an integral equation method which is crucial in achieving better computational efficiency when running on a modern vector computer

Static aeroelastic effects on the flutter of a supercritical wing

It is well known that wings with supercritical airfoils generally have lower transonic flutter speeds than similar wings with conventional airfoils and that small increases in angle of attack from zero and the accompanying static aeroelastic deformations have further detrimental effects on transonic flutter. The results of an effort to calculate the effects of angle of attack and the associated aeroelastic deformation on the flutter of a highly swept supercritical wing (TF 8A) by use of the modified strip analysis employed in previous studies of this wing are presented. The spanwise distributions of steady-state section lift-curve slope and aerodynamic center required as input for these calculations were obtained from static aeroelastic calculations for the wing by use of the FL022 transonic code and an assumed dynamic pressure as that used to calculate the statically deformed shape and loading about which the flutter oscillation occurs. The results show that the unconventional backward turn of the transonic dip in the experimental flutter boundary for angles of attack greater than zero is caused by variations in mass ratio and not by static aeroelastic deformation, although inclusion of the latter appears to be required for quantitative accuracy in the calculations

New Insights on 30 Dor B Revealed by High-Quality Multi-wavelength Observations

The supernova remnant (SNR) 30 Dor B is associated with the \ion{H}{2} region ionized by the OB association LH99. The complex interstellar environment has made it difficult to study the physical structure of this SNR. We have used Hubble Space Telescope H$\alpha$ images to identify SNR shocks and deep Chandra X-ray observations to detect faint diffuse emission. We find that 30 Dor B hosts three zones with very different X-ray surface brightnesses and nebular kinematics that are characteristic of SNRs in different interstellar environments and/or evolutionary stages. The ASKAP 888 MHz map of 30 Dor B shows counterparts to all X-ray emission features except the faint halo. The ASKAP 888 MHz and 1420 MHz observations are used to produce a spectral index map, but its interpretation is complicated by the background thermal emission and the pulsar PSR J0537$-$6910's flat spectral index. The stellar population in the vicinity of 30 Dor B indicates a continuous star formation in the past 8--10 Myr. The observed very massive stars in LH99 cannot be coeval with the progenitor of 30 Dor B's pulsar. Adopting the pulsar's spin-down timescale, 5000 yr, as the age of the SNR, the X-ray shell would be expanding at $\sim$4000 km\,s$^{-1}$ and the post-shock temperature would be 1--2 orders of magnitude higher than that indicated by the X-ray spectra. Thus, the bright central region of 30 Dor B and the X-ray shell requires two separate SN events, and the faint diffuse X-ray halo perhaps other older SN events

Lipopolysaccharide-stimulated Leukocytes Contribute to Platelet Aggregative Dysfunction, Which is Attenuated by Catalase in Rats

Endotoxemia causes several hematological dysfunctions, including platelet degranulation or disseminated intravascular coagulation, which lead to thrombotic and hemorrhagic events. Here, we tested the hypothesis that bacterial lipopolysaccharide (LPS)-stimulated leukocytes contribute to platelet aggregative dysfunction, and this function is attenuated by antioxidants. Plateletrich plasma (PRP) was prepared from whole blood of normal and endotoxemic rats. The ability of platelet aggregation was measured by an aggregometer. LPS (50–100 μg/mL) was incubated with PRP, whole blood and PRP with polymorphonuclear leukocytes (PMNs) for 30 minutes, 60 minutes and 90 minutes, and platelet aggregation was detected. LPS-induced platelet aggregative dysfunction was undetectable in intact PRP which was isolated from normal whole blood, whereas it was detected in PRP isolated from endotoxemic rats and LPS-treated whole blood. Moreover, the effect of LPS-induced platelet aggregative dysfunction on intact PRP was observed when the PMNs were added. LPS-induced platelet aggregative dysfunction was significantly attenuated by catalase alone and in combination with NG-nitro-L-arginine methyl ester, but not by NG-nitro-L-arginine methyl ester alone. These results indicate that LPS-stimulated PMNs modulate platelet aggregation during LPS treatment and the effects are reversed by antioxidants. PMNs serve as an approach to understand LPS-induced platelet aggregative dysfunction during endotoxemia. During this process, the generation of reactive oxygen species, hydrogen peroxide especially, from LPS-stimulated PMNs could be an important potential factor in LPS-induced platelet aggregative dysfunction. Catalase contributes to the prevention of platelet dysfunction during LPS-induced sepsis