Streak generation in wind tunnels

Computational results are presented which co-validate published experimental observations of steady streaks, deliberately generated by the steady wake of a wire placed upstream of a flat plate with a prescribed leading edge. The largest streak occurs when the wake is generated from a wire placed upstream of the wind tunnel contraction. Normal vorticity passing through the contraction leads to the creation of streamwise vorticity in the test-section via tilting and stretching. The computational results allow the original experiment to be reinterpreted as a receptivity experiment that demonstrates the boundary layer is more receptive to steady streamwise vorticity than normal vorticity. It also suggests an interesting mechanism for the generation of Klebanoff streaks in wind tunnels. The effect of shifting the attachment point at the leading edge on receptivity is also demonstrated. The streak growth is compared to the Optimal streak often used in computational studies. The modal growth of the streak generated by free-stream normal vorticity is found to have a streamwise location of peak energy close to the Optimal streak for wavelengths larger than the leading edge thickness. However, the location of the peak energy for the streamwise vorticity streak varies substantially with wavelength. Differences in wall-normal profiles are also noted

Key to the Species of \u3cem\u3eMegarhyssa\u3c/em\u3e (Hymenoptera, Ichneumonidae, Rhyssinae) in America, North of Mexico

A dichotomous and an interactive key to the species of Megarhyssa (Hymenoptera: Ichneumonidae) in America, north of Mexico are presented. A diagnosis accompanied by images is provided for male and female wasps of each of the four species, Megarhyssa atrata, Megarhyssa greenei, Megarhyssa macrurus and Megarhyssa nortoni

Key to the Species of \u3cem\u3eMegarhyssa\u3c/em\u3e (Hymenoptera, Ichneumonidae, Rhyssinae) in America, North of Mexico

A dichotomous and an interactive key to the species of Megarhyssa (Hymenoptera: Ichneumonidae) in America, north of Mexico are presented. A diagnosis accompanied by images is provided for male and female wasps of each of the four species, Megarhyssa atrata, Megarhyssa greenei, Megarhyssa macrurus and Megarhyssa nortoni

Universal Multifractality in Quantum Hall Systems with Long-Range Disorder Potential

We investigate numerically the localization-delocalization transition in quantum Hall systems with long-range disorder potential with respect to multifractal properties. Wavefunctions at the transition energy are obtained within the framework of the generalized Chalker--Coddington network model. We determine the critical exponent $\alpha_0$ characterizing the scaling behavior of the local order parameter for systems with potential correlation length $d$ up to $12$ magnetic lengths $l$. Our results show that $\alpha_0$ does not depend on the ratio $d/l$. With increasing $d/l$, effects due to classical percolation only cause an increase of the microscopic length scale, whereas the critical behavior on larger scales remains unchanged. This proves that systems with long-range disorder belong to the same universality class as those with short-range disorder.Comment: 4 pages, 2 figures, postsript, uuencoded, gz-compresse

Multifractal properties of critical eigenstates in two-dimensional systems with symplectic symmetry

The multifractal properties of electronic eigenstates at the metal-insulator transition of a two-dimensional disordered tight-binding model with spin-orbit interaction are investigated numerically. The correlation dimensions of the spectral measure $\widetilde{D}_{2}$ and of the fractal eigenstate $D_{2}$ are calculated and shown to be related by $D_{2}=2\widetilde{D}_{2}$. The exponent $\eta=0.35\pm 0.05$ describing the energy correlations of the critical eigenstates is found to satisfy the relation $\eta=2-D_{2}$.Comment: 6 pages RevTeX; 3 uuencoded, gzipped ps-figures to appear in J. Phys. Condensed Matte

Impact of surface forcing on Southern Hemisphere atmospheric blocking in the Australia–New Zealand sector

Author Posting. © American Meteorological Society, 2013. This article is posted here by permission of American Meteorological Society for personal use, not for redistribution. The definitive version was published in Journal of Climate 26 (2013): 8476–8494, doi:10.1175/JCLI-D-12-00860.1.Characteristics of atmospheric blocking in the Southern Hemisphere (SH) are explored in atmospheric general circulation model (AGCM) simulations with the Community Atmosphere Model, version 3, with a particular focus on the Australia–New Zealand sector. Preferred locations of blocking in SH observations and the associated seasonal cycle are well represented in the AGCM simulations, but the observed magnitude of blocking is underestimated throughout the year, particularly in late winter and spring. This is related to overly zonal flow due to an enhanced meridional pressure gradient in the model, which results in a decreased amplitude of the longwave trough/ridge pattern. A range of AGCM sensitivity experiments explores the effect on SH blocking of tropical heating, midlatitude sea surface temperatures, and land–sea temperature gradients created over the Australian continent during austral winter. The combined effects of tropical heating and extratropical temperature gradients are further explored in a configuration that is favorable for blocking in the Australia–New Zealand sector with warm SST anomalies to the north of Australia, cold to the southwest of Australia, warm to the southeast, and cool Australian land temperatures. The blocking-favorable configuration indicates a significant strengthening of the subtropical jet and a reduction in midlatitude flow, which results from changes in the thermal wind. While these overall changes in mean climate, predominantly forced by the tropical heating, enhance blocking activity, the magnitude of atmospheric blocking compared to observations is still underestimated. The blocking-unfavorable configuration with surface forcing anomalies of opposite sign results in a weakening subtropical jet, enhanced midlatitude flow, and significantly reduced blocking.C.C.U. received support from the Australian Research Council through funding awarded to the Centre of Excellence for Climate System Science and the Penzance Endowed Fund at WHOI. P.C.M., M.J.P., and J.S.R. were funded by the CSIRO Climate Adaptation Flagship and the Managing Climate Variability R&D Program.2014-05-0

Multifractality of the quantum Hall wave functions in higher Landau levels

To probe the universality class of the quantum Hall system at the metal-insulator critical point, the multifractality of the wave function $\psi$ is studied for higher Landau levels, $N=1,2$, for various range $(\sigma )$ of random potential. We have found that, while the multifractal spectrum $f(\alpha)$ (and consequently the fractal dimension) does vary with $N$, the parabolic form for $f(\alpha)$ indicative of a log-normal distribution of $\psi$ persists in higher Landau levels. If we relate the multifractality with the scaling of localization via the conformal theory, an asymptotic recovery of the single-parameter scaling with increasing $\sigma$ is seen, in agreement with Huckestein's irrelevant scaling field argument.Comment: 10 pages, revtex, 5 figures available on request from [email protected]

Disordered Electrons in a Strong Magnetic Field: Transfer Matrix Approaches to the Statistics of the Local Density of States

We present two novel approaches to establish the local density of states as an order parameter field for the Anderson transition problem. We first demonstrate for 2D quantum Hall systems the validity of conformal scaling relations which are characteristic of order parameter fields. Second we show the equivalence between the critical statistics of eigenvectors of the Hamiltonian and of the transfer matrix, respectively. Based on this equivalence we obtain the order parameter exponent $\alpha_0\approx 3.4$ for 3D quantum Hall systems.Comment: 4 pages, 3 Postscript figures, corrected scale in Fig.

GAA repeat expansion mutation mouse models of Friedreich ataxia exhibit oxidative stress leading to progressive neuronal and cardiac pathology

Friedreich ataxia (FRDA) is a neurodegenerative disorder caused by an unstable GAA repeat expansion mutation within intron 1 of the FXN gene. However, the origins of the GAA repeat expansion, its unstable dynamics within different cells and tissues, and its effects on frataxin expression are not yet completely understood. Therefore, we have chosen to generate representative FRDA mouse models by using the human FXN GAA repeat expansion itself as the genetically modified mutation. We have previously reported the establishment of two lines of human FXN YAC transgenic mice that contain unstable GAA repeat expansions within the appropriate genomic context. We now describe the generation of FRDA mouse models by crossbreeding of both lines of human FXN YAC transgenic mice with heterozygous Fxn knockout mice. The resultant FRDA mice that express only human-derived frataxin show comparatively reduced levels of frataxin mRNA and protein expression, decreased aconitase activity, and oxidative stress, leading to progressive neurodegenerative and cardiac pathological phenotypes. Coordination deficits are present, as measured by accelerating rotarod analysis, together with a progressive decrease in locomotor activity and increase in weight. Large vacuoles are detected within neurons of the dorsal root ganglia (DRG), predominantly within the lumbar regions in 6-month-old mice, but spreading to the cervical regions after 1 year of age. Secondary demyelination of large axons is also detected within the lumbar roots of older mice. Lipofuscin deposition is increased in both DRG neurons and cardiomyocytes, and iron deposition is detected in cardiomyocytes after 1 year of age. These mice represent the first GAA repeat expansion-based FRDA mouse models that exhibit progressive FRDA-like pathology and thus will be of use in testing potential therapeutic strategies, particularly GAA repeat-based strategies. © 2006 Elsevier Inc. All rights reserved

Cellular, molecular and functional characterisation of YAC transgenic mouse models of Friedreich Ataxia

Copyright © 2014 Anjomani Virmouni et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.This article has been made available through the Brunel Open Access Publishing Fund.Background - Friedreich ataxia (FRDA) is an autosomal recessive neurodegenerative disorder, caused by a GAA repeat expansion mutation within intron 1 of the FXN gene. We have previously established and performed preliminary characterisation of several human FXN yeast artificial chromosome (YAC) transgenic FRDA mouse models containing GAA repeat expansions, Y47R (9 GAA repeats), YG8R (90 and 190 GAA repeats) and YG22R (190 GAA repeats). Methodology/Principal Findings - We now report extended cellular, molecular and functional characterisation of these FXN YAC transgenic mouse models. FXN transgene copy number analysis of the FRDA mice demonstrated that the YG22R and Y47R lines each have a single copy of the FXN transgene while the YG8R line has two copies. Single integration sites of all transgenes were confirmed by fluorescence in situ hybridisation (FISH) analysis of metaphase and interphase chromosomes. We identified significant functional deficits, together with a degree of glucose intolerance and insulin hypersensitivity, in YG8R and YG22R FRDA mice compared to Y47R and wild-type control mice. We also confirmed increased somatic GAA repeat instability in the cerebellum and brain of YG22R and YG8R mice, together with significantly reduced levels of FXN mRNA and protein in the brain and liver of YG8R and YG22R compared to Y47R. Conclusions/Significance - Together these studies provide a detailed characterisation of our GAA repeat expansion-based YAC transgenic FRDA mouse models that will help investigations of FRDA disease mechanisms and therapy.European Union, Ataxia UK and FARA