Geometric observation for the Bures fidelity between two states of a qubit

In this Brief Report, we present a geometric observation for the Bures fidelity between two states of a qubit.Comment: 4 pages, 1 figure, RevTex, Accepted by Phys. Rev.

Electron g-Factor Anisotropy in Symmetric (110)-oriented GaAs Quantum Wells

We demonstrate by spin quantum beat spectroscopy that in undoped symmetric (110)-oriented GaAs/AlGaAs single quantum wells even a symmetric spatial envelope wavefunction gives rise to an asymmetric in-plane electron Land\'e-g-factor. The anisotropy is neither a direct consequence of the asymmetric in-plane Dresselhaus splitting nor of the asymmetric Zeeman splitting of the hole bands but is a pure higher order effect that exists as well for diamond type lattices. The measurements for various well widths are very well described within 14 x 14 band k.p theory and illustrate that the electron spin is an excellent meter variable to map out the internal -otherwise hidden- symmetries in two dimensional systems. Fourth order perturbation theory yields an analytical expression for the strength of the g-factor anisotropy, providing a qualitative understanding of the observed effects

Fatigue analysis-based numerical design of stamping tools made of cast iron

This work concerns stress and fatigue analysis of stamping tools made of cast iron with an essentially pearlitic matrix and containing foundry defects. Our approach consists at first, in coupling the stamping numerical processing simulations and structure analysis in order to improve the tool stiffness geometry for minimizing the stress state and optimizing their fatigue lifetime. The method consists in simulating the stamping process by considering the tool as a perfect rigid body. The estimated contact pressure is then used as boundary condition for FEM structure loading analysis of the tool. The result of this analysis is compared with the critical stress limit depending on the automotive model. The acceptance of this test allows calculating the fatigue lifetime of the critical zone by using the S–N curve of corresponding load ratio. If the prescribed tool life requirements are not satisfied, then the critical region of the tool is redesigned and the whole simulation procedures are reactivated. This method is applied for a cast iron EN-GJS-600-3. The stress-failure (S–N) curves for this material is determined at room temperature under push pull loading with different load ratios R0σmin/σmax0−2, R0−1 and R00.1. The effects of the foundry defects are determined by SEM observations of crack initiation sites. Their presence in tested specimens is associated with a reduction of fatigue lifetime by a factor of 2. However, the effect of the load ratio is more important

Frictional drag between quantum wells mediated by phonon exchange

We use the Kubo formalism to evaluate the contribution of acoustic phonon exchange to the frictional drag between nearby two-dimensional electron systems. In the case of free phonons, we find a divergent drag rate ($\tau_{D}^{-1}$). However, $\tau_{D}^{-1}$ becomes finite when phonon scattering from either lattice imperfections or electronic excitations is accounted for. In the case of GaAs quantum wells, we find that for a phonon mean free path $\ell_{ph}$ smaller than a critical value, imperfection scattering dominates and the drag rate varies as $ln (\ell_{ph}/d)$ over many orders of magnitude of the layer separation $d$. When $\ell_{ph}$ exceeds the critical value, the drag rate is dominated by coupling through an electron-phonon collective mode localized in the vicinity of the electron layers. We argue that the coupled electron-phonon mode may be observable for realistic parameters. Our theory is in good agreement with experimental results for the temperature, density, and $d$-dependence of the drag rate.Comment: 45 pages, LaTeX, 8 postscript file figure

Enhanced recovery after surgery: are we ready, and can we afford not to implement these pathways for patients undergoing radical cystectomy?

Enhanced recovery after surgery (ERAS) for radical cystectomy seems logical, but our study has shown a paucity in the level of clinical evidence. As part of the ERAS Society, we welcome global collaboration to collect evidence that will improve patient outcomes

Neurotensin(8–13) analogs as dual NTS1 and NTS2 receptor ligands with enhanced effects on a mouse model of Parkinson's disease

: The modulatory interactions between neurotensin (NT) and the dopaminergic neurotransmitter system in the brain suggest that NT may be associated with the progression of Parkinson's disease (PD). NT exerts its neurophysiological effects by interactions with the human NT receptors type 1 (hNTS1) and 2 (hNTS2). Therefore, both receptor subtypes are promising targets for the development of novel NT-based analogs for the treatment of PD. In this study, we used a virtually guided molecular modeling approach to predict the activity of NT(8-13) analogs by investigating the docking models of ligands designed for binding to the human NTS1 and NTS2 receptors. The importance of the residues at positions 8 and/or 9 for hNTS1 and hNTS2 receptor binding affinity was experimentally confirmed by radioligand binding assays. Further in vitro ADME profiling and in vivo studies revealed that, compared to the parent peptide NT(8-13), compound 10 exhibited improved stability and BBB permeability combined with a significant enhancement of the motor function and memory in a mouse model of PD. The herein reported NTS1/NTS2 dual-specific NT(8-13) analogs represent an attractive tool for the development of therapeutic strategies against PD and potentially other CNS disorders

Intra- and inter-individual genetic differences in gene expression

Genetic variation is known to influence the amount of mRNA produced by a gene. Given that the molecular machines control mRNA levels of multiple genes, we expect genetic variation in the components of these machines would influence multiple genes in a similar fashion. In this study we show that this assumption is correct by using correlation of mRNA levels measured independently in the brain, kidney or liver of multiple, genetically typed, mice strains to detect shared genetic influences. These correlating groups of genes (CGG) have collective properties that account for 40-90% of the variability of their constituent genes and in some cases, but not all, contain genes encoding functionally related proteins. Critically, we show that the genetic influences are essentially tissue specific and consequently the same genetic variations in the one animal may up-regulate a CGG in one tissue but down-regulate the same CGG in a second tissue. We further show similarly paradoxical behaviour of CGGs within the same tissues of different individuals. The implication of this study is that this class of genetic variation can result in complex inter- and intra-individual and tissue differences and that this will create substantial challenges to the investigation of phenotypic outcomes, particularly in humans where multiple tissues are not readily available.

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ERK2 phosphorylation of serine 77 regulates Bmf pro-apoptotic activity

B-cell lymphoma 2 (Bcl-2) homology 3 (BH3)-only proteins represent a class of pro-apoptotic factors that neutralize pro-survival Bcl-2 proteins, and, in some cases, directly activate Bax. The mechanisms of control and the role of BH3-only proteins, such as Bcl-2 like protein 11 extra large and Bad are well studied. By contrast, relatively little is known about the regulation and role of Bcl-2 modifying factor (Bmf). The B-RAF oncogene is mutated in ∼8% of human tumors. We have previously shown that Bmf is upregulated at the transcript level and is required for apoptosis induced by targeting B-RAF signaling in tumor cells harboring mutant B-RAF. In this study, we show that Bmf is regulated at the post-translational level by mutant B-RAF-MEK-ERK2 signaling. Extracellular signal-regulated kinase (ERK2) directly phosphorylates Bmf on serine 74 and serine 77 residues with serine 77 being the predominant site. In addition, serine 77 phosphorylation reduces Bmf pro-apoptotic activity likely through a mechanism independent of altering Bmf localization to the mitochondria and/or interactions with dynein light chain 2 and the pro-survival proteins, B-cell lymphoma extra large, Bcl-2 and Mcl-1. These data identify a novel mode of regulation in Bmf that modulates its pro-apoptotic activity in mutant B-RAF tumor cells