Classical and Non-Relativistic Limits of a Lorentz-Invariant Bohmian Model for a System of Spinless Particles

A completely Lorentz-invariant Bohmian model has been proposed recently for the case of a system of non-interacting spinless particles, obeying Klein-Gordon equations. It is based on a multi-temporal formalism and on the idea of treating the squared norm of the wave function as a space-time probability density. The particle's configurations evolve in space-time in terms of a parameter {\sigma}, with dimensions of time. In this work this model is further analyzed and extended to the case of an interaction with an external electromagnetic field. The physical meaning of {\sigma} is explored. Two special situations are studied in depth: (1) the classical limit, where the Einsteinian Mechanics of Special Relativity is recovered and the parameter {\sigma} is shown to tend to the particle's proper time; and (2) the non-relativistic limit, where it is obtained a model very similar to the usual non-relativistic Bohmian Mechanics but with the time of the frame of reference replaced by {\sigma} as the dynamical temporal parameter

X-Ray Detection of Transient Magnetic Moments Induced by a Spin Current in Cu

We have used a MHz lock-in x-ray spectro-microscopy technique to directly detect changes of magnetic moments in Cu due to spin injection from an adjacent Co layer. The elemental and chemical specificity of x-rays allows us to distinguish two spin current induced effects. We detect the creation of transient magnetic moments of $3\times 10^{-5}$ $\mu_\mathrm{B}$ on Cu atoms within the bulk of the 28 nm thick Cu film due to spin-accumulation. The moment value is compared to predictions by Mott's two current model. We also observe that the hybridization induced existing magnetic moments on Cu interface atoms are transiently increased by about 10% or $4\times 10^{-3}$ $\mu_\mathrm{B}$. This reveals the dominance of spin-torque alignment over Joule heat induced disorder of the interfacial Cu moments during current flow

Microscopic chaos from Brownian motion?

A recent experiment on Brownian motion has been interpreted to exhibit direct evidence for microscopic chaos. In this note we demonstrate that virtually identical results can be obtained numerically using a manifestly microscopically nonchaotic system.Comment: 3 pages, 1 figure, Comment on P. Gaspard et al, Nature vol 394, 865 (1998); rewritten in a more popular styl

Static quarks with improved statistical precision

We present a numerical study for different discretisations of the static action, concerning cut-off effects and the growth of statistical errors with Euclidean time. An error reduction by an order of magnitude can be obtained with respect to the Eichten-Hill action, for time separations beyond 1.3 fm, keeping discretization errors small. The best actions lead to a big improvement on the precision of the quark mass Mb and F_Bs in the static approximation.Comment: 3 pages, 4 figures, Lattice2003(heavy

Mutations in SPG11, encoding spatacsin, are a major cause of spastic paraplegia with thin corpus callosum.

Autosomal recessive hereditary spastic paraplegia (ARHSP) with thin corpus callosum (TCC) is a common and clinically distinct form of familial spastic paraplegia that is linked to the SPG11 locus on chromosome 15 in most affected families. We analyzed 12 ARHSP-TCC families, refined the SPG11 candidate interval and identified ten mutations in a previously unidentified gene expressed ubiquitously in the nervous system but most prominently in the cerebellum, cerebral cortex, hippocampus and pineal gland. The mutations were either nonsense or insertions and deletions leading to a frameshift, suggesting a loss-of-function mechanism. The identification of the function of the gene will provide insight into the mechanisms leading to the degeneration of the corticospinal tract and other brain structures in this frequent form of ARHSP

Longitudinal changes in functional connectivity of cortico-basal ganglia networks in manifests and premanifest huntington's disease

Huntington's disease (HD) is a genetic neurological disorder resulting in cognitive and motor impairments. We evaluated the longitudinal changes of functional connectivity in sensorimotor, associative and limbic cortico-basal ganglia networks. We acquired structural MRI and resting-state fMRI in three visits one year apart, in 18 adult HD patients, 24 asymptomatic mutation carriers (preHD) and 18 gender- and age-matched healthy volunteers from the TRACK-HD study. We inferred topological changes in functional connectivity between 182 regions within cortico-basal ganglia networks using graph theory measures. We found significant differences for global graph theory measures in HD but not in preHD. The average shortest path length (L) decreased, which indicated a change toward the random network topology. HD patients also demonstrated increases in degree k, reduced betweeness centrality bc and reduced clustering C. Changes predominated in the sensorimotor network for bc and C and were observed in all circuits for k. Hubs were reduced in preHD and no longer detectable in HD in the sensorimotor and associative networks. Changes in graph theory metrics (L, k, C and bc) correlated with four clinical and cognitive measures (symbol digit modalities test, Stroop, Burden and UHDRS). There were no changes in graph theory metrics across sessions, which suggests that these measures are not reliable biomarkers of longitudinal changes in HD. preHD is characterized by progressive decreasing hub organization, and these changes aggravate in HD patients with changes in local metrics. HD is characterized by progressive changes in global network interconnectivity, whose network topology becomes more random over time. Hum Brain Mapp, 2016. © 2016 Wiley Periodicals, Inc

Neurofilament light protein in blood as a potential biomarker of neurodegeneration in Huntington's disease: a retrospective cohort analysis

BACKGROUND: Blood biomarkers of neuronal damage could facilitate clinical management of and therapeutic development for Huntington's disease. We investigated whether neurofilament light protein NfL (also known as NF-L) in blood is a potential prognostic marker of neurodegeneration in patients with Huntington's disease. METHODS: We did a retrospective analysis of healthy controls and carriers of CAG expansion mutations in HTT participating in the 3-year international TRACK-HD study. We studied associations between NfL concentrations in plasma and clinical and MRI neuroimaging findings, namely cognitive function, motor function, and brain volume (global and regional). We used random effects models to analyse cross-sectional associations at each study visit and to assess changes from baseline, with and without adjustment for age and CAG repeat count. In an independent London-based cohort of 37 participants (23 HTT mutation carriers and 14 controls), we further assessed whether concentrations of NfL in plasma correlated with those in CSF. FINDINGS: Baseline and follow-up plasma samples were available from 97 controls and 201 individuals carrying HTT mutations. Mean concentrations of NfL in plasma at baseline were significantly higher in HTT mutation carriers than in controls (3·63 [SD 0·54] log pg/mL vs 2·68 [0·52] log pg/mL, p<0·0001) and the difference increased from one disease stage to the next. At any given timepoint, NfL concentrations in plasma correlated with clinical and MRI findings. In longitudinal analyses, baseline NfL concentration in plasma also correlated significantly with subsequent decline in cognition (symbol-digit modality test r=–0·374, p<0·0001; Stroop word reading r=–0·248, p=0·0033), total functional capacity (r=–0·289, p=0·0264), and brain atrophy (caudate r=0·178, p=0·0087; whole-brain r=0·602, p<0·0001; grey matter r=0·518, p<0·0001; white matter r=0·588, p<0·0001; and ventricular expansion r=–0·589, p<0·0001). All changes except Stroop word reading and total functional capacity remained significant after adjustment for age and CAG repeat count. In 104 individuals with premanifest Huntington's disease, NfL concentration in plasma at baseline was associated with subsequent clinical onset during the 3-year follow-up period (hazard ratio 3·29 per log pg/mL, 95% CI 1·48–7·34, p=0·0036). Concentrations of NfL in CSF and plasma were correlated in mutation carriers (r=0·868, p<0·0001). INTERPRETATION: NfL in plasma shows promise as a potential prognostic blood biomarker of disease onset and progression in Huntington's disease

Light Hadron Masses from Lattice QCD

This article reviews lattice QCD results for the light hadron spectrum. We give an overview of different formulations of lattice QCD, with discussions on the fermion doubling problem and improvement programs. We summarize recent developments in algorithms and analysis techniques, that render calculations with light, dynamical quarks feasible on present day computer resources. Finally, we summarize spectrum results for ground state hadrons and resonances using various actions.Comment: 53 pages, 24 figures, one table; Rev.Mod.Phys. (published version); v2: corrected typ

Pion mass dependence of the Kl3K_{l3} semileptonic scalar form factor within finite volume

We calculate the scalar semileptonic kaon decay in finite volume at the momentum transfer $t_{m} = (m_{K} - m_{\pi})^2$, using chiral perturbation theory. At first we obtain the hadronic matrix element to be calculated in finite volume. We then evaluate the finite size effects for two volumes with $L = 1.83 fm$ and $L= 2.73 fm$ and find that the difference between the finite volume corrections of the two volumes are larger than the difference as quoted in \cite{Boyle2007a}. It appears then that the pion masses used for the scalar form factor in ChPT are large which result in large finite volume corrections. If appropriate values for pion mass are used, we believe that the finite size effects estimated in this paper can be useful for Lattice data to extrapolate at large lattice size.Comment: 19 pages, 5 figures, accepted for publication in EPJ

The rooting issue for a lattice fermion formulation similar to staggered fermions but without taste mixing

To investigate the viability of the 4th root trick for the staggered fermion determinant in a simpler setting, we consider a two taste (flavor) lattice fermion formulation with no taste mixing but with exact taste-nonsinglet chiral symmetries analogous to the taste-nonsinglet $U(1)_A$ symmetry of staggered fermions. M. Creutz's objections to the rooting trick apply just as much in this setting. To counter them we show that the formulation has robust would-be zero-modes in topologically nontrivial gauge backgrounds, and that these manifest themselves in a viable way in the rooted fermion determinant and also in the disconnected piece of the pseudoscalar meson propagator as required to solve the U(1) problem. Also, our rooted theory is heuristically seen to be in the right universality class for QCD if the same is true for an unrooted mixed fermion action theory.Comment: 22 revtex pages, to appear in PRD. v4: correction in the relation of the 2-flavor theory to twisted mass fermion