Numerical study of a non-equilibrium interface model

We have carried out extensive computer simulations of one-dimensional models related to the low noise (solid-on-solid) non-equilibrium interface of a two dimensional anchored Toom model with unbiased and biased noise. For the unbiased case the computed fluctuations of the interface in this limit provide new numerical evidence for the logarithmic correction to the subnormal L^(1/2) variance which was predicted by the dynamic renormalization group calculations on the modified Edwards-Wilkinson equation. In the biased case the simulations are in close quantitative agreement with the predictions of the Collective Variable Approximation (CVA), which gives the same L^(2/3) behavior of the variance as the KPZ equation.Comment: 15 pages revtex, 4 Postscript Figure

Noether symmetries for two-dimensional charged particle motion

We find the Noether point symmetries for non-relativistic two-dimensional charged particle motion. These symmetries are composed of a quasi-invariance transformation, a time-dependent rotation and a time-dependent spatial translation. The associated electromagnetic field satisfy a system of first-order linear partial differential equations. This system is solved exactly, yielding three classes of electromagnetic fields compatible with Noether point symmetries. The corresponding Noether invariants are derived and interpreted

Probing New Physics from Top-charm Associated Productions at Linear Colliders

The top-charm associated productions via $e^+ e^-$, $e^- \gamma$ and $\gamma \gamma$ collisions at linear colliders, which are extremely suppressed in the Standard Model (SM), could be significantly enhanced in some extensions of the SM. In this article we calculate the full contribution of the topcolor-assisted technicolor (TC2) to these productions and then compare the results with the existing predictions of the SM, the general two-Higgs-doublet model and the Minimal Supersymmetric Model. We find that the TC2 model predicts much larger production rates than other models and the largest-rate channel is $\gamma \gamma \to t \bar{c}$, which exceeds 10 fb for a large part of the parameter space. From the analysis of the observability of such productions at the future linear colliders, we find that the predictions of the TC2 model can reach the observable level for a large part of the parameter space while the predictions of other models are hardly accessible.Comment: discussions added (version in Eur. Phys. J. C

Cosmology with Hypervelocity Stars

In the standard cosmological model, the merger remnant of the Milky Way and Andromeda (Milkomeda) will be the only galaxy remaining within our event horizon once the Universe has aged by another factor of ten, ~10^{11} years after the Big Bang. After that time, the only extragalactic sources of light in the observable cosmic volume will be hypervelocity stars being ejected continuously from Milkomeda. Spectroscopic detection of the velocity-distance relation or the evolution in the Doppler shifts of these stars will allow a precise measurement of the vacuum mass density as well as the local matter distribution. Already in the near future, the next generation of large telescopes will allow photometric detection of individual stars out to the edge of the Local Group, and may target the ~10^{5+-1} hypervelocity stars that originated in it as cosmological tracers.Comment: 4 pages, 2 figures, accepted for publication in the Journal of Cosmology and Astroparticle Physics (JCAP, 2011

Gains Across WHO Dimensions of Function After Robot-Based Therapy in Stroke Subjects

Background Studies examining the effects of therapeutic interventions after stroke often focus on changes in loss of body function/structure (impairment). However, improvements in activities limitations and participation restriction are often higher patient priorities, and the relationship that these measures have with loss of body function/structure is unclear. Objective This study measured gains across WHO International Classification of Function (ICF) dimensions and examined their interrelationships. Methods Subjects were recruited 11 to 26 weeks after hemiparetic stroke. Over a 3-week period, subjects received 12 sessions of intensive robot-based therapy targeting the distal arm. Each subject was assessed at baseline and at 1 month after end of therapy. Results At baseline, subjects (n = 40) were 134.7 ± 32.4 (mean ± SD) days poststroke and had moderate-severe arm motor deficits (arm motor Fugl-Meyer score of 35.6 ± 14.4) that were stable. Subjects averaged 2579 thumb movements and 1298 wrist movements per treatment session. After robot therapy, there was significant improvement in measures of body function/structure (Fugl-Meyer score) and activity limitations (Action Research Arm Test, Barthel Index, and Stroke Impact Scale–Hand), but not participation restriction (Stroke Specific Quality of Life Scale). Furthermore, while the degree of improvement in loss of body function/structure was correlated with improvement in activity limitations, neither improvement in loss of body function/structure nor improvement in activity limitations was correlated with change in participation restriction. Conclusions After a 3-week course of robotic therapy, there was improvement in body function/structure and activity limitations but no reduction in participation restriction

Gains Across WHO Dimensions of Function After Robot-Based Therapy in Stroke Subjects

Background Studies examining the effects of therapeutic interventions after stroke often focus on changes in loss of body function/structure (impairment). However, improvements in activities limitations and participation restriction are often higher patient priorities, and the relationship that these measures have with loss of body function/structure is unclear. Objective This study measured gains across WHO International Classification of Function (ICF) dimensions and examined their interrelationships. Methods Subjects were recruited 11 to 26 weeks after hemiparetic stroke. Over a 3-week period, subjects received 12 sessions of intensive robot-based therapy targeting the distal arm. Each subject was assessed at baseline and at 1 month after end of therapy. Results At baseline, subjects (n = 40) were 134.7 ± 32.4 (mean ± SD) days poststroke and had moderate-severe arm motor deficits (arm motor Fugl-Meyer score of 35.6 ± 14.4) that were stable. Subjects averaged 2579 thumb movements and 1298 wrist movements per treatment session. After robot therapy, there was significant improvement in measures of body function/structure (Fugl-Meyer score) and activity limitations (Action Research Arm Test, Barthel Index, and Stroke Impact Scale–Hand), but not participation restriction (Stroke Specific Quality of Life Scale). Furthermore, while the degree of improvement in loss of body function/structure was correlated with improvement in activity limitations, neither improvement in loss of body function/structure nor improvement in activity limitations was correlated with change in participation restriction. Conclusions After a 3-week course of robotic therapy, there was improvement in body function/structure and activity limitations but no reduction in participation restriction

Mitochondrial dysfunction and biogenesis: do ICU patients die from mitochondrial failure?

Mitochondrial functions include production of energy, activation of programmed cell death, and a number of cell specific tasks, e.g., cell signaling, control of Ca2+ metabolism, and synthesis of a number of important biomolecules. As proper mitochondrial function is critical for normal performance and survival of cells, mitochondrial dysfunction often leads to pathological conditions resulting in various human diseases. Recently mitochondrial dysfunction has been linked to multiple organ failure (MOF) often leading to the death of critical care patients. However, there are two main reasons why this insight did not generate an adequate resonance in clinical settings. First, most data regarding mitochondrial dysfunction in organs susceptible to failure in critical care diseases (liver, kidney, heart, lung, intestine, brain) were collected using animal models. Second, there is no clear therapeutic strategy how acquired mitochondrial dysfunction can be improved. Only the benefit of such therapies will confirm the critical role of mitochondrial dysfunction in clinical settings. Here we summarized data on mitochondrial dysfunction obtained in diverse experimental systems, which are related to conditions seen in intensive care unit (ICU) patients. Particular attention is given to mechanisms that cause cell death and organ dysfunction and to prospective therapeutic strategies, directed to recover mitochondrial function. Collectively the data discussed in this review suggest that appropriate diagnosis and specific treatment of mitochondrial dysfunction in ICU patients may significantly improve the clinical outcome