Theory of rigid-plane phonon modes in layered crystals

The lattice dynamics of low-frequency rigid-plane modes in metallic (graphene multilayers, GML) and in insulating (hexagonal boron-nitride multilayers, BNML) layered crystals is investigated. The frequencies of shearing and compression (stretching) modes depend on the layer number {\EuScript N} and are presented in the form of fan diagrams. The results for GML and BNML are very similar. In both cases only the interactions (van der Waals and Coulomb) between nearest-neighbor planes are effective, while the interactions between more distant planes are screened. A comparison with recent Raman scattering results on low-frequency shear modes in GML [Tan {\it et al.}, arXiv:1106.1146v1 (2011)] is made. Relations with the low-lying rigid-plane phonon dispersions in the bulk materials are established. Master curves which connect the fan diagram frequencies for any given {\EuScript N} are derived. Static and dynamic thermal correlation functions for rigid-layer shear and compression modes are calculated. The results might be of use for the interpretation of friction force experiments on multilayer crystals

Modifications of Gait as Predictors of Natural Osteoarthritis Progression in STR/Ort Mice

OBJECTIVE: Osteoarthritis (OA) is a common chronic disease for which disease-modifying therapies are not currently available. Studies to seek new targets for slowing the progress of OA rely on mouse models, but these do not allow for longitudinal monitoring of disease development. This study was undertaken to determine whether gait can be used to measure disease severity in the STR/Ort mouse model of spontaneous OA and whether gait changes are related to OA joint pain. METHODS: Gait was monitored using a treadmill-based video system. Correlations between OA severity and gait at 3 treadmill speeds were assessed in STR/Ort mice. Gait and pain behaviors of STR/Ort mice and control CBA mice were analyzed longitudinally, with monthly assessments. RESULTS: The best speed to identify paw area changes associated with OA severity in STR/Ort mice was found to be 17 cm · seconds(−1). Paw area was modified with age in CBA and STR/Ort mice, but this began earlier in STR/Ort mice and correlated with the onset of OA at 20 weeks of age. In addition, task noncompliance appeared at 20 weeks. Surprisingly, STR/Ort mice did not show any signs of pain with OA development, even when treated with the opioid antagonist naloxone, but did exhibit normal pain behaviors in response to complete Freund's adjuvant–induced arthritis. CONCLUSION: The present results identify an animal model in which OA severity and OA pain can be studied in isolation from one another. The findings suggest that paw area and treadmill noncompliance may be useful tools to longitudinally monitor nonpainful OA development in STR/Ort mice. This will help in providing a noninvasive means of assessing new therapies to slow the progression of OA

STATIONS D’EPURATION A LITS FILTRANTS PLANTES DE MACROPHYTES WASTE WATER TREATMENT PLANTS WITH MACROPHYTES

L’utilisation de marais pour l’amélioration de la qualité de l’eau est une technique très ancienne. Depuis que l’homme rejettedes effluents pollués dans le milieu naturel, les marais ont été impliqués – volontairement ou non – dans l’épuration de ceux-ci.De nombreuses recherches sont actuellement menées afin de mieux comprendre les phénomènes intervenant dans le sol pourl’épuration, l’influence des conditions climatiques, les tailles et formes des lits, la charge hydraulique et le type de plantesutilisées. Le présent travail se veut une contribution à la mise en valeur des techniques d’épuration des eaux usées domestiquespar lits plantés de macrophytes

Nanoscale regulation of L-type calcium channels differentiates between ischemic and dilated cardiomyopathies.

Background Subcellular localization and function of L-type calcium channels (LTCCs) play an important role in regulating contraction of cardiomyocytes. Understanding how this is affected by the disruption of transverse tubules during heart failure could lead to new insights into the disease. Methods Cardiomyocytes were isolated from healthy donor hearts, as well as from patients with cardiomyopathies and with left ventricular assist devices. Scanning ion conductance and confocal microscopy was used to study membrane structures in the cells. Super-resolution scanning patch-clamp was used to examine LTCC function in different microdomains. Computational modeling predicted the impact of these changes to arrhythmogenesis at the whole-heart level. Findings We showed that loss of structural organization in failing myocytes leads to re-distribution of functional LTCCs from the T-tubules to the sarcolemma. In ischemic cardiomyopathy, the increased LTCC open probability in the T-tubules depends on the phosphorylation by protein kinase A, whereas in dilated cardiomyopathy, the increased LTCC opening probability in the sarcolemma results from enhanced phosphorylation by calcium-calmodulin kinase II. LVAD implantation corrected LTCCs pathophysiological activity, although it did not improve their distribution. Using computational modeling in a 3D anatomically-realistic human ventricular model, we showed how LTCC location and activity can trigger heart rhythm disorders of different severity. Interpretation Our findings demonstrate that LTCC redistribution and function differentiate between disease aetiologies. The subcellular changes observed in specific microdomains could be the consequence of the action of distinct protein kinases. Funding This work was supported by NIH grant (ROI-HL 126802 to NT-JG) and British Heart Foundation (grant RG/17/13/33173 to JG, project grant PG/16/17/32069 to RAC). Funders had no role in study design, data collection, data analysis, interpretation, writing of the repor

Study of the ηπo\eta\pi^o system in the mass range up to 1200 MeV

The reaction $\pi^-p \to \eta\pi^o n$ has been studied with GAMS-2000 spectrometer in the secondary 38 GeV/c $\pi^-$-beam of the IHEP U-70 accelerator. Partial wave analysis of the reaction has been performed in the $\eta\pi^o$ mass range up to 1200 MeV. The $a_0(980)$-meson is seen as a sharp peak in S-wave. The $t$-dependence of $a_0(980)$ production cross section has been studied. Dominant production of the $a_0(980)$ at a small transfer momentum $t$ confirms the hypothesis of Achasov and Shestakov about significant contribution of the $\rho_2$ exchange ($I^GJ^{PC}=1^+2^{--}$) in the mechanism of $a_0(980)$ meson production in $t$-channel of the reaction.Comment: 4 pages, 3 figures, talk given at HADRON'9

Detection of arcs in Saturn's F ring during the 1995 Sun ring-plane crossing

Observations of the November 1995 Sun crossing of the Saturn's ring-plane made with the 3.6m CFH telescope, using the UHAO adaptive optics system, are presented here. We report the detection of four arcs located in the vicinity of the F ring. They can be seen one day later in HST images. The combination of both data sets gives accurate determinations of their orbits. Semi-major axes range from 140020 km to 140080 km, with a mean of 140060 +- 60 km. This is about 150 km smaller than previous estimates of the F ring radius from Voyager 1 and 2 data, but close to the orbit of another arc observed at the same epoch in HST images.Comment: 8 pages, 3 figures, 1 table, To appear in A&A, for comments : [email protected]

The Protective Effect of Ursodeoxycholic Acid in an in vitro model of the Human Fetal Heart occurs via Targeting Cardiac Fibroblasts

Bile acids are elevated in the blood of women with intrahepatic cholestasis of pregnancy (ICP) and this may lead to fetal arrhythmia, fetal hypoxia and potentially fetal death in utero. The bile acid taurocholic acid (TC) causes abnormal calcium dynamics and contraction in neonatal rat cardiomyocytes. Ursodeoxycholic acid (UDCA), a drug clinically used to treat ICP, prevents adverse effects of TC. During development, the fetus is in a state of relative hypoxia. Although this is essential for the development of the heart and vasculature, resident fibroblasts can transiently differentiate into myofibroblasts and form gap junctions with cardiomyocytes in vitro, resulting in cardiomyocyte depolarization. We expanded on previously published work using an in vitro hypoxia model to investigate the differentiation of human fetal fibroblasts into myofibroblasts.Recent evidence shows that potassium channels are involved in maintaining the membrane potential of ventricular fibroblasts and that ATP-dependent potassium (KATP) channel subunits are expressed in cultured fibroblasts. KATP channels are a valuable target as they are thought to have a cardioprotective role during ischaemic and hypoxic conditions. We investigated whether UDCA could modulate fibroblast membrane potential.We established the isolation and culture of human fetal cardiomyocytes and fibroblasts to investigate the effect of hypoxia, TC and UDCA on human fetal cardiac cells.UDCA hyperpolarized myofibroblasts and prevented TC-induced depolarisation, possibly through the activation of KATP channels that are expressed in cultured fibroblasts. Also, similar to the rat model, UDCA can counteract TC-induced calcium abnormalities in human fetal cultures of cardiomyocytes and myofibroblasts. Under normoxic conditions, we found a higher number of myofibroblasts in cultures derived from human fetal hearts compared to cells isolated from neonatal rat hearts, indicating a possible increased number of myofibroblasts in human fetal hearts. Hypoxia further increased the number of human fetal and rat neonatal myofibroblasts. However, chronically administered UDCA reduced the number of myofibroblasts and prevented hypoxia-induced depolarisation.In conclusion, our results show that the protective effect of UDCA involves both the reduction of fibroblast differentiation into myofibroblasts, and hyperpolarisation of myofibroblasts, most likely through the stimulation of potassium channels, i.e. KATP channels. This could be important in validating UDCA as an antifibrotic and antiarrhythmic drug for treatment of failing hearts and fetal arrhythmia

Lagrangian model for deposition from low-concentrated particles-laden turbulent jets

Paper presented at the 9th International Conference on Heat Transfer, Fluid Mechanics and Thermodynamics, Malta, 16-18 July, 2012.This work presents a simple model that accurately predicts the deposition from low-concentrated particle-laden turbulent jets in different scenarios. Our proposed model is a developed Lagrangian model that takes advantage of the preferential concentration phenomenon. The unidirectional coupling (fluid- sediment) is used in the modelling. This choice is adopted because when the concentration of solid particles is small enough, it does not affect the hydrodynamic development of the jet. The deposition criterion states that the particle deposits when its settling velocity is greater than the vertical component of the entrainment velocity. Six experiments chosen from the available literature are used to validate the model. These experiments cover the cases of horizontal and inclined buoyant jets in stationary ambient, horizontal buoyant jets in coflow current and nonbuoyant horizontal jets in stationary ambient. Good agreement between the experiments and the obtained simulations is revealed. A sensitivity analysis study is conducted in order to investigate the role of the model main variables. We found that the most important variables are respectively the settling velocity of solid particles, the jet initial velocity, ambient velocity and the buoyancy forces.dc201

Junctophilin-2 tethers T-tubules and recruits functional L-type calcium channels to lipid rafts in adult cardiomyocytes

Aim: In cardiomyocytes, transverse tubules (T-tubules) associate with the sarcoplasmic reticulum (SR), forming junctional membrane complexes (JMCs) where L-type calcium channels (LTCCs) are juxtaposed to Ryanodine receptors (RyR). Junctophilin-2 (JPH2) supports the assembly of JMCs by tethering T-tubules to the SR membrane. T-tubule remodeling in cardiac diseases is associated with down-regulation of JPH2 expression suggesting that JPH2 plays a crucial role in T-tubule stability. Furthermore, increasing evidence indicate that JPH2 might additionally act as a modulator of calcium signaling by directly regulating RyR and LTCCs. This study aimed at determining whether JPH2 overexpression restores normal T-tubule structure and LTCC function in cultured cardiomyocytes. Methods and results: Rat ventricular myocytes kept in culture for 4 days showed extensive T-tubule remodeling with impaired JPH2 localization and relocation of the scaffolding protein Caveolin3 (Cav3) from the T-tubules to the outer membrane. Overexpression of JPH2 restored T-tubule structure and Cav3 relocation. Depletion of membrane cholesterol by chronic treatment with Methyl-β-cyclodextrin (MβCD) countered the stabilizing effect of JPH2 overexpression on T-tubules and Cav3. Super-resolution scanning patch-clamp showed that JPH2 overexpression greatly increased the number of functional LTCCs at the plasma membrane. Treatment with MβCD reduced LTCC open probability and activity. Proximity ligation assays showed that MβCD did not affect JPH2 interaction with RyR and the pore-forming LTCC subunit Cav1.2, but strongly impaired JPH2 association with Cav3 and the accessory LTCC subunit Cavβ2. Conclusions: JPH2 promotes T-tubule structural stability and recruits functional LTCCs to the membrane, most likely by directly binding to the channel. Cholesterol is involved in the binding of JPH2 to T-tubules as well as in the modulation of LTCC activity. We propose a model where cholesterol and Cav3 support the assembly of lipid rafts which provide an anchor for JPH2 to form JMCs and a platform for signaling complexes to regulate LTCC activity