Study Of Inertia And Stoichiometric Effect On Surface Diffusion By Monte Carlo Method

In this work, we investigate the inertia and stoichiometric effect on surface diffusion of adsorbates particles. The study is done by means of Monte-Carlo simulation in the framework of the lattice gas model. Only first neighboring repulsive pair interaction is considered. We concentrate on the behaviour of the tracer diffusion coefficient Dt(θ), as a function of surface coverage θ in the case where two type of particles A and B are adsorbed. A and B are only different by their mass. The results shows that θt ordering phenomenon is not strongly influenced. However the diffusion process is decreased by inclusion of heavy particles.w.In this work, we investigate the inertia and stoichiometric effect on surface diffusion of adsorbates particles. The study is done by means of Monte-Carlo simulation in the framework of the lattice gas model. Only first neighboring repulsive pair interaction is considered. We concentrate on the behaviour of the tracer diffusion coefficient Dt(θ), as a function of surface coverage θ in the case where two type of particles A and B are adsorbed. A and B are only different by their mass. The results shows that θt ordering phenomenon is not strongly influenced. However the diffusion process is decreased by inclusion of heavy particles.w

Phase-field modelling of dendritic growth behaviour towards the cooling / heating of pure nickel

We are interested in modelling the dendritic growth occurring during the solidification process of a pure material and especially to see the effect of the cooling / heating on the growth behaviour of this dendrite. For this purpose we use a phase-field model. The obtained partial differential equations are solved numerically by a finite difference method. In order to appreciate the shape of the resulting dendrites we expose some figures obtained from simulations in 2D.We are interested in modelling the dendritic growth occurring during the solidification process of a pure material and especially to see the effect of the cooling / heating on the growth behaviour of this dendrite. For this purpose we use a phase-field model. The obtained partial differential equations are solved numerically by a finite difference method. In order to appreciate the shape of the resulting dendrites we expose some figures obtained from simulations in 2D

Dynamics of diffusive rough interfaces in inhomogeneous systems

We investigate the dynamics of interfaces growth in inhomogeneous systems. The description of the kinetics is based on the mean field master equation in terms of lattice gas model. The existence of repulsive interactions between nearest-neighbour particles creates an order in the system. We show that the order extension has an influence on the localisation of the diffusive interface called "the diffusion front" which delimits disordered region from ordered one. We analyze the time evolution of diffusion fronts by dynamic scaling approach and we find that the scaling behavior of these interfaces is characterized by anomalously large exponents which agree with the experimental and theoretical results.We investigate the dynamics of interfaces growth in inhomogeneous systems. The description of the kinetics is based on the mean field master equation in terms of lattice gas model. The existence of repulsive interactions between nearest-neighbour particles creates an order in the system. We show that the order extension has an influence on the localisation of the diffusive interface called "the diffusion front" which delimits disordered region from ordered one. We analyze the time evolution of diffusion fronts by dynamic scaling approach and we find that the scaling behavior of these interfaces is characterized by anomalously large exponents which agree with the experimental and theoretical results

Mammalian sphingosine kinase (SphK) isoenzymes and isoform expression: Challenges for SphK as an oncotarget

Copyright: © Hatoum et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC-BY), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. The various sphingosine kinase (SphK) isoenzymes (isozymes) and isoforms, key players in normal cellular physiology, are strongly implicated in cancer and other diseases. Mutations in SphKs, that may justify abnormal physiological function, have not been recorded. Nonetheless, there is a large and growing body of evidence demonstrating the contribution of gain or loss of function and the imbalance in the SphK/S1P rheostat to a plethora of pathological conditions including cancer, diabetes and inflammatory diseases. SphK is expressed as two isozymes SphK1 and SphK2, transcribed from genes located on different chromosomes and both isozymes catalyze the phosphorylation of sphingosine to S1P. Expression of each SphK isozyme produces alternately spliced isoforms. In recent years the importance of the contribution of SpK1 expression to treatment resistance in cancer has been highlighted and, additionally, differences in treatment outcome appear to also be dependent upon SphK isoform expression. This review focuses on an exciting emerging area of research involving SphKs functions, expression and subcellular localization, highlighting the complexity of targeting SphK in cancer and also comorbid diseases. This review also covers the SphK isoenzymes and isoforms from a historical perspective, from their first discovery in murine species and then in humans, their role(s) in normal cellular function and in disease processes, to advancement of SphK as an oncotarget

“Dicing and splicing” sphingosine kinase and relevance to cancer

© 2017 by the authors. Licensee MDPI, Basel, Switzerland. Sphingosine kinase (SphK) is a lipid enzyme that maintains cellular lipid homeostasis. Two SphK isozymes, SphK1 and SphK2, are expressed from different chromosomes and several variant isoforms are expressed from each of the isozymes, allowing for the multi-faceted biological diversity of SphK activity. Historically, SphK1 is mainly associated with oncogenicity, however in reality, both SphK1 and SphK2 isozymes possess oncogenic properties and are recognized therapeutic targets. The absence of mutations of SphK in various cancer types has led to the theory that cancer cells develop a dependency on SphK signaling (hyper-SphK signaling) or “non-oncogenic addiction”. Here we discuss additional theories of SphK cellular mislocation and aberrant “dicing and splicing” as contributors to cancer cell biology and as key determinants of the success or failure of SphK/S1P (sphingosine 1 phosphate) based therapeutics

Study of adatoms diffusion through current density fluctuation functions

In this work, we investigate the diffusion process by using a mean field lattice gas dynamical model. The temporal correlation function of the current density is calculated in a probe area of radius R. The latter is considered to test if the developed formulation can be applied to reproduce STM experiments. The obtained results concerning the effective diffusion coefficient exhibit clearly the order disorder transition effect translated by two minima appearing respectively at p=1/3 and p=2/3. The effect of the ordering phase at p=1/3 requires a threshold size more precisely, the minimum size system where, the ordering phase effect begins, to appear here is R=5.In this work, we investigate the diffusion process by using a mean field lattice gas dynamical model. The temporal correlation function of the current density is calculated in a probe area of radius R. The latter is considered to test if the developed formulation can be applied to reproduce STM experiments. The obtained results concerning the effective diffusion coefficient exhibit clearly the order disorder transition effect translated by two minima appearing respectively at p=1/3 and p=2/3. The effect of the ordering phase at p=1/3 requires a threshold size more precisely, the minimum size system where, the ordering phase effect begins, to appear here is R=5

Mammalian sphingosine kinase (SphK) isoenzymes and isoform expression: challenges for SphK as an oncotarget.

The various sphingosine kinase (SphK) isoenzymes (isozymes) and isoforms, key players in normal cellular physiology, are strongly implicated in cancer and other diseases. Mutations in SphKs, that may justify abnormal physiological function, have not been recorded. Nonetheless, there is a large and growing body of evidence demonstrating the contribution of gain or loss of function and the imbalance in the SphK/S1P rheostat to a plethora of pathological conditions including cancer, diabetes and inflammatory diseases. SphK is expressed as two isozymes SphK1 and SphK2, transcribed from genes located on different chromosomes and both isozymes catalyze the phosphorylation of sphingosine to S1P. Expression of each SphK isozyme produces alternately spliced isoforms. In recent years the importance of the contribution of SpK1 expression to treatment resistance in cancer has been highlighted and, additionally, differences in treatment outcome appear to also be dependent upon SphK isoform expression. This review focuses on an exciting emerging area of research involving SphKs functions, expression and subcellular localization, highlighting the complexity of targeting SphK in cancer and also comorbid diseases. This review also covers the SphK isoenzymes and isoforms from a historical perspective, from their first discovery in murine species and then in humans, their role(s) in normal cellular function and in disease processes, to advancement of SphK as an oncotarget

Dynamic model of fracture

We study the failure properties of heterogeneous materials within the framework of the fiber bundle model subject to the global load-sharing rule in which the load failing elements is shared equally among all surviving elements. We develop a simulation technique by using the Langevin equation in order to investigate some characteristics of our model. It is found that the behavior of time to failure tf decreases with an exponential law and the avalanche size distribution present a power law.We study the failure properties of heterogeneous materials within the framework of the fiber bundle model subject to the global load-sharing rule in which the load failing elements is shared equally among all surviving elements. We develop a simulation technique by using the Langevin equation in order to investigate some characteristics of our model. It is found that the behavior of time to failure tf decreases with an exponential law and the avalanche size distribution present a power law