Excitation of the Slichter mode by collision with a meteoroid or pressure variations at the surface and core boundaries

We use a normal-mode formalism to compute the response of a spherical, self-gravitating anelastic PREM-like Earth model to various excitation sources at the Slichter mode period. The formalism makes use of the theory of the Earth's free oscillations based upon an eigenfunction expansion methodology. We determine the complete response in the form of Green's function obtained from a generalization of Betti's reciprocity theorem. Surficial (surface load, fluid core pressure), internal (earthquakes, explosions) and external (object impact) sources of excitation are investigated to show that the translational motion of the inner-core would be best excited by a pressure acting at the core boundaries at time-scales shorter than the Slichter eigenperiods

Surface atmospheric pressure excitation of the translational mode of the inner core

Using hourly atmospheric surface pressure field from ECMWF (European Centre for Medium-Range Weather Forecasts) and from NCEP (National Centers for Environmental Prediction) Climate Forecast System Reanalysis (CFSR) models, we show that atmospheric pressure fluctuations excite the translational oscillation of the inner core, the so-called Slichter mode, to the sub-nanogal level at the Earth surface. The computation is performed using a normal-mode formalism for a spherical, self-gravitating anelastic PREM-like Earth model. We determine the statistical response in the form of power spectral densities of the degree-one spherical harmonic components of the observed pressure field. Both hypotheses of inverted and non-inverted barometer for the ocean response to pressure forcing are considered. Based on previously computed noise levels, we show that the surface excitation amplitude is below the limit of detection of the superconducting gravimeters, making the Slichter mode detection a challenging instrumental task for the near future

Les facteurs neurotrophiques : un mythe thérapeutique ?

peer reviewe

Electrostatic drift instabilities, turbulence and anomalous transport: introduction and basic theory

Experts consider that the enhanced transport observed in fusion devices is the consequence of low frequency instabilities which are elongated along the magnetic field lines and whose free energy sources are the gradients inherent to confinement. The cases k(parallel to)qR >> 1 and k(parallel to)qR similar to 1 will be considered, where k(parallel to) is the parallel wave number and qR the connection length. The first limit is relevant to plasmas with large parallel flow velocity gradients (\partial derivative U-r(phi,i) \similar to c(i)\partial derivative(r) ln N-i\, where (U) over bar (i) and c(i) are the ion bulk and thermal velocities; N-i is the density); here, a local dispersion relation leads to exact stability criteria with the help of the Nyquist diagram technique. The ordering k(parallel to)qR similar to 1 applies otherwise; it requires a non-local analysis leading to a second order differential equation whose complex eigenvalues provide the wave frequencies and growth / decay rates; two sub-cases must be considered according to whether the eigenfunctions are radially or poloidally localised. After reviewing some of the most important micro-instabilities, the non-linear saturation mechanism and ultimate turbulence level will be discussed, as well as the various aspects of anomalous transport theories

Parameter mismatches,variable delay times and synchronization in time-delayed systems

We investigate synchronization between two unidirectionally linearly coupled chaotic non-identical time-delayed systems and show that parameter mismatches are of crucial importance to achieve synchronization. We establish that independent of the relation between the delay time in the coupled systems and the coupling delay time, only retarded synchronization with the coupling delay time is obtained. We show that with parameter mismatch or without it neither complete nor anticipating synchronization occurs. We derive existence and stability conditions for the retarded synchronization manifold. We demonstrate our approach using examples of the Ikeda and Mackey-Glass models. Also for the first time we investigate chaos synchronization in time-delayed systems with variable delay time and find both existence and sufficient stability conditions for the retarded synchronization manifold with the coupling delay lag time. Also for the first time we consider synchronization between two unidirectionally coupled chaotic multi-feedback Ikeda systems and derive existence and stability conditions for the different anticipating, lag, and complete synchronization regimes.Comment: 12 page

Quels espoirs de remyélinisation dans la sclérose en plaques ?

Peer reviewe

Dynamics of broadband dispersive Alfven waves

The properties of amplitude modulated broadband Alfven waves is investigated. In particular, the dynamics of circularly polarized dispersive Alfven waves, governed by a derivative nonlinear Schroedinger equation, is analyzed using the Wigner formalism. The modulational instability of random phase dispersive pump Alfven waves is investigated, and it is shown that the spectral broadening gives rise to a new mode structure.Comment: 9 pages, 2 figures, to appear in Phys. Lett.

Neuregulin-1 modulates the differentiation of neural stem cells in vitro trough an interaction with the Swi/Snf complex.

The neuregulin-1 (Nrg-1) gene is translated into several protein isoforms, which are either secreted or membrane-anchored. In vitro, neural stem cells (NSC) express mainly the cystein-rich-domain NRG (CRD-NRG) isoform, a membrane-anchored type III form. This isoform exhibits a cystein-rich-domain, which constitutes a second transmembrane domain and can be cleaved to release both a signaling EGF-containing domain (ECD) at the cell surface and an intracellular domain (ICD). The main goal of this paper was to determine the exact role of ECD and ICD in NSC survival and differentiation. Using an siRNA approach, we demonstrated that CRD-NRG inhibition was followed by a decrease in NSC proliferation and of neuronal or oligodendroglial differentiation. Overexpression of ICD but not ECD was followed by a decrease in NSC proliferation and an increase in neuronal and oligodendroglial differentiation. Moreover, we showed that ICD physically interacted in cultured NSC with BRM and BAF57, two members of the Swi/Snf remodeling complex, and that ICD stimulation of neuronal cell differentiation is dependent on the presence of BAF57

From Neural Crest Development to Cancer and Vice Versa: How p75NTR and (Pro)neurotrophins Could Act on Cell Migration and Invasion?

The p75 neurotrophin receptor (p75NTR), also known as low-affinity nerve growth factor, belongs to the tumor necrosis factor family of receptors. p75NTR is widely expressed in the nervous system during the development, as well as, in the neural crest population, since p75NTR has been described as ubiquitously expressed and considered as a neural crest marker. Neural crest cells (NCCs) constitute an transient population accurately migrating and invading, with precision, defined sites of the embryo. During migration, NCCs are guided along distinct migratory pathways by specialized molecules present in the extracellular matrix or on the surfaces of those cells. Two main processes direct NCC migration during the development: (1) an epithelial-to-mesenchymal transition and (2) a process known as contact inhibition of locomotion. In adults, p75NTR remains expressed by NCCs and has been identified in an increasing number of cancer cells. Nonetheless, the regulation of the expression of p75NTR and the underlying mechanisms in stem cell biology or cancer cells have not yet been sufficiently addressed. The main objective of this review is therefore to analyze elements of our actual knowledge regarding p75NTR roles during the development (mainly focusing on neural crest development) and see how we can transpose that information from development to cancer (and vice versa) to better understand the link between p75NTR and cell migration and invasion. In this review, we successively analyzed the molecular mechanisms of p75NTR when it interacts with several coreceptors and/or effectors. We then analyzed which signaling pathways are the most activated or linked to NCC migration during the development. Regarding cancer, we analyzed the described molecular pathways underlying cancer cell migration when p75NTR was correlated to cancer cell migration and invasion. From those diverse sources of information, we finally summarized potential molecular mechanisms underlying p75NTR activation in cell migration and invasion that could lead to new research areas to develop new therapeutic protocols