Extended free-form deformation : a sculpturing tool for 3D geometric modeling

Projet SYNTIMCurrent research efforts focus on providing more efficient and effective design methods for 3D modeling systems. In this paper a new deformation technique is presented. Among other things, arbitrarily shaped bump can be designed and surfaces can be bent along arbitrarily shaped curves. The purpose of this research is to define a highly interactive and intuitive modeling technique for designers and stylists. A natural way of thinking is to mimic traditional trades, such as sculpturing and moulding. Furthermore, with this deformation technique, the modeling tool paradigm is introduced. The object is deformed with a user-defined deformation tool. This method is an extension of the Free-Form Deformation (FFD) technique proposed by Sederberg and Parry

Multimessenger astronomy with the Einstein Telescope

Gravitational waves (GWs) are expected to play a crucial role in the development of multimessenger astrophysics. The combination of GW observations with other astrophysical triggers, such as from gamma-ray and X-ray satellites, optical/radio telescopes, and neutrino detectors allows us to decipher science that would otherwise be inaccessible. In this paper, we provide a broad review from the multimessenger perspective of the science reach offered by the third generation interferometric GW detectors and by the Einstein Telescope (ET) in particular. We focus on cosmic transients, and base our estimates on the results obtained by ET's predecessors GEO, LIGO, and Virgo.Comment: 26 pages. 3 figures. Special issue of GRG on the Einstein Telescope. Minor corrections include

Modelling harmonic generation measurements in solids

Harmonic generation measurements typically make use of the plane wave result when extracting values for the nonlinearity parameter, beta, from experimental measurements. This approach, however, ignores the effects of diffraction, attenuation, and receiver integration which are common features in a typical experiment. Our aim is to determine the importance of these effects when making measurements of beta over different sample dimensions, or using different input frequencies. We describe a three-dimensional numerical model designed to accurately predict the results of a typical experiment, based on a quasi-linear assumption. An experiment is designed to measure the axial variation of the fundamental and second harmonic amplitude components in an ultrasonic beam, and the results are compared with those predicted by the model. The absolute b values are then extracted from the experimental data using both the simulation and the standard plane wave result. A difference is observed between the values returned by the two methods, which varies with axial range and input frequency. (C) 2013 Elsevier B. V. All rights reserved.</p

MeCP2 and Rett syndrome: reversibility and potential avenues for therapy

Mutations in the X-linked gene MECP2 (methyl CpG-binding protein 2) are the primary cause of the neurodevelopmental disorder RTT (Rett syndrome), and are also implicated in other neurological conditions. The expression product of this gene, MeCP2, is a widely expressed nuclear protein, especially abundant in mature neurons of the CNS (central nervous system). The major recognized consequences of MECP2 mutation occur in the CNS, but there is growing awareness of peripheral effects contributing to the full RTT phenotype. MeCP2 is classically considered to act as a DNA methylation-dependent transcriptional repressor, but may have additional roles in regulating gene expression and chromatin structure. Knocking out Mecp2 function in mice recapitulates many of the overt neurological features seen in RTT patients, and the characteristic postnatally delayed onset of symptoms is accompanied by aberrant neuronal morphology and deficits in synaptic physiology. Evidence that reactivation of endogenous Mecp2 in mutant mice, even at adult stages, can reverse aspects of RTT-like pathology and result in apparently functionally mature neurons has provided renewed hope for patients, but has also provoked discussion about traditional boundaries between neurodevelopmental disorders and those involving dysfunction at later stages. In the present paper we review the neurobiology of MeCP2 and consider the various genetic (including gene therapy), pharmacological and environmental interventions that have been, and could be, developed to attempt phenotypic rescue in RTT. Such approaches are already providing valuable insights into the potential tractability of RTT and related conditions, and are useful pointers for the development of future therapeutic strategies

How Bursts Shape the STDP Curve in the Presence/Absence of GABAergic Inhibition

It has been known for some time that the synapses of the CA1 pyramidal cells are surprisingly unreliable at signalling the arrival of single spikes to the postsynaptic neuron [2]. On the other hand, bursts of spikes are reliably signalled, because transmitter release is facilitated. In the hippocampus, a single burst can produce long-term synaptic modifications. Bursts of spikes in addition to increasing reliability of synaptic transmission [3], they have been shown to provide effective mechanisms for selective communication between neurons in a network [4]. We investigate via computer simulations how the profile of spike-timing-dependent plasticity (STDP) in the CA1 pyramidal cell synapses is affected when an excitatory burst of spikes applied to dendrites is paired with an excitatory single spike applied to the soma in the absence and presence of a 100Hz GABAergic inhibitory spike train applied to the dendrites. We report that the shape of the STDP curve strongly depends on the burst interspike interval in the presence/absence of GABA A when a presynaptic burst and a postsynaptic spike are paired togethe

Synaptic plasticity deficits in an experimental model of Rett Syndrome: LTP saturation and its pharmacological reversal

Rett syndrome (RTT), a disorder caused almost exclusively by mutations in the X-linked gene, MECP2, has a phenotype thought to be primarily of neurological origin. Disruption of Mecp2 in mice results in a prominent RTT-like phenotype. One of the consequences of MeCP2 absence in the brain is altered functional and structural plasticity. We aimed to characterize synaptic effects related to plasticity in the hippocampus further and establish whether plasticity defects are amenable to pharmacological reversal. Using male mice in which Mecp2 expression was prevented by a stop cassette, we assessed synaptic plasticity in area CA1 at different phenotypic stages, scoring the mice weekly for overt RTT-like signs. Strongly symptomatic Mecp2(stoply) mice displayed reduced long-term potentiation (LIP, 40.2 +/- 1.6% of wild-type), post-tetanic potentiation (PIP, 45 +/- 18.8% of wildtype) and paired-pulse facilitation (PPF, 78 +/- 0.1% of wild type) (all P &lt; 0.05), the impairment increasing with symptom severity score. These plasticity impairments were absent in presymptomatic mice. Repeated high frequency stimulation revealed pronounced LTP saturation in symptomatic Mecp2(stoply) mice, suggesting an LIP 'ceiling' effect. Bath application of the weak NMDA receptor blocker memantine (1 mu M) resulted in partial restoration of a short-term plasticity component. These data support that idea that progressive functional synaptic impairment is a key feature in the RTT brain and demonstrate the potential for the pharmacological restoration of plasticity function

Synaptic plasticity deficits in an experimental model of rett syndrome: long-term potentiation saturation and its pharmacological reversal

[[abstract]]Rett syndrome (RTT), a disorder caused almost exclusively by mutations in the X-linked gene, MECP2, has a phenotype thought to be primarily of neurological origin. Disruption of Mecp2 in mice results in a prominent RTT-like phenotype. One of the consequences of MeCP2 absence in the brain is altered functional and structural plasticity. We aimed to characterize synaptic effects related to plasticity in the hippocampus further and establish whether plasticity defects are amenable to pharmacological reversal. Using male mice in which Mecp2 expression was prevented by a stop cassette, we assessed synaptic plasticity in area CA1 at different phenotypic stages, scoring the mice weekly for overt RTT-like signs. Strongly symptomatic Mecp2stop/y mice displayed reduced long-term potentiation (LTP, 40.2±1.6% of wild-type), post-tetanic potentiation (PTP, 45±18.8% of wild-type) and paired-pulse facilitation (PPF, 78±0.1% of wild type) (all P<0.05), the impairment increasing with symptom severity score. These plasticity impairments were absent in presymptomatic mice. Repeated high frequency stimulation revealed pronounced LTP saturation in symptomatic Mecp2stop/y mice, suggesting an LTP ‘ceiling’ effect. Bath application of the weak NMDA receptor blocker memantine (1 μM) resulted in partial restoration of a short-term plasticity component. These data support that idea that progressive functional synaptic impairment is a key feature in the RTT brain and demonstrate the potential for the pharmacological restoration of plasticity function