Tunable Entanglement, Antibunching and Saturation effects in Dipole Blockade

We report a model that makes it possible to analyze quantitatively the dipole blockade effect on the dynamical evolution of a two two-level atom system driven by an external laser field. The multiple excitations of the atomic sample are taken into account. We find very large concurrence in the dipole blockade regime. We further find that entanglement can be tuned by changing the intensity of the exciting laser. We also report a way to lift the dipole blockade paving the way to manipulate in a controllable way the blockade effects. We finally report how a continuous monitoring of the dipole blockade would be possible using photon-photon correlations of the scattered light in a regime where the spontaneous emission would dominate dissipation in the sample.Comment: 5 pages, 5 figure

Stochastic modelling of regional archaeomagnetic series

SUMMARY We report a new method to infer continuous time series of the declination, inclination and intensity of the magnetic field from archeomagnetic data. Adopting a Bayesian perspective, we need to specify a priori knowledge about the time evolution of the magnetic field. It consists in a time correlation function that we choose to be compatible with present knowledge about the geomagnetic time spectra. The results are presented as distributions of possible values for the declination, inclination or intensity. We find that the methodology can be adapted to account for the age uncertainties of archeological artefacts and we use Markov Chain Monte Carlo to explore the possible dates of observations. We apply the method to intensity datasets from Mari, Syria and to intensity and directional datasets from Paris, France. Our reconstructions display more rapid variations than previous studies and we find that the possible values of geomagnetic field elements are not necessarily normally distributed. Another output of the model is better age estimates of archeological artefacts

Fast quasi-adiabatic dynamics

We work out the theory and applications of a fast quasi-adiabatic approach to speed up slow adiabatic manipulations of quantum systems by driving a control parameter as near to the adiabatic limit as possible over the entire protocol duration. Specifically, we show that the population inversion in a two-level system, the splitting and cotunneling of two-interacting bosons, and the stirring of a Tonks-Girardeau gas on a ring to achieve mesoscopic superpositions of many-body rotating and non-rotating states, can be significantly speeded up.Comment: 5 pages, 6 figure

Glycoprotein L sets the neutralization profile of murid herpesvirus 4

Antibodies readily neutralize acute, epidemic viruses, but are less effective against more indolent pathogens such as herpesviruses. Murid herpesvirus 4 (MuHV-4) provides an accessible model for tracking the fate of antibody-exposed gammaherpesvirus virions. Glycoprotein L (gL) plays a central role in MuHV-4 entry: it allows gH to bind heparan sulfate and regulates fusion-associated conformation changes in gH and gB. However, gL is non-essential: heparan sulfate binding can also occur via gp70, and the gB–gH complex alone seems to be sufficient for membrane fusion. Here, we investigated how gL affects the susceptibility of MuHV-4 to neutralization. Immune sera neutralized gL− virions more readily than gL+ virions, chiefly because heparan sulfate binding now depended on gp70 and was therefore easier to block. However, there were also post-binding effects. First, the downstream, gL-independent conformation of gH became a neutralization target; gL normally prevents this by holding gH in an antigenically distinct heterodimer until after endocytosis. Second, gL− virions were more vulnerable to gB-directed neutralization. This covered multiple epitopes and thus seemed to reflect a general opening up of the gH–gB entry complex, which gL again normally restricts to late endosomes. gL therefore limits MuHV-4 neutralization by providing redundancy in cell binding and by keeping key elements of the virion fusion machinery hidden until after endocytosis

In vivo importance of heparan sulfate-binding glycoproteins for murid herpesvirus-4 infection

Many herpesviruses bind to heparan sulfate (HS). Murid herpesvirus-4 (MuHV-4) does so via its envelope glycoproteins gp70 and gH/gL. MuHV-4 gp150 further regulates an HS-independent interaction to make that HS-dependent too. Cell binding by MuHV-4 virions is consequently strongly HS-dependent. Gp70 and gH/gL show some in vitro redundancy: an antibody-mediated blockade of HS binding by one is well tolerated, whereas a blockade of both severely impairs infection. In order to understand the importance of HS binding for MuHV-4 in vivo, we generated mutants lacking both gL and gp70. As expected, gL−gp70− MuHV-4 showed very poor cell binding. It infected mice at high dose but not at low dose, indicating defective host entry. But once entry occurred, host colonization, which for MuHV-4 is relatively independent of the infection dose, was remarkably normal. The gL−gp70− entry deficit was much greater than that of gL− or gp70− single knockouts. And gp150 disruption, which allows HS-independent cell binding, largely rescued the gL−gp70− cell binding and host entry deficits. Thus, it appeared that MuHV-4 HS binding is important in vivo, principally for efficient host entry

Vast planes of satellites in a high resolution simulation of the Local Group: comparison to Andromeda

We search for vast planes of satellites (VPoS) in a high resolution simulation of the Local Group performed by the CLUES project, which improves significantly the resolution of former similar studies. We use a simple method for detecting planar configurations of satellites, and validate it on the known plane of M31. We implement a range of prescriptions for modelling the satellite populations, roughly reproducing the variety of recipes used in the literature, and investigate the occurence and properties of planar structures in these populations. The structure of the simulated satellite systems is strongly non-random and contains planes of satellites, predominantly co-rotating, with, in some cases, sizes comparable to the plane observed in M31 by Ibata et al.. However the latter is slightly richer in satellites, slightly thinner and has stronger co-rotation, which makes it stand out as overall more exceptional than the simulated planes, when compared to a random population. Although the simulated planes we find are generally dominated by one real structure, forming its backbone, they are also partly fortuitous and are thus not kinematically coherent structures as a whole. Provided that the simulated and observed planes of satellites are indeed of the same nature, our results suggest that the VPoS of M31 is not a coherent disc and that one third to one half of its satellites must have large proper motions perpendicular to the plane

Vaccination with murid herpesvirus-4 glycoprotein B reduces viral lytic replication but does not induce detectable virion neutralization

Herpesviruses characteristically disseminate from immune hosts. Therefore in the context of natural infection, antibody neutralizes them poorly. Murid herpesvirus-4 (MuHV-4) provides a tractable model with which to understand gammaherpesvirus neutralization. MuHV-4 virions blocked for cell binding by immune sera remain infectious for IgG-Fc receptor+ myeloid cells, so broadly neutralizing antibodies must target the virion fusion complex – glycoprotein B (gB) or gH/gL. While gB-specific neutralizing antibodies are rare, its domains I+II (gB-N) contain at least one potent neutralization epitope. Here, we tested whether immunization with recombinant gB presenting this epitope could induce neutralizing antibodies in naive mice and protect them against MuHV-4 challenge. Immunizing with the full-length gB extracellular domain induced a strong gB-specific antibody response and reduced MuHV-4 lytic replication but did not induce detectable neutralization. gB-N alone, which more selectively displayed pre-fusion epitopes including neutralization epitopes, also failed to induce neutralizing responses, and while viral lytic replication was again reduced this depended completely on IgG Fc receptors. gB and gB-N also boosted neutralizing responses in only a minority of carrier mice. Therefore, it appears that neutralizing epitopes on gB are intrinsically difficult for the immune response to target

Melting and Pressure-Induced Amorphization of Quartz

It has recently been shown that amorphization and melting of ice were intimately linked. In this letter, we infer from molecular dynamics simulations on the SiO2 system that the extension of the quartz melting line in the metastable pressure-temperature domain is the pressure-induced amorphization line. It seems therefore likely that melting is the physical phenomenon responsible for pressure induced amorphization. Moreover, we show that the structure of a "pressure glass" is similar to that of a very rapidly (1e+13 to 1e+14 kelvins per second) quenched thermal glass.Comment: 9 pages, 4 figures, LaTeX2

Antibody limits in vivo murid herpesvirus-4 replication by IgG Fc receptor-dependent functions

Antibody is an important antiviral defence. However, it is considered to do little against human gamma-herpesviruses, which establish predominantly latent infections regulated by T cells. One limitation on analysing these infections has been that latency is already well-established at clinical presentation; early infection may still be accessible to antibody. Here, using murid herpesvirus-4 (MuHV-4), we tested the impact of adoptively transferred antibody on early gamma-herpesvirus infection. Immune sera and neutralizing and non-neutralizing monoclonal antibodies (mAbs) all reduced acute lytic MuHV-4 replication. The reductions, even by neutralizing mAbs, were largely or completely dependent on host IgG Fc receptors. Therefore, passive antibody can blunt acute gamma-herpesvirus lytic infection, and does this principally by IgG Fc-dependent functions rather than by neutralization