Collective spin systems in dispersive optical cavity QED: Quantum phase transitions and entanglement

We propose a cavity QED setup which implements a dissipative Lipkin-Meshkov-Glick model -- an interacting collective spin system. By varying the external model parameters the system can be made to undergo both first-and second-order quantum phase transitions, which are signified by dramatic changes in cavity output field properties, such as the probe laser transmission spectrum. The steady-state entanglement between pairs of atoms is shown to peak at the critical points and can be experimentally determined by suitable measurements on the cavity output field. The entanglement dynamics also exhibits pronounced variations in the vicinities of the phase transitions.Comment: 19 pages, 18 figures, shortened versio

ROSAT X-ray sources in the field of the LMC. II.Statistics of background AGN and X-ray binaries

About 200 X-ray sources from a sample of spectrally hard ROSAT PSPC sources, given in the catalog of Haberl & Pietsch (1999), and observed in a ~60 square degree field of the LMC during several archival pointed observations with a wide range of exposure times have been reanalyzed. For these sources accurate count rates and hardness ratios have been recalculated. In comparison to Haberl & Pietsch (1999) we used merged data from all available observations and we derived average source parameters by investigating each source individually. From a simulation powerlaw spectral tracks have been derived in the HR1 - HR2 plane and ~170 sources have been classified as background X-ray sources or as LMC X-ray binaries. 80% of the spectrally hard X-ray sources with more than 50 observed counts have been found to be consistent with background X-ray sources and 20% with LMC X-ray binaries (53 sources with AGN and 15 with X-ray binaries). The discovery of a new supersoft source RX J0529.4-6713 at the southern HI boundary of the supergiant shell LMC4 is reported. We find two new candidate X-ray binary systems which are associated with the optical bar of the LMC and additional candidate X-ray binaries which are associated with supergiant shells.Comment: 13 pages, accepted for publication in A&A, March 22 200

Antigenic diversity is generated by distinct evolutionary mechanisms in African trypanosome species

Antigenic variation enables pathogens to avoid the host immune response by continual switching of surface proteins. The protozoan blood parasite Trypanosoma brucei causes human African trypanosomiasis ("sleeping sickness") across sub-Saharan Africa and is a model system for antigenic variation, surviving by periodically replacing a monolayer of variant surface glycoproteins (VSG) that covers its cell surface. We compared the genome of Trypanosoma brucei with two closely related parasites Trypanosoma congolense and Trypanosoma vivax, to reveal how the variant antigen repertoire has evolved and how it might affect contemporary antigenic diversity. We reconstruct VSG diversification showing that Trypanosoma congolense uses variant antigens derived from multiple ancestral VSG lineages, whereas in Trypanosoma brucei VSG have recent origins, and ancestral gene lineages have been repeatedly co-opted to novel functions. These historical differences are reflected in fundamental differences between species in the scale and mechanism of recombination. Using phylogenetic incompatibility as a metric for genetic exchange, we show that the frequency of recombination is comparable between Trypanosoma congolense and Trypanosoma brucei but is much lower in Trypanosoma vivax. Furthermore, in showing that the C-terminal domain of Trypanosoma brucei VSG plays a crucial role in facilitating exchange, we reveal substantial species differences in the mechanism of VSG diversification. Our results demonstrate how past VSG evolution indirectly determines the ability of contemporary parasites to generate novel variant antigens through recombination and suggest that the current model for antigenic variation in Trypanosoma brucei is only one means by which these parasites maintain chronic infections

A major genetic locus in <i>Trypanosoma brucei</i> is a determinant of host pathology

The progression and variation of pathology during infections can be due to components from both host or pathogen, and/or the interaction between them. The influence of host genetic variation on disease pathology during infections with trypanosomes has been well studied in recent years, but the role of parasite genetic variation has not been extensively studied. We have shown that there is parasite strain-specific variation in the level of splenomegaly and hepatomegaly in infected mice and used a forward genetic approach to identify the parasite loci that determine this variation. This approach allowed us to dissect and identify the parasite loci that determine the complex phenotypes induced by infection. Using the available trypanosome genetic map, a major quantitative trait locus (QTL) was identified on T. brucei chromosome 3 (LOD = 7.2) that accounted for approximately two thirds of the variance observed in each of two correlated phenotypes, splenomegaly and hepatomegaly, in the infected mice (named &lt;i&gt;TbOrg1&lt;/i&gt;). In addition, a second locus was identified that contributed to splenomegaly, hepatomegaly and reticulocytosis (&lt;i&gt;TbOrg2&lt;/i&gt;). This is the first use of quantitative trait locus mapping in a diploid protozoan and shows that there are trypanosome genes that directly contribute to the progression of pathology during infections and, therefore, that parasite genetic variation can be a critical factor in disease outcome. The identification of parasite loci is a first step towards identifying the genes that are responsible for these important traits and shows the power of genetic analysis as a tool for dissecting complex quantitative phenotypic traits

Characterization of renal cell carcinoma-associated constitutional chromosome abnormalities by genome sequencing.

Constitutional translocations, typically involving chromosome 3, have been recognized as a rare cause of inherited predisposition to renal cell carcinoma (RCC) for four decades. However, knowledge of the molecular basis of this association is limited. We have characterized the breakpoints by genome sequencing (GS) of constitutional chromosome abnormalities in five individuals who presented with RCC. In one individual with constitutional t(10;17)(q11.21;p11.2), the translocation breakpoint disrupted two genes: the known renal tumor suppressor gene (TSG) FLCN (and clinical features of Birt-Hogg-Dubé syndrome were detected) and RASGEF1A. In four cases, the rearrangement breakpoints did not disrupt known inherited RCC genes. In the second case without chromosome 3 involvement, the translocation breakpoint in an individual with a constitutional t(2;17)(q21.1;q11.2) mapped 12 Kb upstream of NLK. Interestingly, NLK has been reported to interact indirectly with FBXW7 and a previously reported RCC-associated translocation breakpoint disrupted FBXW7. In two cases of constitutional chromosome 3 translocations, no candidate TSGs were identified in the vicinity of the breakpoints. However, in an individual with a constitutional chromosome 3 inversion, the 3p breakpoint disrupted the FHIT TSG (which has been reported previously to be disrupted in two apparently unrelated families with an RCC-associated t(3;8)(p14.2;q24.1). These findings (a) expand the range of constitutional chromosome rearrangements that may be associated with predisposition to RCC, (b) confirm that chromosome rearrangements not involving chromosome 3 can predispose to RCC, (c) suggest that a variety of molecular mechanisms are involved the pathogenesis of translocation-associated RCC, and (d) demonstrate the utility of GS for investigating such cases

Smoothed Particle Hydrodynamics and Magnetohydrodynamics

This paper presents an overview and introduction to Smoothed Particle Hydrodynamics and Magnetohydrodynamics in theory and in practice. Firstly, we give a basic grounding in the fundamentals of SPH, showing how the equations of motion and energy can be self-consistently derived from the density estimate. We then show how to interpret these equations using the basic SPH interpolation formulae and highlight the subtle difference in approach between SPH and other particle methods. In doing so, we also critique several `urban myths' regarding SPH, in particular the idea that one can simply increase the `neighbour number' more slowly than the total number of particles in order to obtain convergence. We also discuss the origin of numerical instabilities such as the pairing and tensile instabilities. Finally, we give practical advice on how to resolve three of the main issues with SPMHD: removing the tensile instability, formulating dissipative terms for MHD shocks and enforcing the divergence constraint on the particles, and we give the current status of developments in this area. Accompanying the paper is the first public release of the NDSPMHD SPH code, a 1, 2 and 3 dimensional code designed as a testbed for SPH/SPMHD algorithms that can be used to test many of the ideas and used to run all of the numerical examples contained in the paper.Comment: 44 pages, 14 figures, accepted to special edition of J. Comp. Phys. on "Computational Plasma Physics". The ndspmhd code is available for download from http://users.monash.edu.au/~dprice/ndspmhd

Generating coherence and entanglement with a finite-size atomic ensemble in a ring cavity

We propose a model to study the coherence and entanglement resulting from the interaction of a finite-size atomic ensemble with degenerate counter-propagating field modes of a high-Q ring cavity. Our approach applies to an arbitrary number of atoms N and includes the spatial variation of the field throughout the ensemble. We report several new interesting aspects of coherence and entangled behavior that emerge when the size of the atomic ensemble is not taken to the thermodynamic limit of N>>1. Under such conditions, it is found that the counter-propagating cavity modes, although in the thermodynamic limit are mutually incoherent and exhibit no one-photon interference, the modes can, however, be made mutually coherent and exhibit interference after interacting with a finite-size atomic ensemble. It is also found that the spatial redistribution of the atoms over a finite size results in nonorthogonality of the collective bosonic modes. This nonorthogonality leads to the super-bunching effect that the correlations of photons of the individual cavity modes and of different modes are stronger than those of a thermal field. However, we find that the correlations are not strong enough to violate the Cauchy-Schwarz inequality and to produce squeezing and entanglement between the modes. Therefore, we investigate the spectral distributions of the logarithmic negativity and the variances of the output fields. These functions determine squeezing and entanglement properties of the output cavity fields and can be measured by a homodyne technique. We find that the entanglement is redistributed over several components of the spectrum and the finite-size effect is to concentrate the entanglement at the zero-frequency component of the spectrum.Comment: Published versio