WASP-12b as a prolate, inflated and disrupting planet from tidal dissipation

The class of exotic Jupiter-mass planets that orbit very close to their parent stars were not explicitly expected before their discovery. The recently found transiting planet WASP-12b has a mass Mp = 1.4(+/-0.1) Jupiter masses (MJ), a mean orbital distance of only 3.1 stellar radii (meaning it is subject to intense tidal forces), and a period of 1.1 days. Its radius 1.79(+/- 0.09) RJ is unexpectedly large and its orbital eccentricity 0.049(+/-0:015) is even more surprising as such close orbits are in general quickly circularized. Here we report an analysis of its properties, which reveals that the planet is losing mass to its host star at a rate ~ 10^-7 MJ yr^-1. The planets surface is distorted by the stars gravity and the light curve produced by its prolate shape will differ by about ten per cent from that of a spherical planet. We conclude that dissipation of the stars tidal perturbation in the planets convective envelope provides the energy source for its large volume. We predict up to 10mJy CO band-head (2.292 micron) emission from a tenuous disk around the host star, made up of tidally stripped planetary gas. It may also contain a detectable resonant super-Earth, as a hypothetical perturber that continually stirs up WASP-12b's eccentricity.Comment: Accepted to Nature, 14 pages, 1 figur

Activation of the Listeria monocytogenes Virulence Program by a Reducing Environment.

Upon entry into the host cell cytosol, the facultative intracellular pathogen Listeria monocytogenes coordinates the expression of numerous essential virulence factors by allosteric binding of glutathione (GSH) to the Crp-Fnr family transcriptional regulator PrfA. Here, we report that robust virulence gene expression can be recapitulated by growing bacteria in a synthetic medium containing GSH or other chemical reducing agents. Bacteria grown under these conditions were 45-fold more virulent in an acute murine infection model and conferred greater immunity to a subsequent lethal challenge than bacteria grown in conventional media. During cultivation in vitro, PrfA activation was completely dependent on the intracellular levels of GSH, as a glutathione synthase mutant (ΔgshF) was activated by exogenous GSH but not reducing agents. PrfA activation was repressed in a synthetic medium supplemented with oligopeptides, but the repression was relieved by stimulation of the stringent response. These data suggest that cytosolic L. monocytogenes interprets a combination of metabolic and redox cues as a signal to initiate robust virulence gene expression in vivoIMPORTANCE Intracellular pathogens are responsible for much of the worldwide morbidity and mortality from infectious diseases. These pathogens have evolved various strategies to proliferate within individual cells of the host and avoid the host immune response. Through cellular invasion or the use of specialized secretion machinery, all intracellular pathogens must access the host cell cytosol to establish their replicative niches. Determining how these pathogens sense and respond to the intracellular compartment to establish a successful infection is critical to our basic understanding of the pathogenesis of each organism and for the rational design of therapeutic interventions. Listeria monocytogenes is a model intracellular pathogen with robust in vitro and in vivo infection models. Studies of the host-sensing and downstream signaling mechanisms evolved by L. monocytogenes often describe themes of pathogenesis that are broadly applicable to less tractable pathogens. Here, we describe how bacteria use external redox states as a cue to activate virulence

Symmetry and designability for lattice protein models

Native protein folds often have a high degree of symmetry. We study the relationship between the symmetries of native proteins, and their designabilities -- how many different sequences encode a given native structure. Using a two-dimensional lattice protein model based on hydrophobicity, we find that those native structures that are encoded by the largest number of different sequences have high symmetry. However only certain symmetries are enhanced, e.g. x/y-mirror symmetry and $180^o$ rotation, while others are suppressed. If it takes a large number of mutations to destabilize the native state of a protein, then, by definition, the state is highly designable. Hence, our findings imply that insensitivity to mutation implies high symmetry. It appears that the relationship between designability and symmetry results because protein substructures are also designable. Native protein folds may therefore be symmetric because they are composed of repeated designable substructures.Comment: 13 pages, 10 figure

On pattern structures of the N-soliton solution of the discrete KP equation over a finite field

The existence and properties of coherent pattern in the multisoliton solutions of the dKP equation over a finite field is investigated. To that end, starting with an algebro-geometric construction over a finite field, we derive a "travelling wave" formula for $N$-soliton solutions in a finite field. However, despite it having a form similar to its analogue in the complex field case, the finite field solutions produce patterns essentially different from those of classical interacting solitons.Comment: 12 pages, 3 figure

Coupling Non-Gravitational Fields with Simplicial Spacetimes

The inclusion of source terms in discrete gravity is a long-standing problem. Providing a consistent coupling of source to the lattice in Regge Calculus (RC) yields a robust unstructured spacetime mesh applicable to both numerical relativity and quantum gravity. RC provides a particularly insightful approach to this problem with its purely geometric representation of spacetime. The simplicial building blocks of RC enable us to represent all matter and fields in a coordinate-free manner. We provide an interpretation of RC as a discrete exterior calculus framework into which non-gravitational fields naturally couple with the simplicial lattice. Using this approach we obtain a consistent mapping of the continuum action for non-gravitational fields to the Regge lattice. In this paper we apply this framework to scalar, vector and tensor fields. In particular we reconstruct the lattice action for (1) the scalar field, (2) Maxwell field tensor and (3) Dirac particles. The straightforward application of our discretization techniques to these three fields demonstrates a universal implementation of coupling source to the lattice in Regge calculus.Comment: 10 pages, no figures, Latex, fixed typos and minor corrections

Development of high temperature refractory-based multi-principle-component alloys by thermodynamic calculations and rapid alloy prototyping

Recently, new refractory-based high entropy alloys (HEAs) have been investigated for potential use as high temperature structural alloys, and some alloys exhibit excellent high temperature strength and ductility. While the high entropy alloy community is generally concerned with obtaining single phase solid-solution phases, secondary strengthening phases are usually required to achieve an adequate balance of mechanical and physical properties for structural applications. This contribution will report on new Mo,Nb-based alloys that have been developed using HEA design guidelines, as well as new tools that enable thermodynamic property predictions and rapid alloy prototyping and assessment. An elemental palette of Mo-Nb-Hf-Ta-Ti-V-W-Zr was chosen in order to promote the formation of a single body-centered cubic (BCC) solid-solution phase upon solidification, which facilitates homogenization heat treatments. Al, Cr, and Si were also included to promote secondary phase formation. These 11 elements were then used to calculate the phases present and their reaction temperatures of 3-, 4-, 5-, and 6-component alloy compositions from all of the available PandatTM databases. Mo and Nb were required to be present in each alloy composition in order to maintain modest alloy costs and densities. Please click Additional Files below to see the full abstract

Impaired β-glucocerebrosidase activity and processing in frontotemporal dementia due to progranulin mutations.

Loss-of-function mutations in progranulin (GRN) are a major autosomal dominant cause of frontotemporal dementia. Most pathogenic GRN mutations result in progranulin haploinsufficiency, which is thought to cause frontotemporal dementia in GRN mutation carriers. Progranulin haploinsufficiency may drive frontotemporal dementia pathogenesis by disrupting lysosomal function, as patients with GRN mutations on both alleles develop the lysosomal storage disorder neuronal ceroid lipofuscinosis, and frontotemporal dementia patients with GRN mutations (FTD-GRN) also accumulate lipofuscin. The specific lysosomal deficits caused by progranulin insufficiency remain unclear, but emerging data indicate that progranulin insufficiency may impair lysosomal sphingolipid-metabolizing enzymes. We investigated the effects of progranulin insufficiency on sphingolipid-metabolizing enzymes in the inferior frontal gyrus of FTD-GRN patients using fluorogenic activity assays, biochemical profiling of enzyme levels and posttranslational modifications, and quantitative neuropathology. Of the enzymes studied, only β-glucocerebrosidase exhibited impairment in FTD-GRN patients. Brains from FTD-GRN patients had lower activity than controls, which was associated with lower levels of mature β-glucocerebrosidase protein and accumulation of insoluble, incompletely glycosylated β-glucocerebrosidase. Immunostaining revealed loss of neuronal β-glucocerebrosidase in FTD-GRN patients. To investigate the effects of progranulin insufficiency on β-glucocerebrosidase outside of the context of neurodegeneration, we investigated β-glucocerebrosidase activity in progranulin-insufficient mice. Brains from Grn-/- mice had lower β-glucocerebrosidase activity than wild-type littermates, which was corrected by AAV-progranulin gene therapy. These data show that progranulin insufficiency impairs β-glucocerebrosidase activity in the brain. This effect is strongest in neurons and may be caused by impaired β-glucocerebrosidase processing