Shocks and a Giant Planet in the Disk Orbiting BP Piscium?

Spitzer IRS spectroscopy supports the interpretation that BP Piscium, a gas and dust enshrouded star residing at high Galactic latitude, is a first-ascent giant rather than a classical T Tauri star. Our analysis suggests that BP Piscium's spectral energy distribution can be modeled as a disk with a gap that is opened by a giant planet. Modeling the rich mid-infrared emission line spectrum indicates that the solid-state emitting grains orbiting BP Piscium are primarily composed of ~75 K crystalline, magnesium-rich olivine; ~75 K crystalline, magnesium-rich pyroxene; ~200 K amorphous, magnesium-rich pyroxene; and ~200 K annealed silica ('cristobalite'). These dust grains are all sub-micron sized. The giant planet and gap model also naturally explains the location and mineralogy of the small dust grains in the disk. Disk shocks that result from disk-planet interaction generate the highly crystalline dust which is subsequently blown out of the disk mid-plane and into the disk atmosphere.Comment: 25 pages, 4 figures, 1 table. Accepted to Ap

Superconducting gap structure of the 115's revisited

Density functional theory calculations of the electronic structure of Ce- and Pu-based heavy fermion superconductors in the so-called 115 family are performed. The gap equation is used to consider which superconducting order parameters are most favorable assuming a pairing interaction that is peaked at (\pi,\pi,q_z) - the wavevector for the antiferromagnetic ordering found in close proximity. In addition to the commonly accepted $d_{x^2-y^2}$ order parameter, there is evidence that an extended s-wave order parameter with nodes is also plausible. We discuss whether these results are consistent with current observations and possible measurements that could help distinguish between these scenarios.Comment: 8 pages, 4 figures; Accepted for publication in JPC

Suppression of mitochondrial respiration through recruitment of p160 myb binding protein to PGC-1α : modulation by p38 MAPK

The transcriptional coactivator PPAR gamma coactivator 1 α (PGC-1α) is a key regulator of metabolic processes such as mitochondrial biogenesis and respiration in muscle and gluconeogenesis in liver. Reduced levels of PGC-1α in humans have been associated with type II diabetes. PGC-1α contains a negative regulatory domain that attenuates its transcriptional activity. This negative regulation is removed by phosphorylation of PGC-1α by p38 MAPK, an important kinase downstream of cytokine signaling in muscle and β-adrenergic signaling in brown fat. We describe here the identification of p160 myb binding protein (p160MBP) as a repressor of PGC-1α. The binding and repression of PGC-1α by p160MBP is disrupted by p38 MAPK phosphorylation of PGC-1α. Adenoviral expression of p160MBP in myoblasts strongly reduces PGC-1α's ability to stimulate mitochondrial respiration and the expression of the genes of the electron transport system. This repression does not require removal of PGC-1α from chromatin, suggesting that p160MBP is or recruits a direct transcriptional suppressor. Overall, these data indicate that p160MBP is a powerful negative regulator of PGC-1α function and provide a molecular mechanism for the activation of PGC-1α by p38 MAPK. The discovery of p160MBP as a PGC-1α regulator has important implications for the understanding of energy balance and diabetes

Time--Splitting Schemes and Measure Source Terms for a Quasilinear Relaxing System

Several singular limits are investigated in the context of a $2 \times 2$ system arising for instance in the modeling of chromatographic processes. In particular, we focus on the case where the relaxation term and a $L^2$ projection operator are concentrated on a discrete lattice by means of Dirac measures. This formulation allows to study more easily some time-splitting numerical schemes

Copious amounts of hot and cold dust orbiting the main sequence A-type stars HD 131488 and HD 121191

We report two new dramatically dusty main sequence stars: HD 131488 (A1 V) and HD 121191 (A8 V). HD 131488 is found to have substantial amounts of dust in its terrestrial planet zone (L IR/L bol ≈ 4 × 10-3), cooler dust farther out in its planetary sy

The Luminosity Profiles of Brightest Cluster Galaxies

(Abridged) We have derived detailed R band luminosity profiles and structural parameters for a total of 430 brightest cluster galaxies (BCGs), down to a limiting surface brightness of 24.5 mag/arcsec^2. Light profiles were initially fitted with a Sersic's R^(1/n) model, but we found that 205 (~48) BCGs require a double component model to accurately match their light profiles. The best fit for these 205 galaxies is an inner Sersic model, with indices n~1-7, plus an outer exponential component. Thus, we establish the existence of two categories of the BCGs luminosity profiles: single and double component profiles. We found that double profile BCGs are brighter ~0.2 mag than single profile BCG. In fact, the Kolmogorov-Smirnov test applied to these subsamples indicates that they have different total magnitude distributions, with mean values M_R=-23.8 +/- 0.6 mag for single profile BCGs and M_R=-24.0 +/- 0.5 mag for double profile BCGs. We find that partial luminosities for both subsamples are indistinguishable up to r = 15 kpc, while for r > 20 kpc the luminosities we obtain are on average 0.2 mag brighter for double profile BCGs. This result indicates that extra-light for double profile BCGs does not come from the inner region but from the outer regions of these galaxies. The best fit slope of the Kormendy relation for the whole sample is a = 3.13 +/- 0.04$. However, when fitted separately, single and double profile BCGs show different slopes: a_(single) = 3.29 +/- 0.06 and a_(double)= 2.79 +/- 0.08. On the other hand, we did not find differences between these two BCGs categories when we compared global cluster properties such as the BCG-projected position relative to the cluster X-ray center emission, X-ray luminosity, or BCG orientation with respect to the cluster position angle.Comment: August 2011 issue of ApJS, volume 195, 15 http://iopscience.iop.org/0067-0049/195/2/1

Multiform antimicrobial resistance from a metabolic mutation

A critical challenge for microbiology and medicine is how to cure infections by bacteria that survive antibiotic treatment by persistence or tolerance. Seeking mechanisms behind such high survival, we developed a forward-genetic method for efficient isolation of high24 survival mutants in any culturable bacterial species. We found that perturbation of an essential biosynthetic pathway (arginine biosynthesis) in a mycobacterium generated three distinct forms of resistance to diverse antibiotics, each mediated by induction of WhiB7— high persistence and tolerance to kanamycin, high survival upon exposure to rifampicin, and MIC-shifted resistance to clarithromycin. As little as one base change in a gene encoding a metabolic pathway component conferred multiple forms of resistance to multiple antibiotics with different targets. This extraordinary resilience may help explain how sub31 sterilizing exposure to one antibiotic in a regimen can induce resistance to others and invites development of drugs targeting the mediator of multiform resistance, WhiB7

Partnership of PGC-1α and HNF4α in the regulation of lipoprotein metabolism

Peroxisome proliferator-activated receptor γ coactivator-1α (PGC-1α) is a transcriptional coactivator involved in several aspects of energy metabolism. It is induced or activated under different stimuli in a highly tissue-specific manner and subsequently partners with certain transcription factors in those tissues to execute various biological programs. In the fasted liver, PGC-1α is induced and interacts with hepatocyte nuclear factor 4α (HNF4α) and other transcription factors to activate gluconeogenesis and increase hepatic glucose output. Given the broad spectrum of liver genes responsive to HNF4α, we sought to determine those that were specifically targeted by the combination of PGC-1α and HNF4α. Coexpression of these two molecules in murine stem cells reveals a high induction of mRNA for apolipoproteins A-IV and C-II. Forced expression of PGC-1α in mouse and human hepatoma cells increases the mRNA of a subset of apolipoproteins implicated in very low density lipoprotein and triglyceride metabolism, including apolipoproteins A-IV, C-II, and C-III. Coactivation of the apoC-III/A-IV promoter region by PGC-1α occurs through a highly conserved HNF4α response element, the loss of which completely abolishes activation by PGC-1α and HNF4α. Adenoviral infusion of PGC-1α into live mice increases hepatic expression of apolipoproteins A-IV, C-II, and C-III and increases serum and very low density lipoprotein triglyceride levels. Conversely, knock down of PGC-1α in vivo causes a decrease in both apolipoprotein expression and serum triglyceride levels. These data point to a crucial role for the PGC-1α/HNF4α partnership in hepatic lipoprotein metabolism