Stability of Horava-Lifshitz Black Holes in the Context of AdS/CFT

The anti--de Sitter/conformal field theory (AdS/CFT) correspondence is a powerful tool that promises to provide new insights toward a full understanding of field theories under extreme conditions, including but not limited to quark-gluon plasma, Fermi liquid and superconductor. In many such applications, one typically models the field theory with asymptotically AdS black holes. These black holes are subjected to stringy effects that might render them unstable. Ho\v{r}ava-Lifshitz gravity, in which space and time undergo different transformations, has attracted attentions due to its power-counting renormalizability. In terms of AdS/CFT correspondence, Ho\v{r}ava-Lifshitz black holes might be useful to model holographic superconductors with Lifshitz scaling symmetry. It is thus interesting to study the stringy stability of Ho\v{r}ava-Lifshitz black holes in the context of AdS/CFT. We find that uncharged topological black holes in $\lambda=1$ Ho\v{r}ava-Lifshitz theory are nonperturbatively stable, unlike their counterparts in Einstein gravity, with the possible exceptions of negatively curved black holes with detailed balance parameter $\epsilon$ close to unity. Sufficiently charged flat black holes for $\epsilon$ close to unity, and sufficiently charged positively curved black holes with $\epsilon$ close to zero, are also unstable. The implication to the Ho\v{r}ava-Lifshitz holographic superconductor is discussed.Comment: 15 pages, 6 figures. Updated version accepted by Phys. Rev. D, with corrections to various misprints. References update

Dissipationless Anomalous Hall Current in the Ferromagnetic Spinel CuCr2_2Se4−x_{4-x}Brx_x

In a ferromagnet, an applied electric field $\bf E$ invariably produces an anomalous Hall current ${\bf J}_H$ that flows perpendicular to the plane defined by $\bf E$ and $\bf M$ (the magnetization). For decades, the question whether ${\bf J}_H$ is dissipationless (independent of the scattering rate), has been keenly debated without experimental resolution. In the ferromagnetic spinel CuCr$_2$Se$_{4-x}$Br$_x$, the resistivity $\rho$ (at low temperature) may be increased 1000 fold by varying $x$(Br), without degrading the $\bf M$. We show that ${\bf J}_H/E$ (normalized per carrier, at 5 K) remains unchanged throughout. In addition to resolving the controversy experimentally, our finding has strong bearing on the generation and study of spin-Hall currents in bulk samples.Comment: 7 pages, 6 figure

Thermal Hall Conductivity as a Probe of Gap Structure in Multi-band Superconductors: The Case of Ba1−xKxFe2As2\rm Ba_{1-x}K_xFe_2As_2

The sign and profile of the thermal Hall conductivity $\kappa_{xy}$ gives important insights into the gap structure of multi-band superconductors. With this perspective, we have investigated $\kappa_{xy}$ and the thermal conductivity $\kappa_{xx}$ in $\rm Ba_{1-x}K_xFe_2As_2$ which display large peak anomalies in the superconducting state. The anomalies imply that a large hole-like quasiparticle (qp) population exists below the critical temperature $T_c$. We show that the qp mean-free-path inferred from $\kappa_{xx}$ reproduces the observed anomaly in $\kappa_{xy}$, providing a consistent estimate of a large qp population. Further, we demonstrate that the hole-like signal is consistent with a theoretical scenario where despite potentially large gap variations on the electron pockets, the minimal homogeneous gap of the superconducting phase resides at a hole pocket. Implications for probing the gap structure in the broader class of pnictide superconductors are discussed.Comment: 5 pages, 4 figures. Orientation significantly updated from previous (0811.4668v1) reflecting new theoretical understanding of experimental results and physical implications. Introduction, discussion, and figures updated including additional figure for model calculatio

Empires and Percolation: Stochastic Merging of Adjacent Regions

We introduce a stochastic model in which adjacent planar regions $A, B$ merge stochastically at some rate $\lambda(A,B)$, and observe analogies with the well-studied topics of mean-field coagulation and of bond percolation. Do infinite regions appear in finite time? We give a simple condition on $\lambda$ for this {\em hegemony} property to hold, and another simple condition for it to not hold, but there is a large gap between these conditions, which includes the case $\lambda(A,B) \equiv 1$. For this case, a non-rigorous analytic argument and simulations suggest hegemony.Comment: 13 page

Integrin α2β1 Expression Regulates Matrix Metalloproteinase-1-Dependent Bronchial Epithelial Repair in Pulmonary Tuberculosis.

Pulmonary tuberculosis (TB) is caused by inhalation of Mycobacterium tuberculosis, which damages the bronchial epithelial barrier to establish local infection. Matrix metalloproteinase-1 plays a crucial role in the immunopathology of TB, causing breakdown of type I collagen and cavitation, but this collagenase is also potentially involved in bronchial epithelial repair. We hypothesized that the extracellular matrix (ECM) modulates M. tuberculosis-driven matrix metalloproteinase-1 expression by human bronchial epithelial cells (HBECs), regulating respiratory epithelial cell migration and repair. Medium from monocytes stimulated with M. tuberculosis induced collagenase activity in bronchial epithelial cells, which was reduced by ~87% when cells were cultured on a type I collagen matrix. Matrix metalloproteinase-1 had a focal localization, which is consistent with cell migration, and overall secretion decreased by 32% on type I collagen. There were no associated changes in the specific tissue inhibitors of metalloproteinases. Decreased matrix metalloproteinase-1 secretion was due to ligand-binding to the α2β1 integrin and was dependent on the actin cytoskeleton. In lung biopsies, samples from patients with pulmonary TB, integrin α2β1 is highly expressed on the bronchial epithelium. Areas of lung with disrupted collagen matrix showed an increase in matrix metalloproteinases-1 expression compared with areas where collagen was comparable to control lung. Type I collagen matrix increased respiratory epithelial cell migration in a wound-healing assay, and this too was matrix metalloproteinase-dependent, since it was blocked by the matrix metalloproteinase inhibitor GM6001. In summary, we report a novel mechanism by which α2β1-mediated signals from the ECM modulate matrix metalloproteinase-1 secretion by HBECs, regulating their migration and epithelial repair in TB

Optical investigation of the charge-density-wave phase transitions in NbSe3NbSe_{3}

We have measured the optical reflectivity $R(\omega)$ of the quasi one-dimensional conductor $NbSe_{3}$ from the far infrared up to the ultraviolet between 10 and 300 $K$ using light polarized along and normal to the chain axis. We find a depletion of the optical conductivity with decreasing temperature for both polarizations in the mid to far-infrared region. This leads to a redistribution of spectral weight from low to high energies due to partial gapping of the Fermi surface below the charge-density-wave transitions at 145 K and 59 K. We deduce the bulk magnitudes of the CDW gaps and discuss the scattering of ungapped free charge carriers and the role of fluctuations effects

Structural and molecular basis of the assembly of the TRPP2/PKD1 complex

Mutations in PKD1 and TRPP2 account for nearly all cases of autosomal dominant polycystic kidney disease (ADPKD). These 2 proteins form a receptor/ion channel complex on the cell surface. Using a combination of biochemistry, crystallography, and a single-molecule method to determine the subunit composition of proteins in the plasma membrane of live cells, we find that this complex contains 3 TRPP2 and 1 PKD1. A newly identified coiled-coil domain in the C terminus of TRPP2 is critical for the formation of this complex. This coiled-coil domain forms a homotrimer, in both solution and crystal structure, and binds to a single coiled-coil domain in the C terminus of PKD1. Mutations that disrupt the TRPP2 coiled-coil domain trimer abolish the assembly of both the full-length TRPP2 trimer and the TRPP2/PKD1 complex and diminish the surface expression of both proteins. These results have significant implications for the assembly, regulation, and function of the TRPP2/PKD1 complex and the pathogenic mechanism of some ADPKD-producing mutations

The relationship of circulating fibroblast growth factor 21 levels with pericardial fat: The Multi-Ethnic Study of Atherosclerosis.

Previous small studies have reported an association between circulating fibroblast growth factor 21 (FGF21) levels and pericardial fat volume in post-menopausal women and high cardiovascular disease (CVD) risk patients. In this study, we investigated the relationship of FGF21 levels with pericardial fat volume in participants free of clinical CVD at baseline. We analysed data from 5765 men and women from the Multi-Ethnic Study of Atherosclerosis (MESA) with both pericardial fat volume and plasma FGF21 levels measured at baseline. 4746 participants had pericardial fat volume measured in at least one follow-up exam. After adjusting for confounding factors, ln-transformed FGF21 levels were positively associated with pericardial fat volume at baseline (β = 0.055, p < 0.001). When assessing change in pericardial fat volume over a mean duration of 3.0 years using a linear mixed-effects model, higher baseline FGF21 levels were associated with higher pericardial fat volume at baseline (2.381 cm3 larger in pericardial fat volume per one SD increase in ln-transformed FGF21 levels), but less pericardial fat accumulation over time (0.191 cm3/year lower per one SD increase in ln-transformed FGF21 levels). Cross-sectionally, higher plasma FGF21 levels were significantly associated with higher pericardial fat volume, independent of traditional CVD risk factors and inflammatory markers. However, higher FGF21 levels tended to be associated with less pericardial fat accumulation over time. Nevertheless, such change in pericardial fat volume is very modest and could be due to measurement error. Further studies are needed to elucidate the longitudinal relationship of baseline FGF21 levels with pericardial fat accumulation