Anomalous Roughening in Experiments of Interfaces in Hele-Shaw Flows with Strong Quenched Disorder

We report experimental evidences of anomalous kinetic roughening in the stable displacement of an oil-air interface in a Hele-Shaw cell with strong quenched disorder. The disorder consists on a random modulation of the gap spacing transverse to the growth direction (tracks). We have performed experiments varying average interface velocity and gap spacing, and measured the scaling exponents. We have obtained beta=0.50, beta*=0.25, alpha=1.0, alpha_l=0.5, and z=2. When there is no fluid injection, the interface is driven solely by capillary forces, and a higher value of beta around beta=0.65 is measured. The presence of multiscaling and the particular morphology of the interfaces, characterized by high slopes that follow a L\'evy distribution, confirms the existence of anomalous scaling. From a detailed study of the motion of the oil--air interface we show that the anomaly is a consequence of different local velocities over tracks plus the coupling in the motion between neighboring tracks. The anomaly disappears at high interface velocities, weak capillary forces, or when the disorder is not sufficiently persistent in the growth direction. We have also observed the absence of scaling when the disorder is very strong or when a regular modulation of the gap spacing is introduced.Comment: 14 pages, 17 figure

Physical properties of FeSe0.5_{0.5}Te0.5_{0.5} single crystals grown under different conditions

We report on structural, magnetic, conductivity, and thermodynamic studies of FeSe$_{0.5}$Te$_{0.5}$ single crystals grown by self-flux and Bridgman methods. The samples were prepared from starting materials of different purity at various temperatures and cooling rates. The lowest values of the susceptibility in the normal state, the highest transition temperature $T_c$ of 14.5 K, and the largest heat-capacity anomaly at $T_c$ were obtained for pure (oxygen-free) samples. The critical current density $j_c$ of $8 \times 10^4$ A/cm$^2$ (at 2 K) achieved in pure samples is attributed to intrinsic inhomogeneity due to disorder at the cation and anion sites. The impure samples show increased $j_c$ up to $2.3 \times 10^5$ A/cm$^2$ due to additional pinning centers of Fe$_3$O$_4$. The upper critical field $H_{c2}$ of $\sim 500$ kOe is estimated from the resistivity study in magnetic fields parallel to the \emph{c}-axis. The anisotropy of the upper critical field $\gamma_{H_{c2}} = H_{_{c2}}^{ab}/H_{_{c2}}^{c}$ reaches a value $\sim 6$ at $T\longrightarrow T_c$. Extremely low values of the residual Sommerfeld coefficient for pure samples indicate a high volume fraction of the superconducting phase (up to 97%). The electronic contribution to the specific heat in the superconducting state is well described within a single-band BCS model with a temperature dependent gap $\Delta_0 = 27(1)$ K. A broad cusp-like anomaly in the electronic specific heat of samples with suppressed bulk superconductivity is ascribed to a splitting of the ground state of the interstitial Fe$^{2+}$ ions. This contribution is fully suppressed in the ordered state in samples with bulk superconductivity.Comment: 11 pages, 11 figures, 3 table

Treatable traits in the European U-BIOPRED adult asthma cohorts

No abstract availabl

Critical behavior at m-axial Lifshitz points: field-theory analysis and ϵ\epsilon-expansion results

The critical behavior of d-dimensional systems with an n-component order parameter is reconsidered at (m,d,n)-Lifshitz points, where a wave-vector instability occurs in an m-dimensional subspace of ${\mathbb R}^d$. Our aim is to sort out which ones of the previously published partly contradictory $\epsilon$-expansion results to second order in $\epsilon=4+\frac{m}{2}-d$ are correct. To this end, a field-theory calculation is performed directly in the position space of $d=4+\frac{m}{2}-\epsilon$ dimensions, using dimensional regularization and minimal subtraction of ultraviolet poles. The residua of the dimensionally regularized integrals that are required to determine the series expansions of the correlation exponents $\eta_{l2}$ and $\eta_{l4}$ and of the wave-vector exponent $\beta_q$ to order $\epsilon^2$ are reduced to single integrals, which for general m=1,...,d-1 can be computed numerically, and for special values of m, analytically. Our results are at variance with the original predictions for general m. For m=2 and m=6, we confirm the results of Sak and Grest [Phys. Rev. B {\bf 17}, 3602 (1978)] and Mergulh{\~a}o and Carneiro's recent field-theory analysis [Phys. Rev. B {\bf 59},13954 (1999)].Comment: Latex file with one figure (eps-file). Latex file uses texdraw to generate figures that are included in the tex

The genetic architecture of the human cerebral cortex

INTRODUCTION The cerebral cortex underlies our complex cognitive capabilities. Variations in human cortical surface area and thickness are associated with neurological, psychological, and behavioral traits and can be measured in vivo by magnetic resonance imaging (MRI). Studies in model organisms have identified genes that influence cortical structure, but little is known about common genetic variants that affect human cortical structure. RATIONALE To identify genetic variants associated with human cortical structure at both global and regional levels, we conducted a genome-wide association meta-analysis of brain MRI data from 51,665 individuals across 60 cohorts. We analyzed the surface area and average thickness of the whole cortex and 34 cortical regions with known functional specializations. RESULTS We identified 306 nominally genome-wide significant loci (P < 5 × 10−8) associated with cortical structure in a discovery sample of 33,992 participants of European ancestry. Of the 299 loci for which replication data were available, 241 loci influencing surface area and 14 influencing thickness remained significant after replication, with 199 loci passing multiple testing correction (P < 8.3 × 10−10; 187 influencing surface area and 12 influencing thickness). Common genetic variants explained 34% (SE = 3%) of the variation in total surface area and 26% (SE = 2%) in average thickness; surface area and thickness showed a negative genetic correlation (rG = −0.32, SE = 0.05, P = 6.5 × 10−12), which suggests that genetic influences have opposing effects on surface area and thickness. Bioinformatic analyses showed that total surface area is influenced by genetic variants that alter gene regulatory activity in neural progenitor cells during fetal development. By contrast, average thickness is influenced by active regulatory elements in adult brain samples, which may reflect processes that occur after mid-fetal development, such as myelination, branching, or pruning. When considered together, these results support the radial unit hypothesis that different developmental mechanisms promote surface area expansion and increases in thickness. To identify specific genetic influences on individual cortical regions, we controlled for global measures (total surface area or average thickness) in the regional analyses. After multiple testing correction, we identified 175 loci that influence regional surface area and 10 that influence regional thickness. Loci that affect regional surface area cluster near genes involved in the Wnt signaling pathway, which is known to influence areal identity. We observed significant positive genetic correlations and evidence of bidirectional causation of total surface area with both general cognitive functioning and educational attainment. We found additional positive genetic correlations between total surface area and Parkinson’s disease but did not find evidence of causation. Negative genetic correlations were evident between total surface area and insomnia, attention deficit hyperactivity disorder, depressive symptoms, major depressive disorder, and neuroticism. CONCLUSION This large-scale collaborative work enhances our understanding of the genetic architecture of the human cerebral cortex and its regional patterning. The highly polygenic architecture of the cortex suggests that distinct genes are involved in the development of specific cortical areas. Moreover, we find evidence that brain structure is a key phenotype along the causal pathway that leads from genetic variation to differences in general cognitive function

Identification of CCR₉^- murine plasmacytoid DC precursors with plasticity to differentiate into conventional DCs.

Whereas the final differentiation of conventional dendritic cells (CDCs) from committed precursors occurs locally in secondary lymphoid or peripheral tissues, plasmacytoid dendritic cells (PDCs) are thought to fully develop in the bone marrow from common DC progenitors before migrating to the periphery. In our study, we define, for the first time, a subpopulation of CCR9(-) major histocompatibility complex class II(low) PDCs in murine bone marrow, which express E2-2 and are immediate precursors of CCR9(+) fully differentiated PDCs. However, CCR9(-) PDCs have the plasticity to acquire the phenotype and function of CD11b(+) CD8&alpha;(-) major histocompatibility complex class II(high) CDC-like cells under the influence of soluble factors produced by intestinal epithelial cells or recombinant GM-CSF. This deviation from the PDC lineage commitment is regulated on the level of transcription factors reflected by down-regulation of E2-2 and up-regulation of ID2, PU.1, and BATF3. Thus, CCR9(-) PDCs are immediate PDC precursors that can be reprogrammed to differentiate into CDC-like cells with higher antigen-presenting and cytokine-producing capacity under the influence of the local tissue microenvironment