Nonlinear screening and percolative transition in a two-dimensional electron liquid

A novel variational method is proposed for calculating the percolation threshold, the real-space structure, and the thermodynamical compressibility of a disordered two-dimensional electron liquid. Its high accuracy is verified against prior numerical results and newly derived exact asymptotics. The inverse compressibility is shown to have a strongly asymmetric minimum at a density that is approximately the triple of the percolation threshold. This implies that the experimentally observed metal-insulator transition takes place well before the percolation point is reached.Comment: 4 pages, 2 figures. (v2) minor changes (v3) reference added (v4) few more references adde

Effect of FET geometry on charge ordering of transition metal oxides

We examine the effect of an FET geometry on the charge ordering phase diagram of transition metal oxides using numerical simulations of a semiclassical model including long-range Coulomb fields, resulting in nanoscale pattern formation. We find that the phase diagram is unchanged for insulating layers thicker than approximately twice the magnetic correlation length. For very thin insulating layers, the onset of a charge clump phase is shifted to lower values of the strength of the magnetic dipolar interaction, and intermediate diagonal stripe and geometric phases can be suppressed. Our results indicate that, for sufficiently thick insulating layers, charge injection in an FET geometry can be used to experimentally probe the intrinsic charge ordering phases in these materials.Comment: 4 pages, 4 postscript figure

Two-Dimensional Wigner Crystal in Anisotropic Semiconductor

We investigate the effect of mass anisotropy on the Wigner crystallization transition in a two-dimensional (2D) electron gas. The static and dynamical properties of a 2D Wigner crystal have been calculated for arbitrary 2D Bravais lattices in the presence of anisotropic mass, as may be obtainable in Si MOSFETs with (110) surface. By studying the stability of all possible lattices, we find significant change in the crystal structure and melting density of the electron lattice with the lowest ground state energy.Comment: 4 pages, revtex, 4 figure

Lattice Pseudospin Model for ν=1\nu=1 Quantum Hall Bilayers

We present a new theoretical approach to the study of $\nu=1$ quantum Hall bilayer that is based on a systematic mapping of the microscopic Hamiltonian to an anisotropic SU(4) spin model on a lattice. To study the properties of this model we generalize the Heisenberg model Schwinger boson mean field theory (SBMFT) of Arovas and Auerbach to spin models with anisotropy. We calculate the temperature dependence of experimentally observable quantities, including the spin magnetization, and the differential interlayer capacitance. Our theory represents a substantial improvement over the conventional Hartree-Fock picture which neglects quantum and thermal fluctuations, and has advantages over long-wavelength effective models that fail to capture important microscopic physics at all realistic layer separations. The formalism we develop can be generalized to treat quantum Hall bilayers at filling factor $\nu=2$.Comment: 26 pages, 10 figures. The final version, to appear in PR

Quantitative Treatment of Decoherence

We outline different approaches to define and quantify decoherence. We argue that a measure based on a properly defined norm of deviation of the density matrix is appropriate for quantifying decoherence in quantum registers. For a semiconductor double quantum dot qubit, evaluation of this measure is reviewed. For a general class of decoherence processes, including those occurring in semiconductor qubits, we argue that this measure is additive: It scales linearly with the number of qubits.Comment: Revised version, 26 pages, in LaTeX, 3 EPS figure

Lateral geniculate nucleus volume changes after optic neuritis in neuromyelitis optica: a longitudinal study

OBJECTIVES: Lateral geniculate nucleus (LGN) volume is reduced after optic neuritis (ON) in neuromyelitis optica spectrum disorders (NMOSD). We aimed at a longitudinal assessment of LGN volume in NMOSD. METHODS: Twenty-nine patients with aquaporin 4-IgG seropositive NMOSD (age: 47.8 ± 14.6 years (y), female: n = 27, history of ON (NMO-ON): n = 17, median time since ON: 3[1.2-12.1]y) and 18 healthy controls (HC; age: 39.3 ± 15.8y; female: n = 13) were included. Median follow-up was 4.1[1.1-4.7]y for patients and 1.7[0.9-3.2]y for HC. LGN volume was measured using a multi-atlas-based approach of automated segmentation on 3 Tesla magnetic resonance images. Retinal optical coherence tomography and probabilistic tractography of the optic radiations (OR) were also performed. RESULTS: At baseline, NMO-ON patients had lower LGN volumes (395.4 ± 48.9 mm(3)) than patients without ON (NMO-NON: 450.7 ± 55.6 mm(3); p = 0.049) and HC (444.5 ± 61.5 mm(3), p = 0.025). LGN volume was associated with retinal neuroaxonal loss and microstructural OR damage. Longitudinally, there was no change in LGN volumes in the absence of ON, neither in all patients (B = -0.6, SE = 1.4, p = 0.670), nor in NMO-ON (B = -0.8, SE = 1.6, p = 0.617) and NMO-NON (B = 1.7, SE = 3.5, p = 0.650). However, in four patients with new ON during follow-up, LGN volume was reduced at last visit (median time since ON: 2.6 [1.8-3.9]y) compared to the measurement before ON (352 ± 52.7 vs. 371.1 ± 55.9 mm(3); t = -3.6, p = 0.036). CONCLUSION: Although LGN volume is reduced after ON in NMOSD, this volume loss is not progressive over longer follow-up or independent of ON. Thus, our findings -at least in this relatively small cohort- do not support occult neurodegeneration of the afferent visual pathway in NMOSD

Novel genetic loci associated with hippocampal volume

The hippocampal formation is a brain structure integrally involved in episodic memory, spatial navigation, cognition and stress responsiveness. Structural abnormalities in hippocampal volume and shape are found in several common neuropsychiatric disorders. To identify the genetic underpinnings of hippocampal structure here we perform a genome-wide association study (GWAS) of 33,536 individuals and discover six independent loci significantly associated with hippocampal volume, four of them novel. Of the novel loci, three lie within genes (ASTN2, DPP4 and MAST4) and one is found 200 kb upstream of SHH. A hippocampal subfield analysis shows that a locus within the MSRB3 gene shows evidence of a localized effect along the dentate gyrus, subiculum, CA1 and fissure. Further, we show that genetic variants associated with decreased hippocampal volume are also associated with increased risk for Alzheimer's disease (rg =-0.155). Our findings suggest novel biological pathways through which human genetic variation influences hippocampal volume and risk for neuropsychiatric illness

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

Verbal memory impairments in schizophrenia associated with cortical thinning

Verbal memory (VM) represents one of the most affected cognitive domains in schizophrenia. Multiple studies have shown that schizophrenia is associated with cortical abnormalities, but it remains unclear whether these are related to VM impairments. Considering the vast literature demonstrating the role of the frontal cortex, the parahippocampal cortex, and the hippocampus in VM, we examined the cortical thickness/volume of these regions. We used a categorical approach whereby 27 schizophrenia patients with ‘moderate to severe’ VM impairments were compared to 23 patients with ‘low to mild’ VM impairments and 23 healthy controls. A series of between-group vertex-wise GLM on cortical thickness were performed for specific regions of interest defining the parahippocampal gyrus and the frontal cortex. When compared to healthy controls, patients with ‘moderate to severe’ VM impairments revealed significantly thinner cortex in the left frontal lobe, and the parahippocampal gyri. When compared to patients with ‘low to mild’ VM impairments, patients with ‘moderate to severe’ VM impairments showed a trend of thinner cortex in similar regions. Virtually no differences were observed in the frontal area of patients with ‘low to mild’ VM impairments relative to controls. No significant group differences were observed in the hippocampus. Our results indicate that patients with greater VM impairments demonstrate significant cortical thinning in regions known to be important in VM performance. Treating VM deficits in schizophrenia could have a positive effect on the brain; thus, subgroups of patients with more severe VM deficits should be a prioritized target in the development of new cognitive treatments