A frustrated quantum spin-{\boldmath s} model on the Union Jack lattice with spins {\boldmath s>1/2}

The zero-temperature phase diagrams of a two-dimensional frustrated quantum antiferromagnetic system, namely the Union Jack model, are studied using the coupled cluster method (CCM) for the two cases when the lattice spins have spin quantum number $s=1$ and $s=3/2$. The system is defined on a square lattice and the spins interact via isotropic Heisenberg interactions such that all nearest-neighbour (NN) exchange bonds are present with identical strength $J_{1}>0$, and only half of the next-nearest-neighbour (NNN) exchange bonds are present with identical strength $J_{2} \equiv \kappa J_{1} > 0$. The bonds are arranged such that on the $2 \times 2$ unit cell they form the pattern of the Union Jack flag. Clearly, the NN bonds by themselves (viz., with $J_{2}=0$) produce an antiferromagnetic N\'{e}el-ordered phase, but as the relative strength $\kappa$ of the frustrating NNN bonds is increased a phase transition occurs in the classical case ($s \rightarrow \infty$) at $\kappa^{\rm cl}_{c}=0.5$ to a canted ferrimagnetic phase. In the quantum cases considered here we also find strong evidence for a corresponding phase transition between a N\'{e}el-ordered phase and a quantum canted ferrimagnetic phase at a critical coupling $\kappa_{c_{1}}=0.580 \pm 0.015$ for $s=1$ and $\kappa_{c_{1}}=0.545 \pm 0.015$ for $s=3/2$. In both cases the ground-state energy $E$ and its first derivative $dE/d\kappa$ seem continuous, thus providing a typical scenario of a second-order phase transition at $\kappa=\kappa_{c_{1}}$, although the order parameter for the transition (viz., the average ground-state on-site magnetization) does not go to zero there on either side of the transition.Comment: 1

Polycrystalline {\gamma}-boron: As hard as polycrystalline cubic boron nitride

The Vickers hardness of polycrystalline {\gamma}-B was measured using a diamond indentation method. The elastic properties of polycrystalline {\gamma}-B (B=213.9 GPa, G=227.2 GPa, and E=503.3 GPa) were determined using ultrasonic measurement at ambient condition. Under the loading force up to 20 N, our test gave an average Vickers hardness in the asymptotic-hardness region of 30.3 GPa. The average fracture toughness was measured as 4.1MPa m1/2. Additionally, We also measured the hardness and elastic properties of polycrystalline {\beta}-B and PcBN for comparison. The hardness and elastic properties for polycrystalline {\gamma}-B was found to be very close to that of PcBN. Our results suggest that the polycrystalline {\gamma}-B could be a superhard polycrystalline material for industrial applications.Comment: 16 page

The response of a classical Hodgkin–Huxley neuron to an inhibitory input pulse

A population of uncoupled neurons can often be brought close to synchrony by a single strong inhibitory input pulse affecting all neurons equally. This mechanism is thought to underlie some brain rhythms, in particular gamma frequency (30–80 Hz) oscillations in the hippocampus and neocortex. Here we show that synchronization by an inhibitory input pulse often fails for populations of classical Hodgkin–Huxley neurons. Our reasoning suggests that in general, synchronization by inhibitory input pulses can fail when the transition of the target neurons from rest to spiking involves a Hopf bifurcation, especially when inhibition is shunting, not hyperpolarizing. Surprisingly, synchronization is more likely to fail when the inhibitory pulse is stronger or longer-lasting. These findings have potential implications for the question which neurons participate in brain rhythms, in particular in gamma oscillations

The spin-1/2 J1-J2 Heisenberg antiferromagnet on the square lattice: Exact diagonalization for N=40 spins

We present numerical exact results for the ground state and the low-lying excitations for the spin-1/2 J1-J2 Heisenberg antiferromagnet on finite square lattices of up to N=40 sites. Using finite-size extrapolation we determine the ground-state energy, the magnetic order parameters, the spin gap, the uniform susceptibility, as well as the spin-wave velocity and the spin stiffness as functions of the frustration parameter J2/J1. In agreement with the generally excepted scenario we find semiclassical magnetically ordered phases for J2 < J2^{c1} and J2 > J2^{c2} separated by a gapful quantum paramagnetic phase. We estimate J2^{c1} \approx 0.35J1 and J2^{c2} \approx 0.66J1.Comment: 16 pages, 2 tables, 11 figure

Structural brain abnormalities in the common epilepsies assessed in a worldwide ENIGMA study

Progressive functional decline in the epilepsies is largely unexplained. We formed the ENIGMA-Epilepsy consortium to understand factors that influence brain measures in epilepsy, pooling data from 24 research centres in 14 countries across Europe, North and South America, Asia, and Australia. Structural brain measures were extracted from MRI brain scans across 2149 individuals with epilepsy, divided into four epilepsy subgroups including idiopathic generalized epilepsies (n =367), mesial temporal lobe epilepsies with hippocampal sclerosis (MTLE; left, n = 415; right, n = 339), and all other epilepsies in aggregate (n = 1026), and compared to 1727 matched healthy controls. We ranked brain structures in order of greatest differences between patients and controls, by meta-analysing effect sizes across 16 subcortical and 68 cortical brain regions. We also tested effects of duration of disease, age at onset, and age-by-diagnosis interactions on structural measures. We observed widespread patterns of altered subcortical volume and reduced cortical grey matter thickness. Compared to controls, all epilepsy groups showed lower volume in the right thalamus (Cohen's d = -0.24 to -0.73; P < 1.49 × 10-4), and lower thickness in the precentral gyri bilaterally (d = -0.34 to -0.52; P < 4.31 × 10-6). Both MTLE subgroups showed profound volume reduction in the ipsilateral hippocampus (d = -1.73 to -1.91, P < 1.4 × 10-19), and lower thickness in extrahippocampal cortical regions, including the precentral and paracentral gyri, compared to controls (d = -0.36 to -0.52; P < 1.49 × 10-4). Thickness differences of the ipsilateral temporopolar, parahippocampal, entorhinal, and fusiform gyri, contralateral pars triangularis, and bilateral precuneus, superior frontal and caudal middle frontal gyri were observed in left, but not right, MTLE (d = -0.29 to -0.54; P < 1.49 × 10-4). Contrastingly, thickness differences of the ipsilateral pars opercularis, and contralateral transverse temporal gyrus, were observed in right, but not left, MTLE (d = -0.27 to -0.51; P < 1.49 × 10-4). Lower subcortical volume and cortical thickness associated with a longer duration of epilepsy in the all-epilepsies, all-other-epilepsies, and right MTLE groups (beta, b < -0.0018; P < 1.49 × 10-4). In the largest neuroimaging study of epilepsy to date, we provide information on the common epilepsies that could not be realistically acquired in any other way. Our study provides a robust ranking of brain measures that can be further targeted for study in genetic and neuropathological studies. This worldwide initiative identifies patterns of shared grey matter reduction across epilepsy syndromes, and distinctive abnormalities between epilepsy syndromes, which inform our understanding of epilepsy as a network disorder, and indicate that certain epilepsy syndromes involve more widespread structural compromise than previously assumed

A systems-level analysis highlights microglial activation as a modifying factor in common epilepsies

Aims: The causes of distinct patterns of reduced cortical thickness in the common human epilepsies, detectable on neuroimaging and with important clinical consequences, are unknown. We investigated the underlying mechanisms of cortical thinning using a systems-level analysis. // Methods: Imaging-based cortical structural maps from a large-scale epilepsy neuroimaging study were overlaid with highly spatially resolved human brain gene expression data from the Allen Human Brain Atlas. Cell-type deconvolution, differential expression analysis and cell-type enrichment analyses were used to identify differences in cell-type distribution. These differences were followed up in post-mortem brain tissue from humans with epilepsy using Iba1 immunolabelling. Furthermore, to investigate a causal effect in cortical thinning, cell-type specific depletion was used in a murine model of acquired epilepsy. // Results: We identified elevated fractions of microglia and endothelial cells in regions of reduced cortical thickness. Differentially expressed genes showed enrichment for microglial markers, and in particular, activated microglial states. Analysis of post-mortem brain tissue from humans with epilepsy confirmed excess activated microglia. In the murine model, transient depletion of activated microglia during the early phase of the disease development prevented cortical thinning and neuronal cell loss in the temporal cortex. Although the development of chronic seizures was unaffected, the epileptic mice with early depletion of activated microglia did not develop deficits in a non-spatial memory test seen in epileptic mice not depleted of microglia. // Conclusions: These convergent data strongly implicate activated microglia in cortical thinning, representing a new dimension for concern and disease modification in the epilepsies, potentially distinct from seizure control

Pan-cancer analysis of whole genomes

Cancer is driven by genetic change, and the advent of massively parallel sequencing has enabled systematic documentation of this variation at the whole-genome scale(1-3). Here we report the integrative analysis of 2,658 whole-cancer genomes and their matching normal tissues across 38 tumour types from the Pan-Cancer Analysis of Whole Genomes (PCAWG) Consortium of the International Cancer Genome Consortium (ICGC) and The Cancer Genome Atlas (TCGA). We describe the generation of the PCAWG resource, facilitated by international data sharing using compute clouds. On average, cancer genomes contained 4-5 driver mutations when combining coding and non-coding genomic elements; however, in around 5% of cases no drivers were identified, suggesting that cancer driver discovery is not yet complete. Chromothripsis, in which many clustered structural variants arise in a single catastrophic event, is frequently an early event in tumour evolution; in acral melanoma, for example, these events precede most somatic point mutations and affect several cancer-associated genes simultaneously. Cancers with abnormal telomere maintenance often originate from tissues with low replicative activity and show several mechanisms of preventing telomere attrition to critical levels. Common and rare germline variants affect patterns of somatic mutation, including point mutations, structural variants and somatic retrotransposition. A collection of papers from the PCAWG Consortium describes non-coding mutations that drive cancer beyond those in the TERT promoter(4); identifies new signatures of mutational processes that cause base substitutions, small insertions and deletions and structural variation(5,6); analyses timings and patterns of tumour evolution(7); describes the diverse transcriptional consequences of somatic mutation on splicing, expression levels, fusion genes and promoter activity(8,9); and evaluates a range of more-specialized features of cancer genomes(8,10-18).Peer reviewe