Numerical wave propagation for the triangular P1DGP1_{DG}-P2P2 finite element pair

Inertia-gravity mode and Rossby mode dispersion properties are examined for discretisations of the linearized rotating shallow-water equations using the $P1_{DG}$-$P2$ finite element pair on arbitrary triangulations in planar geometry. A discrete Helmholtz decomposition of the functions in the velocity space based on potentials taken from the pressure space is used to provide a complete description of the numerical wave propagation for the discretised equations. In the $f$-plane case, this decomposition is used to obtain decoupled equations for the geostrophic modes, the inertia-gravity modes, and the inertial oscillations. As has been noticed previously, the geostrophic modes are steady. The Helmholtz decomposition is used to show that the resulting inertia-gravity wave equation is third-order accurate in space. In general the \pdgp finite element pair is second-order accurate, so this leads to very accurate wave propagation. It is further shown that the only spurious modes supported by this discretisation are spurious inertial oscillations which have frequency $f$, and which do not propagate. The Helmholtz decomposition also allows a simple derivation of the quasi-geostrophic limit of the discretised $P1_{DG}$-$P2$ equations in the $\beta$-plane case, resulting in a Rossby wave equation which is also third-order accurate.Comment: Revised version prior to final journal submissio

Reverse Monte Carlo modeling of amorphous silicon

An implementation of the Reverse Monte Carlo algorithm is presented for the study of amorphous tetrahedral semiconductors. By taking into account a number of constraints that describe the tetrahedral bonding geometry along with the radial distribution function, we construct a model of amorphous silicon using the reverse monte carlo technique. Starting from a completely random configuration, we generate a model of amorphous silicon containing 500 atoms closely reproducing the experimental static structure factor and bond angle distribution and in improved agreement with electronic properties. Comparison is made to existing Reverse Monte Carlo models, and the importance of suitable constraints beside experimental data is stressed.Comment: 6 pages, 4 PostScript figure

Sapling size influences shade tolerance ranking among southern boreal tree species

1 Traditional rankings of shade tolerance of trees make little reference to individual size. However, greater respiratory loads with increasing sapling size imply that larger individuals will be less able to tolerate shade than smaller individuals of the same species and that there may be shifts among species in shade tolerance with size. 2 We tested this hypothesis using maximum likelihood estimation to develop individual-tree-based models of the probability of mortality as a function of recent growth rate for seven species: trembling aspen, paper birch, yellow birch, mountain maple, white spruce, balsam fir and eastern white cedar. 3 Shade tolerance of small individuals, as quantified by risk of mortality at low growth, was mostly consistent with traditional shade tolerance rankings such that cedar > balsam fir > white spruce > yellow birch > mountain maple = paper birch > aspen. 4 Differences in growth-dependent mortality were greatest between species in the smallest size classes. With increasing size, a reduced tolerance to shade was observed for all species except trembling aspen and thus species tended to converge in shade tolerance with size. At a given level of radial growth larger trees, apart from aspen, had a higher probability of mortality than smaller trees. 5 Successional processes associated with shade tolerance may thus be most important in the seedling stage and decrease with ontogeny

Coeliac disease-associated risk variants in TNFAIP3 and REL implicate altered NF-kappaB signalling

Objective: Our previous coeliac disease genome-wide association study (GWAS) implicated risk variants in the human leucocyte antigen (HLA) region and eight novel risk regions. To identify more coeliac disease loci, we selected 458 single nucleotide polymorphisms (SNPs) that showed more modest association in the GWAS for genotyping and analysis in four independent cohorts. Design: 458 SNPs were assayed in 1682 cases and 3258 controls from three populations (UK, Irish and Dutch). We combined the results with the original GWAS cohort (767 UK cases and 1422 controls); six SNPs showed association with p Results: We identified two novel coeliac disease risk regions: 6q23.3 (OLIG3-TNFAIP3) and 2p16.1 (REL), both of which reached genome-wide significance in the combined analysis of all 2987 cases and 5273 controls (rs2327832 p= 1.3x10(-08), and rs842647 p= 5.26x10(-07)). We investigated the expression of these genes in the RNA isolated from biopsies and from whole blood RNA. We did not observe any changes in gene expression, nor in the correlation of genotype with gene expression. Conclusions: Both TNFAIP3 (A20, at the protein level) and REL are key mediators in the nuclear factor kappa B (NF-kappa B) inflammatory signalling pathway. For the first time, a role for primary heritable variation in this important biological pathway predisposing to coeliac disease has been identified. Currently, the HLA risk factors and the 10 established non-HLA risk factors explain similar to 40% of the heritability of coeliac disease

Epistemic Entanglement due to Non-Generating Partitions of Classical Dynamical Systems

Quantum entanglement relies on the fact that pure quantum states are dispersive and often inseparable. Since pure classical states are dispersion-free they are always separable and cannot be entangled. However, entanglement is possible for epistemic, dispersive classical states. We show how such epistemic entanglement arises for epistemic states of classical dynamical systems based on phase space partitions that are not generating. We compute epistemically entangled states for two coupled harmonic oscillators.Comment: 13 pages, no figures; International Journal of Theoretical Physics, 201

A family tree of optical transients from narrow-line Seyfert 1 galaxies

Galaxie

Quantitative computed tomography predicts outcomes in idiopathic pulmonary fibrosis

First published: 25 July 2022Background and objective: Prediction of disease course in patients with progressive pulmonary fibrosis remains challenging. The purpose of this study was to assess the prognostic value of lung fibrosis extent quantified at computed tomography (CT) using data-driven texture analysis (DTA) in a large cohort of well-characterized patients with idiopathic pulmonary fibrosis (IPF) enrolled in a national registry. Methods: This retrospective analysis included participants in the Australian IPF Registry with available CT between 2007 and 2016. CT scans were analysed using the DTA method to quantify the extent of lung fibrosis. Demographics, longitudinal pulmonary function and quantitative CT metrics were compared using descriptive statistics. Linear mixed models, and Cox analyses adjusted for age, gender, BMI, smoking history and treatment with anti-fibrotics were performed to assess the relationships between baseline DTA, pulmonary function metrics and outcomes. Results: CT scans of 393 participants were analysed, 221 of which had available pulmonary function testing obtained within 90 days of CT. Linear mixed-effect modelling showed that baseline DTA score was significantly associated with annual rate of decline in forced vital capacity and diffusing capacity of carbon monoxide. In multivariable Cox proportional hazard models, greater extent of lung fibrosis was associated with poorer transplant-free survival (hazard ratio [HR] 1.20, p < 0.0001) and progression-free survival (HR 1.14, p < 0.0001). Conclusion: In a multi-centre observational registry of patients with IPF, the extent of fibrotic abnormality on baseline CT quantified using DTA is associated with outcomes independent of pulmonary function.Stephen M. Humphries, John A. Mackintosh, Helen E. Jo, Simon L. F. Walsh, Mario Silva, Lucio Calandriello, Sally Chapman, Samantha Ellis, Ian Glaspole, Nicole Goh, Christopher Grainge, Peter M. A. Hopkins, Gregory J. Keir, Yuben Moodley, Paul N. Reynolds, E. Haydn Walters, David Baraghoshi, Athol U. Wells, David A. Lynch, Tamera J. Cort

HLA-DQB1 6672G>C (rs113332494) is associated with clozapine-induced neutropenia and agranulocytosis in individuals of European ancestry

The atypical antipsychotic clozapine is the only effective medication for treatment-resistant schizophrenia. However, it can also induce serious adverse drug reactions, including agranulocytosis and neutropenia. The mechanism by which it does so is largely unknown, but there is evidence for contributing genetic factors. Several studies identified HLA-DQB1 variants and especially a polymorphism located in HLA-DQB1 (6672G>C, rs113332494) as associated with clozapine-induced agranulocytosis and neutropenia. We analysed the risk allele distribution of SNP rs113332494 in a sample of 1396 controls and 178 neutropenia cases of which 60 developed agranulocytosis. Absolute neutrophil counts of 500/mm3 and 1500/mm3 were used for defining agranulocytosis and neutropenia cases, respectively. We also performed association analyses and analysed local ancestry patterns in individuals of European ancestry, seeking replication and extension of earlier findings. HLA-DQB1 (6672G>C, rs113332494) was associated with neutropenia (OR = 6.20, P = 2.20E−06) and agranulocytosis (OR = 10.49, P = 1.83E−06) in individuals of European ancestry. The association signal strengthened after including local ancestry estimates (neutropenia: OR = 10.38, P = 6.05E−08; agranulocytosis: OR = 16.31, P = 1.39E−06), with effect sizes being considerably larger for agranulocytosis. Using local ancestry estimates for prediction, the sensitivity of rs113332494 increased from 11.28 to 55.64% for neutropenia and from 16.67 to 53.70% for agranulocytosis. Our study further strengthens the evidence implicating HLA-DQB1 in agranulocytosis and neutropenia, suggesting components of the immune system as contributing to this serious adverse drug reaction. Using local ancestry estimates might help in identifying risk variants and improve prediction of haematological adverse effects