An introduction to network psychometrics:Relating ising network models to item response theory models

In recent years, network models have been proposed as an alternative representation of psychometric constructs such as depression. In such models, the covariance between observables (e.g., symptoms like depressed mood, feelings of worthlessness, and guilt) is explained in terms of a pattern of causal interactions between these observables, which contrasts with classical interpretations in which the observables are conceptualized as the effects of a reflective latent variable. However, few investigations have been directed at the question how these different models relate to each other. To shed light on this issue, the current paper explores the relation between one of the most important network models—the Ising model from physics—and one of the most important latent variable models—the Item Response Theory (IRT) model from psychometrics. The Ising model describes the interaction between states of particles that are connected in a network, whereas the IRT model describes the probability distribution associated with item responses in a psychometric test as a function of a latent variable. Despite the divergent backgrounds of the models, we show a broad equivalence between them and also illustrate several opportunities that arise from this connection

The influence of the rare earth ions radii on the Low Spin to Intermediate Spin state transition in lanthanide cobaltite perovskites: LaCoO3 vs. HoCoO3

We present first principles LDA+U calculations of electronic structure and magnetic state for LaCoO3 and HoCoO3. Low Spin to Intermediate Spin state transition was found in our calculations using experimental crystallographic data for both materials with a much higher transition temperature for HoCoO3, which agrees well with the experimental estimations. Low Spin state t6e0 (non-magnetic) to Intermediate Spin state t5e1 (magnetic) transition of Co(3+) ions happens due to the competition between crystal field t_2g-e_g splitting and effective exchange interaction between 3$d$ spin-orbitals. We show that the difference in crystal structure parameters for HoCoO3 and LaCoO3 due to the smaller ionic radius of Ho ion comparing with La ion results in stronger crystal field splitting for HoCoO3 (0.09 eV ~ 1000 K larger than for LaCoO3) and hence tip the balance between the Low Spin and Intermediate Spin states to the non-magnetic solution in HoCoO3.Comment: 13 pages, 6 figure

Analysis of the vector form factors fKπ+(Q2)f^+_{K\pi}(Q^2) and fKπ−(Q2)f^-_{K\pi}(Q^2) with light-cone QCD sum rules

In this article, we calculate the vector form factors $f^+_{K\pi}(Q^2)$ and $f^-_{K\pi}(Q^2)$ within the framework of the light-cone QCD sum rules approach. The numerical values of the $f^+_{K\pi}(Q^2)$ are compatible with the existing theoretical calculations, the central value of the $f^+_{K\pi}(0)$, $f^+_{K\pi}(0)=0.97$, is in excellent agreement with the values from the chiral perturbation theory and lattice QCD. The values of the $|f^-_{K\pi}(0)|$ are very large comparing with the theoretical calculations and experimental data, and can not give any reliable predictions. At large momentum transfers with $Q^2> 5GeV^2$, the form factors $f^+_{K\pi}(Q^2)$ and $|f^-_{K\pi}(Q^2)|$ can either take up the asymptotic behavior of $\frac{1}{Q^2}$ or decrease more quickly than $\frac{1}{Q^2}$, more experimental data are needed to select the ideal sum rules.Comment: 22 pages, 16 figures, revised version, to appear in Eur. Phys. J.

Genome-wide association and Mendelian randomisation analysis provide insights into the pathogenesis of heart failure

Heart failure (HF) is a leading cause of morbidity and mortality worldwide. A small proportion of HF cases are attributable to monogenic cardiomyopathies and existing genome-wide association studies (GWAS) have yielded only limited insights, leaving the observed heritability of HF largely unexplained. We report results from a GWAS meta-analysis of HF comprising 47,309 cases and 930,014 controls. Twelve independent variants at 11 genomic loci are associated with HF, all of which demonstrate one or more associations with coronary artery disease (CAD), atrial fibrillation, or reduced left ventricular function, suggesting shared genetic aetiology. Functional analysis of non-CAD-associated loci implicate genes involved in cardiac development (MYOZ1, SYNPO2L), protein homoeostasis (BAG3), and cellular senescence (CDKN1A). Mendelian randomisation analysis supports causal roles for several HF risk factors, and demonstrates CAD-independent effects for atrial fibrillation, body mass index, and hypertension. These findings extend our knowledge of the pathways underlying HF and may inform new therapeutic strategies