Structural models of genome-wide covariance identify multiple common dimensions in autism.

Common genetic variation has been associated with multiple phenotypic features in Autism Spectrum Disorder (ASD). However, our knowledge of shared genetic factor structures contributing to this highly heterogeneous phenotypic spectrum is limited. Here, we developed and implemented a structural equation modelling framework to directly model genomic covariance across core and non-core ASD phenotypes, studying autistic individuals of European descent with a case-only design.

What makes fixation of femoral neck fractures fail? A systematic review and meta-analysis of risk factors.

Introduction: This systematic review aims to provide an overview of predictors for failure of treatment of displaced femoral neck fracture (dFNF) with internal fixation and quantify their risk of fixation failure in a meta-analysis.

Patients And Methods: PubMed, Embase, Web of Science, Cochrane Library, and EMCare were searched for original studies published from January 2000, including adult patients with an internally fixated dFNF, that reported data on predictors for fixation failure defined as revision surgery due to non-union, avascular femoral head necrosis or cut-out of implant. RevMan version 5 software was used to pool univariable Odds Ratio's (OR) for predictors of fixation failure by means of a random effects model.

Polygenic risk for mental disorder reveals distinct association profiles across social behaviour in the general population.

Many mental health conditions present a spectrum of social difficulties that overlaps with social behaviour in the general population including shared but little characterised genetic links. Here, we systematically investigate heterogeneity in shared genetic liabilities with attention-deficit/hyperactivity disorder (ADHD), autism spectrum disorders (ASD), bipolar disorder (BP), major depression (MD) and schizophrenia across a spectrum of different social symptoms. Longitudinally assessed low-prosociality and peer-problem scores in two UK population-based cohorts (4-17 years; parent- and teacher-reports; Avon Longitudinal Study of Parents and Children(ALSPAC): N ≤ 6,174; Twins Early Development Study(TEDS): N ≤ 7,112) were regressed on polygenic risk scores for disorder, as informed by genome-wide summary statistics from large consortia, using negative binomial regression models.