Course Engagement as a Mediator between Student-Instructor Personality Fit and Academic Outcomes

While the positive effects of personality similarity on attraction are well established, this research has made a limited transition to the person-environment (P-E) fit research. Following Schneider’s (1987) attraction-selection-attrition model based on similarity-attraction literature, the following study proposes that student-instructor relationships characterized by high levels of perceived personality congruence (i.e., fit) will lead to more motivated and engaged students. The study proposes a model to explain the relationship between student-instructor fit, student course engagement, and student outcomes, whereby engagement should mediate the relationship between perceived student-instructor personality fit and student outcomes of course performance, course satisfaction, and commitment to the academic discipline. A sample of introductory psychology course students completed perceived personality fit and student course engagement questionnaires midway through the semester and final course evaluations at the close of the semester. The proposed theoretical model was not supported; however, findings indicated a significant relationship between personality fit and elements of engagement. Furthermore, some factors of engagement discriminately predicted course outcomes. The proposed role of engagement as a mediating variable was only moderately supported in the fit-satisfaction relationship. Modifications to the proposed model are explored and implications for future research in student-instructor fit and student course engagement are discussed

A common cardiac sodium channel variant associated with sudden infant death in African Americans, SCN5A S1103Y.

Thousands die each year from sudden infant death syndrome (SIDS). Neither the cause nor basis for varied prevalence in different populations is understood. While 2 cases have been associated with mutations in type Valpha, cardiac voltage-gated sodium channels (SCN5A), the "Back to Sleep" campaign has decreased SIDS prevalence, consistent with a role for environmental influences in disease pathogenesis. Here we studied SCN5A in African Americans. Three of 133 SIDS cases were homozygous for the variant S1103Y. Among controls, 120 of 1,056 were carriers of the heterozygous genotype, which was previously associated with increased risk for arrhythmia in adults. This suggests that infants with 2 copies of S1103Y have a 24-fold increased risk for SIDS. Variant Y1103 channels were found to operate normally under baseline conditions in vitro. As risk factors for SIDS include apnea and respiratory acidosis, Y1103 and wild-type channels were subjected to lowered intracellular pH. Only Y1103 channels gained abnormal function, demonstrating late reopenings suppressible by the drug mexiletine. The variant appeared to confer susceptibility to acidosis-induced arrhythmia, a gene-environment interaction. Overall, homozygous and rare heterozygous SCN5A missense variants were found in approximately 5% of cases. If our findings are replicated, prospective genetic testing of SIDS cases and screening with counseling for at-risk families warrant consideration

A Multi-Code Analysis Toolkit for Astrophysical Simulation Data

The analysis of complex multiphysics astrophysical simulations presents a unique and rapidly growing set of challenges: reproducibility, parallelization, and vast increases in data size and complexity chief among them. In order to meet these challenges, and in order to open up new avenues for collaboration between users of multiple simulation platforms, we present yt (available at http://yt.enzotools.org/), an open source, community-developed astrophysical analysis and visualization toolkit. Analysis and visualization with yt are oriented around physically relevant quantities rather than quantities native to astrophysical simulation codes. While originally designed for handling Enzo's structure adaptive mesh refinement (AMR) data, yt has been extended to work with several different simulation methods and simulation codes including Orion, RAMSES, and FLASH. We report on its methods for reading, handling, and visualizing data, including projections, multivariate volume rendering, multi-dimensional histograms, halo finding, light cone generation and topologically-connected isocontour identification. Furthermore, we discuss the underlying algorithms yt uses for processing and visualizing data, and its mechanisms for parallelization of analysis tasks.Comment: 18 pages, 6 figures, emulateapj format. Resubmitted to Astrophysical Journal Supplement Series with revisions from referee. yt can be found at http://yt.enzotools.org

The Formation of Population III Binaries from Cosmological Initial Conditions

Previous high resolution cosmological simulations predict the first stars to appear in the early universe to be very massive and to form in isolation. Here we discuss a cosmological simulation in which the central 50M{sub {circle_dot}} clump breaks up into two cores, having a mass ratio of two to one, with one fragment collapsing to densities of 10{sup -8}g cm{sup -3}. The second fragment, at a distance of {approx}800 astronomical units, is also optically thick to its own cooling radiation from molecular hydrogen lines, but is still able to cool via collision-induced emission. The two dense peaks will continue to accrete from the surrounding cold gas reservoir over a period of {approx} 10{sup 5} years and will likely form a binary star system

Mulching woody ornamentals with organic materials

A wide variety of materials are sold as mulches and used in landscapes. This publication discusses mulching woody ornamentals (trees and shrubs) with organic materials. It covers the reasons for mulching, how to apply mulch, and how to maintain its beneficial effects over time. The information is presented in a question-and-answer format. The general principles described here also apply to a wide range of other organic materials. A table is included to help you compare the characteristics of materials used as mulches in western Oregon.Published March 2009. Reviewed December 2013. Please look for up-to-date information in the OSU Extension Catalog: http://extension.oregonstate.edu/catalo

Rare deleterious mutations of the gene EFR3A in autism spectrum disorders

Background: Whole-exome sequencing studies in autism spectrum disorder (ASD) have identified de novo mutations in novel candidate genes, including the synaptic gene Eighty-five Requiring 3A (EFR3A). EFR3A is a critical component of a protein complex required for the synthesis of the phosphoinositide PtdIns4P, which has a variety of functions at the neural synapse. We hypothesized that deleterious mutations in EFR3A would be significantly associated with ASD. Methods: We conducted a large case/control association study by deep resequencing and analysis of whole-exome data for coding and splice site variants in EFR3A. We determined the potential impact of these variants on protein structure and function by a variety of conservation measures and analysis of the Saccharomyces cerevisiae Efr3 crystal structure. We also analyzed the expression pattern of EFR3A in human brain tissue. Results: Rare nonsynonymous mutations in EFR3A were more common among cases (16 / 2,196 = 0.73%) than matched controls (12 / 3,389 = 0.35%) and were statistically more common at conserved nucleotides based on an experiment-wide significance threshold (P = 0.0077, permutation test). Crystal structure analysis revealed that mutations likely to be deleterious were also statistically more common in cases than controls (P = 0.017, Fisher exact test). Furthermore, EFR3A is expressed in cortical neurons, including pyramidal neurons, during human fetal brain development in a pattern consistent with ASD-related genes, and it is strongly co-expressed (P < 2.2 × 10−16, Wilcoxon test) with a module of genes significantly associated with ASD. Conclusions: Rare deleterious mutations in EFR3A were found to be associated with ASD using an experiment-wide significance threshold. Synaptic phosphoinositide metabolism has been strongly implicated in syndromic forms of ASD. These data for EFR3A strengthen the evidence for the involvement of this pathway in idiopathic autism

Molecular Cytogenetic Analysis and Resequencing of Contactin Associated Protein-Like 2 in Autism Spectrum Disorders

Autism spectrum disorders (ASD) are a group of related neurodevelopmental syndromes with complex genetic etiology.1 We identified a de novo chromosome 7q inversion disrupting Autism susceptibility candidate 2 (AUTS2) and Contactin Associated Protein-Like 2 (CNTNAP2) in a child with cognitive and social delay. We focused our initial analysis on CNTNAP2 based on our demonstration of disruption of Contactin 4 (CNTN4) in a patient with ASD;2 the recent finding of rare homozygous mutations in CNTNAP2 leading to intractable seizures and autism;3 and in situ and biochemical analyses reported herein that confirm expression in relevant brain regions and demonstrate the presence of CNTNAP2 in the synaptic plasma membrane fraction of rat forebrain lysates. We comprehensively resequenced CNTNAP2 in 635 patients and 942 controls. Among patients, we identified a total of 27 nonsynonymous changes; 13 were rare and unique to patients and 8 of these were predicted to be deleterious by bioinformatic approaches and/or altered residues conserved across all species. One variant at a highly conserved position, I869T, was inherited by four affected children in three unrelated families, but was not found in 4010 control chromosomes (p = 0.014). Overall, this resequencing data demonstrated a modest nonsignificant increase in the burden of rare variants in cases versus controls. Nonethless, when viewed in light of two independent studies published in this issue of AJHG showing a relationship between ASD and common CNTNAP2 alleles,4,5 the cytogenetic and mutation screening data suggest that rare variants may also contribute to the pathophysiology of ASD, but place limits on the magnitude of this contribution

No Evidence for Association of Autism with Rare Heterozygous Point Mutations in Contactin-Associated Protein-Like 2 (CNTNAP2), or in Other Contactin-Associated Proteins or Contactins

Contactins and Contactin-Associated Proteins, and Contactin-Associated Protein-Like 2 (CNTNAP2) in particular, have been widely cited as autism risk genes based on findings from homozygosity mapping, molecular cytogenetics, copy number variation analyses, and both common and rare single nucleotide association studies. However, data specifically with regard to the contribution of heterozygous single nucleotide variants (SNVs) have been inconsistent. In an effort to clarify the role of rare point mutations in CNTNAP2 and related gene families, we have conducted targeted next-generation sequencing and evaluated existing sequence data in cohorts totaling 2704 cases and 2747 controls. We find no evidence for statistically significant association of rare heterozygous mutations in any of the CNTN or CNTNAP genes, including CNTNAP2, placing marked limits on the scale of their plausible contribution to risk