Professor-Student Rapport Scale: Psychometric properties of the brief version

The original Professor-Student Rapport Scale contained 34 items and predicted several single-item student outcomes. A high level of internal consistency encouraged the development of a shorter measure in order to address apparent redundancy. Our goals in the current study were to provide psychometric data for the brief version of the scale and to evaluate its ability to predict student outcomes based on more rigorous student-outcome assessments. We found the brief version of the scale demonstrated reliability and validity and significantly predicted rigorous assessments of student outcomes. We suggest that the brief version of the Professor-Student Rapport Scale, with only 6 items, can be used for formative assessment. Instructors can address issues concerning rapport and potentially enhance student outcomes

Professor Age and Gender Affect Student Perceptions and Grades

Student evaluations provide rich information about teaching performance, but a number of factors beyond teacher effectiveness influence student evaluations. In this study we examined the effects of professor gender and perceived age on ratings of effectiveness and rapport as well as academic performance. Participants (N = 308) saw a picture of either a young or old male or female professor while listening to an audio lecture. Students reported greater perceived rapport with the female relative to the male professors and for younger versus older professors. However, students reported the male professors as more competent than the female professors. An interaction revealed that among female professors only, younger women were rated higher on rapport than comparison conditions. Thus, age and gender bias likely impact student evaluations of teaching. Our study also revealed higher quiz grades in the older-female condition, perhaps best explained by the older woman activating a schema for “mom.” Taken together, our results indicate that professor competence and kindness may foster learning best in the context of high expectations

AXTAR: Mission Design Concept

The Advanced X-ray Timing Array (AXTAR) is a mission concept for X-ray timing of compact objects that combines very large collecting area, broadband spectral coverage, high time resolution, highly flexible scheduling, and an ability to respond promptly to time-critical targets of opportunity. It is optimized for submillisecond timing of bright Galactic X-ray sources in order to study phenomena at the natural time scales of neutron star surfaces and black hole event horizons, thus probing the physics of ultradense matter, strongly curved spacetimes, and intense magnetic fields. AXTAR's main instrument, the Large Area Timing Array (LATA) is a collimated instrument with 2-50 keV coverage and over 3 square meters effective area. The LATA is made up of an array of supermodules that house 2-mm thick silicon pixel detectors. AXTAR will provide a significant improvement in effective area (a factor of 7 at 4 keV and a factor of 36 at 30 keV) over the RXTE PCA. AXTAR will also carry a sensitive Sky Monitor (SM) that acts as a trigger for pointed observations of X-ray transients in addition to providing high duty cycle monitoring of the X-ray sky. We review the science goals and technical concept for AXTAR and present results from a preliminary mission design study.Comment: 19 pages, 10 figures, to be published in Space Telescopes and Instrumentation 2010: Ultraviolet to Gamma Ray, Proceedings of SPIE Volume 773

Genome-wide association and epidemiological analyses reveal common genetic origins between uterine leiomyomata and endometriosis

Abstract: Uterine leiomyomata (UL) are the most common neoplasms of the female reproductive tract and primary cause for hysterectomy, leading to considerable morbidity and high economic burden. Here we conduct a GWAS meta-analysis in 35,474 cases and 267,505 female controls of European ancestry, identifying eight novel genome-wide significant (P < 5 × 10−8) loci, in addition to confirming 21 previously reported loci, including multiple independent signals at 10 loci. Phenotypic stratification of UL by heavy menstrual bleeding in 3409 cases and 199,171 female controls reveals genome-wide significant associations at three of the 29 UL loci: 5p15.33 (TERT), 5q35.2 (FGFR4) and 11q22.3 (ATM). Four loci identified in the meta-analysis are also associated with endometriosis risk; an epidemiological meta-analysis across 402,868 women suggests at least a doubling of risk for UL diagnosis among those with a history of endometriosis. These findings increase our understanding of genetic contribution and biology underlying UL development, and suggest overlapping genetic origins with endometriosis

Genome-wide meta-analyses reveal novel loci for verbal short-term memory and learning

Understanding the genomic basis of memory processes may help in combating neurodegenerative disorders. Hence, we examined the associations of common genetic variants with verbal short-term memory and verbal learning in adults without dementia or stroke (N = 53,637). We identified novel loci in the intronic region of CDH18, and at 13q21 and 3p21.1, as well as an expected signal in the APOE/APOC1/TOMM40 region. These results replicated in an independent sample. Functional and bioinformatic analyses supported many of these loci and further implicated POC1. We showed that polygenic score for verbal learning associated with brain activation in right parieto-occipital region during working memory task. Finally, we showed genetic correlations of these memory traits with several neurocognitive and health outcomes. Our findings suggest a role of several genomic loci in verbal memory processes.Peer reviewe

Identification of common genetic risk variants for autism spectrum disorder

Autism spectrum disorder (ASD) is a highly heritable and heterogeneous group of neurodevelopmental phenotypes diagnosed in more than 1% of children. Common genetic variants contribute substantially to ASD susceptibility, but to date no individual variants have been robustly associated with ASD. With a marked sample-size increase from a unique Danish population resource, we report a genome-wide association meta-analysis of 18,381 individuals with ASD and 27,969 controls that identified five genome-wide-significant loci. Leveraging GWAS results from three phenotypes with significantly overlapping genetic architectures (schizophrenia, major depression, and educational attainment), we identified seven additional loci shared with other traits at equally strict significance levels. Dissecting the polygenic architecture, we found both quantitative and qualitative polygenic heterogeneity across ASD subtypes. These results highlight biological insights, particularly relating to neuronal function and corticogenesis, and establish that GWAS performed at scale will be much more productive in the near term in ASD

Polygenic prediction of educational attainment within and between families from genome-wide association analyses in 3 million individuals

We conduct a genome-wide association study (GWAS) of educational attainment (EA) in a sample of ~3 million individuals and identify 3,952 approximately uncorrelated genome-wide-significant single-nucleotide polymorphisms (SNPs). A genome-wide polygenic predictor, or polygenic index (PGI), explains 12-16% of EA variance and contributes to risk prediction for ten diseases. Direct effects (i.e., controlling for parental PGIs) explain roughly half the PGI's magnitude of association with EA and other phenotypes. The correlation between mate-pair PGIs is far too large to be consistent with phenotypic assortment alone, implying additional assortment on PGI-associated factors. In an additional GWAS of dominance deviations from the additive model, we identify no genome-wide-significant SNPs, and a separate X-chromosome additive GWAS identifies 57

Association studies of up to 1.2 million individuals yield new insights into the genetic etiology of tobacco and alcohol use

Tobacco and alcohol use are leading causes of mortality that influence risk for many complex diseases and disorders 1 . They are heritable 2,3 and etiologically related 4,5 behaviors that have been resistant to gene discovery efforts 6–11 . In sample sizes up to 1.2 million individuals, we discovered 566 genetic variants in 406 loci associated with multiple stages of tobacco use (initiation, cessation, and heaviness) as well as alcohol use, with 150 loci evidencing pleiotropic association. Smoking phenotypes were positively genetically correlated with many health conditions, whereas alcohol use was negatively correlated with these conditions, such that increased genetic risk for alcohol use is associated with lower disease risk. We report evidence for the involvement of many systems in tobacco and alcohol use, including genes involved in nicotinic, dopaminergic, and glutamatergic neurotransmission. The results provide a solid starting point to evaluate the effects of these loci in model organisms and more precise substance use measures

Rare and low-frequency coding variants alter human adult height

Height is a highly heritable, classic polygenic trait with ~700 common associated variants identified so far through genome - wide association studies . Here , we report 83 height - associated coding variants with lower minor allele frequenc ies ( range of 0.1 - 4.8% ) and effects of up to 2 16 cm /allele ( e.g. in IHH , STC2 , AR and CRISPLD2 ) , >10 times the average effect of common variants . In functional follow - up studies, rare height - increasing alleles of STC2 (+1 - 2 cm/allele) compromise d proteolytic inhibition of PAPP - A and increased cleavage of IGFBP - 4 in vitro , resulting in higher bioavailability of insulin - like growth factors . The se 83 height - associated variants overlap genes mutated in monogenic growth disorders and highlight new biological candidates ( e.g. ADAMTS3, IL11RA, NOX4 ) and pathways ( e.g . proteoglycan/ glycosaminoglycan synthesis ) involved in growth . Our results demonstrate that sufficiently large sample sizes can uncover rare and low - frequency variants of moderate to large effect associated with polygenic human phenotypes , and that these variants implicate relevant genes and pathways