The manifest association structure of the single-factor model: insights from partial correlations

The association structure between manifest variables arising from the single-factor model is investigated using partial correlations. The additional insights to the practitioner provided by partial correlations for detecting a single-factor model are discussed. The parameter space for the partial correlations is presented, as are the patterns of signs in a matrix containing the partial correlations that are not compatible with a single-factor model

Elastic p-3He and n-3H scattering with two- and three-body forces

We report on a microscopic calculation of n-3H and p-3He scattering employing the Argonne v_{18} and v_8' nucleon-nucleon potentials with and without additional three-nucleon force. An R-matrix analysis of the p-3He and n-3H scattering data is presented. Comparisons are made for the phase shifts and a selection of measurements in both scattering systems. Differences between our calculation and the R-matrix results or the experimental data can be attributed to only two partial waves (3P0 and 3P2). We find the effect of the Urbana IX and the Texas-Los Alamos three-nucleon forces on the phase shifts to be negligible.Comment: submitted to Phys. Rev.

Questions of fairness and anti-doping in US cycling: The contrasting experiences of professionals and amateurs

The focus of researchers, media and policy on doping in cycling is often limited to the professional level of the sport. However, anti-doping test results since 2001 demonstrate that banned substances are also used by US cyclists at lower levels of the sport, necessitating a broader view of the patterns and motivations of substance use within the sport. In this article, we describe and explain the doping culture that has emerged in domestic US cycling among amateur and semi-professionals. Through analysis of records from sports governing bodies and journalistic reports, we assess the range of violation types and discuss the detection and punishing of riders who were not proven to have intended to cheat but became "collateral damage" in the war on doping. We argue that the phenomenon of doping is more complex than what has been shown to occur in elite sport, as it includes a wider variety of behaviours, situations and motivations. We develop fresh insights by examining cases where doping has been accidental, intrinsically motivated, non-performance enhancing or the result of prescribed medical treatments banned by anti-doping authorities. Such trends call into question the fairness of anti-doping measures, and we discuss the possibility of developing localised solutions to testing and sanctioning amateur athletes

The influence of first generation fertility and economic status on second generation fertility

This paper examines the impact of parental economic status and family size on the actual and expected fertility of adult children using longitudinal data from two generations of families participating in the Panel Study of Income Dynamics. There was a modest positive relationship between first generation family size and second generation fertility. More importantly, the ideal family size of the parental family was more closely related to fertility behavior and plans in the second generation than was actual parental family size. In addition, the data revealed the hypothesized negative correlation between parental financial status and second generation fertility behavior and plans. Several mechanisms which could produce the correlation between parental characteristics and the fertility of their children are explored.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/43511/1/11111_2005_Article_BF01253070.pd

Novel genetic loci associated with hippocampal volume

The hippocampal formation is a brain structure integrally involved in episodic memory, spatial navigation, cognition and stress responsiveness. Structural abnormalities in hippocampal volume and shape are found in several common neuropsychiatric disorders. To identify the genetic underpinnings of hippocampal structure here we perform a genome-wide association study (GWAS) of 33,536 individuals and discover six independent loci significantly associated with hippocampal volume, four of them novel. Of the novel loci, three lie within genes (ASTN2, DPP4 and MAST4) and one is found 200 kb upstream of SHH. A hippocampal subfield analysis shows that a locus within the MSRB3 gene shows evidence of a localized effect along the dentate gyrus, subiculum, CA1 and fissure. Further, we show that genetic variants associated with decreased hippocampal volume are also associated with increased risk for Alzheimer's disease (rg =-0.155). Our findings suggest novel biological pathways through which human genetic variation influences hippocampal volume and risk for neuropsychiatric illness

The genetic architecture of the human cerebral cortex

INTRODUCTION The cerebral cortex underlies our complex cognitive capabilities. Variations in human cortical surface area and thickness are associated with neurological, psychological, and behavioral traits and can be measured in vivo by magnetic resonance imaging (MRI). Studies in model organisms have identified genes that influence cortical structure, but little is known about common genetic variants that affect human cortical structure. RATIONALE To identify genetic variants associated with human cortical structure at both global and regional levels, we conducted a genome-wide association meta-analysis of brain MRI data from 51,665 individuals across 60 cohorts. We analyzed the surface area and average thickness of the whole cortex and 34 cortical regions with known functional specializations. RESULTS We identified 306 nominally genome-wide significant loci (P < 5 × 10−8) associated with cortical structure in a discovery sample of 33,992 participants of European ancestry. Of the 299 loci for which replication data were available, 241 loci influencing surface area and 14 influencing thickness remained significant after replication, with 199 loci passing multiple testing correction (P < 8.3 × 10−10; 187 influencing surface area and 12 influencing thickness). Common genetic variants explained 34% (SE = 3%) of the variation in total surface area and 26% (SE = 2%) in average thickness; surface area and thickness showed a negative genetic correlation (rG = −0.32, SE = 0.05, P = 6.5 × 10−12), which suggests that genetic influences have opposing effects on surface area and thickness. Bioinformatic analyses showed that total surface area is influenced by genetic variants that alter gene regulatory activity in neural progenitor cells during fetal development. By contrast, average thickness is influenced by active regulatory elements in adult brain samples, which may reflect processes that occur after mid-fetal development, such as myelination, branching, or pruning. When considered together, these results support the radial unit hypothesis that different developmental mechanisms promote surface area expansion and increases in thickness. To identify specific genetic influences on individual cortical regions, we controlled for global measures (total surface area or average thickness) in the regional analyses. After multiple testing correction, we identified 175 loci that influence regional surface area and 10 that influence regional thickness. Loci that affect regional surface area cluster near genes involved in the Wnt signaling pathway, which is known to influence areal identity. We observed significant positive genetic correlations and evidence of bidirectional causation of total surface area with both general cognitive functioning and educational attainment. We found additional positive genetic correlations between total surface area and Parkinson’s disease but did not find evidence of causation. Negative genetic correlations were evident between total surface area and insomnia, attention deficit hyperactivity disorder, depressive symptoms, major depressive disorder, and neuroticism. CONCLUSION This large-scale collaborative work enhances our understanding of the genetic architecture of the human cerebral cortex and its regional patterning. The highly polygenic architecture of the cortex suggests that distinct genes are involved in the development of specific cortical areas. Moreover, we find evidence that brain structure is a key phenotype along the causal pathway that leads from genetic variation to differences in general cognitive function