A Model of Habitability Within the Milky Way Galaxy

We present a model of the Galactic Habitable Zone (GHZ), described in terms of the spatial and temporal dimensions of the Galaxy that may favour the development of complex life. The Milky Way galaxy is modelled using a computational approach by populating stars and their planetary systems on an individual basis using Monte-Carlo methods. We begin with well-established properties of the disk of the Milky Way, such as the stellar number density distribution, the initial mass function, the star formation history, and the metallicity gradient as a function of radial position and time. We vary some of these properties, creating four models to test the sensitivity of our assumptions. To assess habitability on the Galactic scale, we model supernova rates, planet formation, and the time required for complex life to evolve. Our study improves on other literature on the GHZ by populating stars on an individual basis and by modelling SNII and SNIa sterilizations by selecting their progenitors from within this preexisting stellar population. Furthermore, we consider habitability on tidally locked and non-tidally locked planets separately, and study habitability as a function of height above and below the Galactic midplane. In the model that most accurately reproduces the properties of the Galaxy, the results indicate that an individual SNIa is ~5.6 \times more lethal than an individual SNII on average. In addition, we predict that ~1.2% of all stars host a planet that may have been capable of supporting complex life at some point in the history of the Galaxy. Of those stars with a habitable planet, ~75% of planets are predicted to be in a tidally locked configuration with their host star. The majority of these planets that may support complex life are found towards the inner Galaxy, distributed within, and significantly above and below, the Galactic midplane.Comment: Accepted for publication in Astrobiology. 40 pages, 12 figures, 3 table

Clock drawing performance in cognitively normal elderly

The Clock Drawing Test (CDT) is a common neuropsychological measure sensitive to cognitive changes and functional skills (e.g., driving test performance) among older adults. However, normative data have not been adequately developed. We report the distribution of CDT scores using three common scoring systems [Mendez, M. F., Ala, T., & Underwood, K. L. (1992). Development of scoring criteria for the Clock Drawing Task in Alzheimer's Disease. Journal of the American Geriatrics Society, 40, 1095-1099; Cahn, D. A., Salmon, D. P., Monsch, A. U., Butters, N., Wiederholt, W. C., & Corey-Bloom, J. (1996). Screening for dementia of the Alzheimer type in the community: The utility of the Clock Drawing Test. Archives of Clinical Neuropsychology, 11(6), 529-539], among 207 cognitively normal elderly. The systems were well correlated, took little time to use, and had high inter-rater reliability. We found statistically significant differences in CDT scores based on age and WRAT-3 Reading score, a marker of education quality. We present means, standard deviations, and t- and z-scores based on these subgroups. We found that "normal" CDT performance includes a wider distribution of scores than previously reported. Our results may serve as useful comparisons for clinicians wishing to know whether their patients perform in the general range of cognitively normal elderly. © 2007 National Academy of Neuropsychology

An integrated map of structural variation in 2,504 human genomes

Structural variants are implicated in numerous diseases and make up the majority of varying nucleotides among human genomes. Here we describe an integrated set of eight structural variant classes comprising both balanced and unbalanced variants, which we constructed using short-read DNA sequencing data and statistically phased onto haplotype blocks in 26 human populations. Analysing this set, we identify numerous gene-intersecting structural variants exhibiting population stratification and describe naturally occurring homozygous gene knockouts that suggest the dispensability of a variety of human genes. We demonstrate that structural variants are enriched on haplotypes identified by genome-wide association studies and exhibit enrichment for expression quantitative trait loci. Additionally, we uncover appreciable levels of structural variant complexity at different scales, including genic loci subject to clusters of repeated rearrangement and complex structural variants with multiple breakpoints likely to have formed through individual mutational events. Our catalogue will enhance future studies into structural variant demography, functional impact and disease association. © 2015 Macmillan Publishers Limited. All rights reserved