Dating Methods and Techniques at the John Hallowes Site (44WM6): A Seventeenth-Century Example

The John Hallowes site (44WM6) in Westmoreland County, Virginia, was excavated between July 1968 and August 1969. No report of the excavations was completed at that time, although an article summarizing the findings was published in Historical Archaeology in 1971, dating the site’s occupation to the period from the 1680s to 1716. From 2010 to 2012, a systematic reanalysis of the site, features, history, and artifacts was conducted by archaeologists at the University of Tennessee, Knoxville. Benefiting from nearly 40 years of advances in Chesapeake archaeology, the reanalysis has challenged accepted dates for the site’s occupation, which is now placed at 1647–1681. In this article, we will discuss the multiple lines of evidence in support of the newly interpreted date range

The association of genetic predisposition to depressive symptoms with non-suicidal and suicidal self-Injuries

Non-suicidal and suicidal self-injury are very destructive, yet surprisingly common behaviours. Depressed mood is a major risk factor for non-suicidal self-injury (NSSI), suicidal ideation and suicide attempts. We conducted a genetic risk prediction study to examine the polygenic overlap of depressive symptoms with lifetime NSSI, suicidal ideation, and suicide attempts in a sample of 6237 Australian adult twins and their family members (3740 females, mean age\ua0=\ua042.4\ua0years). Polygenic risk scores for depressive symptoms significantly predicted suicidal ideation, and some predictive ability was found for suicide attempts; the polygenic risk scores explained a significant amount of variance in suicidal ideation (lowest p\ua0=\ua00.008, explained variance ranging from 0.10 to 0.16\ua0%) and, less consistently, in suicide attempts (lowest p\ua0=\ua00.04, explained variance ranging from 0.12 to 0.23\ua0%). Polygenic risk scores did not significantly predict NSSI. Results highlight that individuals genetically predisposed to depression are also more likely to experience suicidal ideation/behaviour, whereas we found no evidence that this is also the case for NSSI

Kin-Aggregations Explain Chaotic Genetic Patchiness, a Commonly Observed Genetic Pattern, in a Marine Fish

The phenomenon of chaotic genetic patchiness is a pattern commonly seen in marine organisms, particularly those with demersal adults and pelagic larvae. This pattern is usually associated with sweepstakes recruitment and variable reproductive success. Here we investigate the biological underpinnings of this pattern in a species of marine goby Coryphopterus personatus. We find that populations of this species show tell-tale signs of chaotic genetic patchiness including: small, but significant, differences in genetic structure over short distances; a non-equilibrium or “chaotic” pattern of differentiation among locations in space; and within locus, within population deviations from the expectations of Hardy-Weinberg equilibrium (HWE). We show that despite having a pelagic larval stage, and a wide distribution across Caribbean coral reefs, this species forms groups of highly related individuals at small spatial scales (metres). These spatially clustered family groups cause the observed deviations from HWE and local population differentiation, a finding that is rarely demonstrated, but could be more common than previously thought

Scanning tunneling spectroscopy of methyl- and ethyl-terminated Si(111) surfaces

Methyl- and ethyl-terminated Si(111) surfaces prepared by a two-step chlorination/alkylation method were characterized by low temperature scanning tunneling spectroscopy (STS). The STS data showed remarkably low levels of midgap states on the CH3- and C2H5-terminated Si surfaces. A large conductance gap relative to the Si band gap was observed for both surfaces as well as for the hydrogen-terminated Si(111) surface. This large gap is ascribed to scanning tunneling microscope tip-induced band bending resulting from a low density of midgap states which avoid pinning of the Fermi levels on these passivated surfaces

Chlorination−Methylation of the Hydrogen-Terminated Silicon(111) Surface Can Induce a Stacking Fault in the Presence of Etch Pits

Recently, we reported STM images of the methylated Si(111) surface [prepared through chlorination−alkylation of the Si(111)−H surface] taken at 4.7 K, indicating that the torsion angle of the methyl group with respect to the subsurface silicon layer is φ = 23 ± 3°. Repulsions between H atoms in adjacent methyl groups are minimized at 30°, while repulsions between H atoms and second layer Si atoms are minimized at 60°. The experimental result of 23° is surprising because it suggests a tendency of the methyl group toward the eclipsed configuration (0°) rather than staggered (60°). In contrast, extensive fully periodic quantum mechanical Density Functional Theory studies of this surface give an equilibrium torsion angle of 37.5°, indicating a tendency toward the staggered configuration. This discrepancy can be resolved by showing that the CH_3 on the step edges and etch pits interacts repulsively with the CH_3 on the surface terraces unless a stacking fault is introduced between the first and second silicon layers of the Si(111)−CH_3 surface terraces. We propose that this could occur during the chlorination−alkylation of the Si(111)−H surface. This stacking fault model predicted φ = 22.5° measured with respect to the bulk (corresponding to φ = 37.5° with respect to the second layer Si atoms). This model can be tested by measuring the orientation of the CH_3 within the etch pits, which should have φ = 37.5°, or by making a surface without etch pits, which should have φ = 37.5°

Genotypic and phenotypic analyses of a Pseudomonas aeruginosa chronic bronchiectasis isolate reveal differences from cystic fibrosis and laboratory strains

Background Pseudomonas aeruginosa is an environmentally ubiquitous Gram-negative bacterium and important opportunistic human pathogen, causing severe chronic respiratory infections in patients with underlying conditions such as cystic fibrosis (CF) or bronchiectasis. In order to identify mechanisms responsible for adaptation during bronchiectasis infections, a bronchiectasis isolate, PAHM4, was phenotypically and genotypically characterized. Results This strain displays phenotypes that have been associated with chronic respiratory infections in CF including alginate over-production, rough lipopolysaccharide, quorum-sensing deficiency, loss of motility, decreased protease secretion, and hypermutation. Hypermutation is a key adaptation of this bacterium during the course of chronic respiratory infections and analysis indicates that PAHM4 encodes a mutated mutS gene responsible for a ~1,000-fold increase in mutation rate compared to wild-type laboratory strain P. aeruginosa PAO1. Antibiotic resistance profiles and sequence data indicate that this strain acquired numerous mutations associated with increased resistance levels to β-lactams, aminoglycosides, and fluoroquinolones when compared to PAO1. Sequencing of PAHM4 revealed a 6.38 Mbp genome, 5.9 % of which were unrecognized in previously reported P. aeruginosa genome sequences. Transcriptome analysis suggests a general down-regulation of virulence factors, while metabolism of amino acids and lipids is up-regulated when compared to PAO1 and metabolic modeling identified further potential differences between PAO1 and PAHM4. Conclusions This work provides insights into the potential differential adaptation of this bacterium to the lung of patients with bronchiectasis compared to other clinical settings such as cystic fibrosis, findings that should aid the development of disease-appropriate treatment strategies for P. aeruginosa infections

International meta-analysis of PTSD genome-wide association studies identifies sex- and ancestry-specific genetic risk loci.

The risk of posttraumatic stress disorder (PTSD) following trauma is heritable, but robust common variants have yet to be identified. In a multi-ethnic cohort including over 30,000 PTSD cases and 170,000 controls we conduct a genome-wide association study of PTSD. We demonstrate SNP-based heritability estimates of 5-20%, varying by sex. Three genome-wide significant loci are identified, 2 in European and 1 in African-ancestry analyses. Analyses stratified by sex implicate 3 additional loci in men. Along with other novel genes and non-coding RNAs, a Parkinson's disease gene involved in dopamine regulation, PARK2, is associated with PTSD. Finally, we demonstrate that polygenic risk for PTSD is significantly predictive of re-experiencing symptoms in the Million Veteran Program dataset, although specific loci did not replicate. These results demonstrate the role of genetic variation in the biology of risk for PTSD and highlight the necessity of conducting sex-stratified analyses and expanding GWAS beyond European ancestry populations