Increased atmospheric SO₂ detected from changes in leaf physiognomy across the Triassic-Jurassic boundary interval of East Greenland

This is the final version of the article. Available from the publisher via the DOI in this record.The Triassic-Jurassic boundary (Tr-J; ∼201 Ma) is marked by a doubling in the concentration of atmospheric CO2, rising temperatures, and ecosystem instability. This appears to have been driven by a major perturbation in the global carbon cycle due to massive volcanism in the Central Atlantic Magmatic Province. It is hypothesized that this volcanism also likely delivered sulphur dioxide (SO2) to the atmosphere. The role that SO2 may have played in leading to ecosystem instability at the time has not received much attention. To date, little direct evidence has been presented from the fossil record capable of implicating SO2 as a cause of plant extinctions at this time. In order to address this, we performed a physiognomic leaf analysis on well-preserved fossil leaves, including Ginkgoales, bennettites, and conifers from nine plant beds that span the Tr-J boundary at Astartekløft, East Greenland. The physiognomic responses of fossil taxa were compared to the leaf size and shape variations observed in nearest living equivalent taxa exposed to simulated palaeoatmospheric treatments in controlled environment chambers. The modern taxa showed a statistically significant increase in leaf roundness when fumigated with SO2. A similar increase in leaf roundness was also observed in the Tr-J fossil taxa immediately prior to a sudden decrease in their relative abundances at Astartekløft. This research reveals that increases in atmospheric SO2 can likely be traced in the fossil record by analyzing physiognomic changes in fossil leaves. A pattern of relative abundance decline following increased leaf roundness for all six fossil taxa investigated supports the hypothesis that SO2 had a significant role in Tr-J plant extinctions. This finding highlights that the role of SO2 in plant biodiversity declines across other major geological boundaries coinciding with global scale volcanism should be further explored using leaf physiognomy.KLB acknowledges funding through a UCD Research Demonstratorship and Science Foundation Ireland (SFI 11/PI/1103). CMB acknowledges funding through a European Union Marie Curie Intra-European Fellowship FILE PIEF-GA-2009-253780 and a Marie Curie Career Integration Grant PyroMap PCIG10-GA- 2011-303610. MH acknowledges funding though PEA-IEF-2010-275626. JMC acknowledges funding through Science Foundation Ireland (SFI 11/PI/1103) and a European Research Council Starting Investigator Grant (ERC-2001-StG_279962). JMC, CMB, and MH acknowledge funding through a Marie Curie research grant (MEXT-CT-2006-042531)

Common DNA markers can account for more than half of the genetic influence on cognitive abilities

For nearly a century, twin and adoption studies have yielded substantial estimates of heritability for cognitive abilities, although it has proved difficult for genomewide-association studies to identify the genetic variants that account for this heritability (i.e., the missing-heritability problem). However, a new approach, genomewide complex-trait analysis (GCTA), forgoes the identification of individual variants to estimate the total heritability captured by common DNA markers on genotyping arrays. In the same sample of 3,154 pairs of 12-year-old twins, we directly compared twin-study heritability estimates for cognitive abilities (language, verbal, nonverbal, and general) with GCTA estimates captured by 1.7 million DNA markers. We found that DNA markers tagged by the array accounted for .66 of the estimated heritability, reaffirming that cognitive abilities are heritable. Larger sample sizes alone will be sufficient to identify many of the genetic variants that influence cognitive abilities

From observational to dynamic genetics.

Twin and family studies have shown that most traits are at least moderately heritable. But what are the implications of finding genetic influence for the design of intervention and prevention programs? For complex traits, heritability does not mean immutability, and research has shown that genetic influences can change with age, context, and in response to behavioral and drug interventions. The most significant implications for intervention will come when we move from observational genetics to investigating dynamic genetics, including genetically sensitive interventions. Future interventions should be designed to overcome genetic risk and draw upon genetic strengths by changing the environment

Common Genetic Variants Explain the Majority of the Correlation Between Height and Intelligence : The Generation Scotland Study

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Emotional over- and under-eating in early childhood are learned not inherited

Emotional overeating (EOE) has been associated with increased obesity risk, while emotional undereating (EUE) may be protective. Interestingly, EOE and EUE tend to correlate positively, but it is unclear whether they reflect different aspects of the same underlying trait, or are distinct behaviours with different aetiologies. Data were from 2054 five-year-old children from the Gemini twin birth cohort, including parental ratings of child EOE and EUE using the Child Eating Behaviour Questionnaire. Genetic and environmental influences on variation and covariation in EUE and EOE were established using a bivariate Twin Model. Variation in both behaviours was largely explained by aspects of the environment completely shared by twin pairs (EOE: C = 90%, 95% CI: 89%-92%; EUE: C = 91%, 95% CI: 90%-92%). Genetic influence was low (EOE: A = 7%, 95% CI: 6%-9%; EUE: A = 7%, 95% CI: 6%-9%). EOE and EUE correlated positively (r = 0.43, p < 0.001), and this association was explained by common shared environmental influences (BivC = 45%, 95% CI: 40%-50%). Many of the shared environmental influences underlying EUE and EOE were the same (rC = 0.50, 95% CI: 0.44, 0.55). Childhood EOE and EUE are etiologically distinct. The tendency to eat more or less in response to emotion is learned rather than inherited

Impact of facial conformation on canine health: Brachycephalic Obstructive Airway Syndrome

The domestic dog may be the most morphologically diverse terrestrial mammalian species known to man; pedigree dogs are artificially selected for extreme aesthetics dictated by formal Breed Standards, and breed-related disorders linked to conformation are ubiquitous and diverse. Brachycephaly–foreshortening of the facial skeleton–is a discrete mutation that has been selected for in many popular dog breeds e.g. the Bulldog, Pug, and French Bulldog. A chronic, debilitating respiratory syndrome, whereby soft tissue blocks the airways, predominantly affects dogs with this conformation, and thus is labelled Brachycephalic Obstructive Airway Syndrome (BOAS). Despite the name of the syndrome, scientific evidence quantitatively linking brachycephaly with BOAS is lacking, but it could aid efforts to select for healthier conformations. Here we show, in (1) an exploratory study of 700 dogs of diverse breeds and conformations, and (2) a confirmatory study of 154 brachycephalic dogs, that BOAS risk increases sharply in a non-linear manner as relative muzzle length shortens. BOAS only occurred in dogs whose muzzles comprised less than half their cranial lengths. Thicker neck girths also increased BOAS risk in both populations: a risk factor for human sleep apnoea and not previously realised in dogs; and obesity was found to further increase BOAS risk. This study provides evidence that breeding for brachycephaly leads to an increased risk of BOAS in dogs, with risk increasing as the morphology becomes more exaggerated. As such, dog breeders and buyers should be aware of this risk when selecting dogs, and breeding organisations should actively discourage exaggeration of this high-risk conformation in breed standards and the show ring

Longitudinal analysis of vertebral fracture and BMD in a Canadian cohort of adult cystic fibrosis patients

<p>Abstract</p> <p>Background</p> <p>Vertebral fractures in patients with cystic fibrosis (CF) may contribute to an accelerated decline in lung function and can be a contraindication to lung transplantation. In this study, we examined longitudinal change in bone mineral density (BMD) and the prevalence of vertebral fractures in adult CF patients, without lung-transplant, attending a Canadian specialty clinic.</p> <p>Methods</p> <p>Retrospective chart review of all patients attending an Adult Cystic Fibrosis Clinic at Hamilton Health Sciences in Hamilton, Canada. Forty-nine of 56 adults met inclusion criteria. Chest radiographs were graded by consensus approach using Genant's semi-quantitative method to identify and grade fractured vertebrae. Dual x-ray absorptiometry (DXA) scans were also reviewed.</p> <p>Results</p> <p>The mean age of the cohort was 25.2 years (SD 9.4), 43% were male. The mean body mass index (BMI) was 19.8 (2.8) for males and 21.7 (5.1) for females. At baseline, the rate of at least one vertebral fracture was 16.3%; rising to 21.3% (prevalent and incident) after a 3-year follow-up. The mean BMD T-or Z-scores at baseline were -0.80 (SD 1.1) at the lumbar spine, -0.57 (SD 0.97) at the proximal femur, and -0.71 (SD 1.1) at the whole body. Over approximately 4-years, the mean percent change in BMD was -1.93% at the proximal femur and -0.73% at the lumbar spine.</p> <p>Conclusion</p> <p>Approximately one in five CF patients demonstrated at least one or more vertebral fractures. Moderate declines in BMD were observed. Given the high rate of vertebral fractures noted in this cohort of adult CF patients, and the negative impact they have on compromised lung functioning, regular screening for vertebral fractures should be considered on routine chest radiographs.</p

Endosialin (TEM1, CD248) is a marker of stromal fibroblasts and is not selectively expressed on tumour endothelium

AbstractFibroblasts are a diverse cell type and display clear topographic differentiation and positional memory. In a screen for fibroblast specific markers we have characterized four monoclonal antibodies to endosialin (TEM1/CD248). Previous studies have reported that endosialin is a tumour endothelium marker and is localized intracellularly. We demonstrate conclusively that endosialin is a cell surface glycoprotein and is predominantly expressed by fibroblasts and a subset of pericytes associated with tumour vessels but not by tumour endothelium. These novel antibodies will facilitate the isolation and classification of fibroblast and pericyte lineages as well as the further functional analysis of endosialin

Gene-Environment Interaction in the Etiology of Mathematical Ability Using SNP Sets

Mathematics ability and disability is as heritable as other cognitive abilities and disabilities, however its genetic etiology has received relatively little attention. In our recent genome-wide association study of mathematical ability in 10-year-old children, 10 SNP associations were nominated from scans of pooled DNA and validated in an individually genotyped sample. In this paper, we use a ‘SNP set’ composite of these 10 SNPs to investigate gene-environment (GE) interaction, examining whether the association between the 10-SNP set and mathematical ability differs as a function of ten environmental measures in the home and school in a sample of 1888 children with complete data. We found two significant GE interactions for environmental measures in the home and the school both in the direction of the diathesis-stress type of GE interaction: The 10-SNP set was more strongly associated with mathematical ability in chaotic homes and when parents are negative

Genetic architecture of Environmental Sensitivity reflects multiple heritable components: a twin study with adolescents

Humans differ substantially in how strongly they respond to similar experiences. Theory suggests that such individual differences in susceptibility to environmental influences have a genetic basis. The present study investigated the genetic architecture of Environmental Sensitivity (ES) by estimating its heritability, exploring the presence of multiple heritable components and its genetic overlap with common personality traits. ES was measured with the Highly Sensitive Child (HSC) questionnaire and heritability estimates were obtained using classic twin design methodology in a sample of 2868 adolescent twins. Results indicate that the heritability of sensitivity was 0.47, and that the genetic influences underlying sensitivity to negative experiences are relatively distinct from sensitivity to more positive aspects of the environment, supporting a multi-dimensional genetic model of ES. The correlation between sensitivity, neuroticism and extraversion was largely explained by shared genetic influences, with differences between these traits mainly attributed to unique environmental influences operating on each trait