Transitions in coral reef accretion rates linked to intrinsic ecological shifts on turbid-zone nearshore reefs

This is the final version of the article. Available from the Geological Society of America via the DOI in this record.Nearshore coral communities within turbid settings are typically perceived to have limited reef-building capacity. However, several recent studies have reported reef growth over millennial time scales within such environments and have hypothesized that depth-variable community assemblages may act as equally important controls on reef growth as they do in clear-water settings. Here, we explicitly test this idea using a newly compiled chronostratigraphic record (31 cores, 142 radiometric dates) from seven proximal (but discrete) nearshore coral reefs located along the central Great Barrier Reef (Australia). Uniquely, these reefs span distinct stages of geomorphological maturity, as reflected in their elevations below sea level. Integrated age-depth and ecological data sets indicate that contemporary coral assemblage shifts, associated with changing light availability and wave exposure as reefs shallowed, coincided with transitions in accretion rates at equivalent core depths. Reef initiation followed a regional ∼1 m drop in sea level (1200–800 calibrated yr B.P.) which would have lowered the photic floor and exposed new substrate for coral recruitment by winnowing away fine seafloor sediments. We propose that a two-way feedback mechanism exists where past growth history influences current reef morphology and ecology, ultimately driving future reef accumulation and morphological change. These findings provide the first empirical evidence that nearshore reef growth trajectories are intrinsically driven by changes in coral community structure as reefs move toward sea level, a finding of direct significance for predicting the impacts of extrinsically driven ecological change (e.g., coral-algal phase shifts) on reef growth potential within the wider coastal zone on the Great Barrier Reef.This work was supported by Natural Environment Research Council (NERC) grant NE/J023329/1 to Perry and Smithers and NERC Radiocarbon Dating Allocations 1727.1013 and 1838.1014 to Morgan, Perry, and Gulliver

Projections of coral cover and habitat change on turbid reefs under future sea-level rise

This is the final version. Available on open access from the Royal Society via the DOI in this recordData accessibility: All field datasets are available from the NERC datacentre: http://www.bgs.ac.uk/services/ngdc/accessions/index.html?simpleText=Great%20Barrier%20Reef#item76769. The model data that support the findings of this study are openly available at: https://github.com/rudyarthur/coral.Global sea-level rise (SLR) is projected to increase water depths above coral reefs. Although the impacts of climate disturbance events on coral cover and three-dimensional complexity are well documented, knowledge of how higher sea levels will influence future reef habitat extent and bioconstruction is limited. Here, we use 31 reef cores, coupled with detailed benthic ecological data, from turbid reefs on the central Great Barrier Reef, Australia, to model broad-scale changes in reef habitat following adjustments to reef geomorphology under different SLR scenarios. Model outputs show that modest increases in relative water depth above reefs (Representative Concentration Pathway (RCP) 4.5) over the next 100 years will increase the spatial extent of habitats with low coral cover and generic diversity. More severe SLR (RCP8.5) will completely submerge reef flats and move reef slope coral communities below the euphotic depth, despite the high vertical accretion rates that characterize these reefs. Our findings suggest adverse future trajectories associated with high emission climate scenarios which could threaten turbid reefs globally and their capacity to act as coral refugia from climate change.Natural Environment Research Council (NERC

Social relationships and the risk of incident heart failure: results from a prospective population-based study of older men

Aims: Limited social relationships, particularly in older adults, have been implicated as a risk factor for cardiovascular disease. However, little is known about the associations between poor social relationships and heart failure incidence. Methods and results: Prospective study of socially representative men aged 60-79 years drawn from general practices in 24 British towns and followed up for a maximum of 18 years. A total of 3698 participants with no previous diagnosis of heart failure were included. Information on social relationships was based on a combination of marital status, living circumstances, and social contacts with friends and family. These provided information on contact frequency, contact satisfaction, and a social relationship score (low to high) combining frequency and satisfaction with contact. Heart failure included both incidents non-fatal heart failure and death from heart failure. Among 3698 participants, 330 developed heart failure. Men with low compared to high frequency of contact with family and friends had an increased risk of incident heart failure [hazard ratio (HR) 1.59, 95% confidence interval (CI) 1.15-2.18]; this remained statistically significant after adjustment for social class, behavioural, and biological risk factors. Low compared to high scores for satisfaction with contacts was associated with increased risk of heart failure (adjusted HR = 1.54; 95% CI 1.14-2.07). Lower social relationship scores (combining frequency and satisfaction with contact) were associated with greater risk of incident heart failure (adjusted HR = 1.38, 95% CI 1.02-1.87). Marital status and living alone were not significantly associated with heart failure. Conclusion: Weaker social relationships appear to increase the risk of developing heart failure in older age. Further research is needed to investigate pathways underlying these associations and to test whether interventions to strengthen social relationships can reduce the risk of heart failure

Polymorphism in TGFB1 is associated with worse non-relapse mortality and overall survival after stem cell transplantation with unrelated donors.

Transforming growth factor beta-1, encoded by the TGFB1 gene, is a cytokine that plays a central role in many physiological and pathogenic processes. We have sequenced TGFB1 regulatory region and assigned allelic genotypes in a large cohort of hematopoietic stem cell transplantation patients and donors. In this study, we analyzed 522 unrelated donor-patient pairs and examined the combined effect of all the common polymorphisms in this genomic region. In univariate analysis, we found that patients carrying a specific allele, 'p001', showed significantly reduced overall survival (5-year overall survival 30.7% for p001/ p001 patients vs. 41.6% others; P=0.032) and increased non-relapse mortality (1-year nonrelapse mortality: 39.0% vs. 25.4%; P=0.039) after transplantation. In multivariate analysis, the presence of a p001/ p001 genotype in patients was confirmed as an independent factor for reduced overall survival [hazard ratio=1.53 (1.04-2.24); P=0.031], and increased non-relapse mortality [hazard ratio=1.73 (1.06-2.83); P=0.030]. In functional experiments we found a trend towards a higher percentage of surface transforming growth factor beta-1-positive regulatory T cells after activation when the cells had a p001 allele (P=0.07). Higher or lower production of transforming growth factor beta-1 in the inflammatory context of hematopoietic stem cell transplantation may influence the development of complications in these patients. Findings indicate that TGFB1 genotype could potentially be of use as a prognostic factor in hematopoietic stem cell transplantation risk assessment algorithms

Towards a formal description of foraminiferal assemblage formation in shallow-water environments: Qualitative and quantitative concepts

© 2014 Elsevier B.V. The use of foraminifera in palaeoenvironmental reconstructions (e.g. sea level) may be complicated by processes such as infaunal test production, taphonomic degradation and bioturbation which act to modify contemporary analogue (surface) assemblages during and subsequent to burial. Understanding the palaeoenvironmental significance of these processes is limited by the absence of a clear theoretical description of the mechanics of foraminiferal assemblage formation. A conceptual framework is proposed which describes assemblage formation in terms of the balance of test inputs and losses within a volume of sediment undergoing burial through the upper sedimentary zones of test production, taphonomic processes and bioturbation. A corresponding mathematical model is described and shown to explain empirical dead test distributions in terms of empirically-defined standing crops, sedimentation and mixing rates, together with model estimates of standing crop turnover and/or taphonomic decay rates. This approach provides a quantitative basis for understanding assemblage formation and for comparing assemblage forming processes between species, environments and study sites. Rates of standing crop turnover and taphonomic loss are identified as the primary unknowns in the study of foraminiferal assemblage formation. These multiple unknowns make interpretations of cored data ambiguous, emphasising the need for a detailed and coherent framework of theory and assumptions for understanding the mechanics assemblage formation if interpretations are to be clear and conclusive

Social relationships and the risk of incident heart failure: results from a prospective population-based study of older men.

Aims: Limited social relationships, particularly in older adults, have been implicated as a risk factor for cardiovascular disease. However, little is known about the associations between poor social relationships and heart failure incidence. Methods and results: Prospective study of socially representative men aged 60-79 years drawn from general practices in 24 British towns and followed up for a maximum of 18 years. A total of 3698 participants with no previous diagnosis of heart failure were included. Information on social relationships was based on a combination of marital status, living circumstances, and social contacts with friends and family. These provided information on contact frequency, contact satisfaction, and a social relationship score (low to high) combining frequency and satisfaction with contact. Heart failure included both incidents non-fatal heart failure and death from heart failure. Among 3698 participants, 330 developed heart failure. Men with low compared to high frequency of contact with family and friends had an increased risk of incident heart failure [hazard ratio (HR) 1.59, 95% confidence interval (CI) 1.15-2.18]; this remained statistically significant after adjustment for social class, behavioural, and biological risk factors. Low compared to high scores for satisfaction with contacts was associated with increased risk of heart failure (adjusted HR = 1.54; 95% CI 1.14-2.07). Lower social relationship scores (combining frequency and satisfaction with contact) were associated with greater risk of incident heart failure (adjusted HR = 1.38, 95% CI 1.02-1.87). Marital status and living alone were not significantly associated with heart failure. Conclusion: Weaker social relationships appear to increase the risk of developing heart failure in older age. Further research is needed to investigate pathways underlying these associations and to test whether interventions to strengthen social relationships can reduce the risk of heart failure

Genome-wide association study with 1000 genomes imputation identifies signals for nine sex hormone-related phenotypes.

PublishedJournal ArticleResearch Support, Non-U.S. Gov'tThis is the final version of the article. Available from Nature Publishing Group via the DOI in this record.Genetic factors contribute strongly to sex hormone levels, yet knowledge of the regulatory mechanisms remains incomplete. Genome-wide association studies (GWAS) have identified only a small number of loci associated with sex hormone levels, with several reproductive hormones yet to be assessed. The aim of the study was to identify novel genetic variants contributing to the regulation of sex hormones. We performed GWAS using genotypes imputed from the 1000 Genomes reference panel. The study used genotype and phenotype data from a UK twin register. We included 2913 individuals (up to 294 males) from the Twins UK study, excluding individuals receiving hormone treatment. Phenotypes were standardised for age, sex, BMI, stage of menstrual cycle and menopausal status. We tested 7,879,351 autosomal SNPs for association with levels of dehydroepiandrosterone sulphate (DHEAS), oestradiol, free androgen index (FAI), follicle-stimulating hormone (FSH), luteinizing hormone (LH), prolactin, progesterone, sex hormone-binding globulin and testosterone. Eight independent genetic variants reached genome-wide significance (P<5 × 10(-8)), with minor allele frequencies of 1.3-23.9%. Novel signals included variants for progesterone (P=7.68 × 10(-12)), oestradiol (P=1.63 × 10(-8)) and FAI (P=1.50 × 10(-8)). A genetic variant near the FSHB gene was identified which influenced both FSH (P=1.74 × 10(-8)) and LH (P=3.94 × 10(-9)) levels. A separate locus on chromosome 7 was associated with both DHEAS (P=1.82 × 10(-14)) and progesterone (P=6.09 × 10(-14)). This study highlights loci that are relevant to reproductive function and suggests overlap in the genetic basis of hormone regulation.We thank Roche Diagnostics Australia Pty Limited, Castle Hill, Australia, who provided support for the analysis of the hormones. We thank the volunteer twins for their participation in the study. Twins UK received funding support from NIHR Biomedical Research Centre (grant to Guys’ and St Thomas’ Hospitals and King’s College London); the Chronic Disease Research Foundation; Canadian Institutes of Health Research, the Canadian Foundation for Innovation, the Fonds de la Recherche en Santé Québec, The Lady Davis Institute, the Jewish General Hospital and Ministère du Développement économique, de l'Innovation et de l'Exportation du Quebec. The Australian National Health and Medical Research Council (NHMRC project grants 1010494, 1048216), and Sir Charles Gairdner Hospital Research (grant PP2009/028). This work was supported by funding from the Wellcome Trust (092447/Z/10/Z) and Medical Research Council (MC_U106179472)

Genome-wide association study meta-analysis for quantitative ultrasound parameters of bone identifies five novel loci for broadband ultrasound attenuation.

Osteoporosis is a common and debilitating bone disease that is characterised by low bone mineral density, typically assessed using dual-energy X-ray absorptiometry. Quantitative ultrasound (QUS), commonly utilising the two parameters velocity of sound (VOS) and broadband ultrasound attenuation (BUA), is an alternative technology used to assess bone properties at peripheral skeletal sites. The genetic influence on the bone qualities assessed by QUS remains an under-studied area. We performed a comprehensive GWAS including low-frequency variants (MAF ≥0.005) for BUA and VOS using a discovery population of individuals with whole-genome sequence (WGS) data from the UK10K project (n=1,268). These results were then meta-analysed with those from two deeply imputed GWAS replication cohorts (n=1,610 and 13,749). In the gender-combined analysis, we identified eight loci associated with BUA and five with VOS at the genome-wide significance level, including three novel loci for BUA at 8p23.1 (PPP1R3B), 11q23.1 (LOC387810) and 22q11.21 (SEPT5) (P = 2.4 × 10-8-1.6 × 10-9). Gene-based association testing in the gender-combined dataset revealed eight loci associated with BUA and seven with VOS at the genome-wide significance level, with one novel locus for BUA at FAM167A (8p23.1) (P = 1.4 × 10-6). An additional novel locus for BUA was seen in the male-specific analysis at DEFB103B (8p23.1) (P = 1.8 × 10-6). Fracture analysis revealed significant associations between variation at the WNT16 and RSPO3 loci and fracture risk (P = 0.004 and 4.0 × 10-4 respectively). In conclusion, by performing a large GWAS meta-analysis for QUS parameters of bone using a combination of WGS and deeply imputed genotype data, we have identified five novel genetic loci associated with BUA

Quantifying Risk Factors for Human Brucellosis in Rural Northern Tanzania

Brucellosis is a zoonosis of veterinary, public health and economic significance in most developing countries. Human brucellosis is a severely debilitating disease that requires prolonged treatment with a combination of antibiotics. The disease can result in permanent and disabling sequel, and results in considerable medical expenses in addition to loss of income due to loss of working hours. A study was conducted in Northern Tanzania to determine the risk factors for transmission of brucellosis to humans in Tanzania. This was a matched case-control study. Any patient with a positive result by a competitive ELISA (c-ELISA) test for brucellosis, and presenting to selected hospitals with at least two clinical features suggestive of brucellosis such as headache, recurrent or continuous fever, sweating, joint pain, joint swelling, general body malaise or backache, was defined as a case. For every case in a district, a corresponding control was traced and matched by sex using multistage cluster sampling. Other criteria for inclusion as a control included a negative c-ELISA test result and that the matched individual would present to hospital if falls sick. Multivariable analysis showed that brucellosis was associated with assisted parturition during abortion in cattle, sheep or goat. It was shown that individuals living in close proximity to other households had a higher risk of brucellosis. People who were of Christian religion were found to have a higher risk of brucellosis compared to other religions. The study concludes that assisting an aborting animal, proximity to neighborhoods, and Christianity were associated with brucellosis infection. There was no association between human brucellosis and Human Immunodeficiency Virus (HIV) serostatus. Protecting humans against contact with fluids and tissues during assisted parturition of livestock may be an important means of reducing the risk of transferring brucellosis from livestock to humans. These can be achieved through health education to the communities where brucellosis is common