67 research outputs found

    The Olive Ridley Project (ORP): A successful example of how to engage researchers, conservation practitioners and civil society

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    The Olive Ridley Project (ORP) was set up to protect sea turtles and their habitats. The project was formed in 2013, and it became a registered charity in the UK in 2016. From its inception, ORP took a multidisciplinary approach to achieve its goals. Part of its objectives, and the reason why the charity came to fruition, are related to the issue of olive ridley sea turtle (Lepidochelys olivacea) entanglement in abandoned, lost or discarded fishing gear (also known as ‘ghost gear’ or ‘ghost nets’), and the search for ghost gear and turtle entanglement ‘hot spots’ throughout the Indian Ocean. The initial ORP research questions were soon challenged by societal interests to develop inclusive educational programmes in local communities and tourist resorts that could raise awareness about the need for conservation of all sea turtle species. In February 2017, ORP opened the first veterinarian-run, fully equipped Marine Turtle Rescue Centre in the Maldives, bringing together the work of researchers, citizen scientists, volunteers, environmentalists, marine biologists and veterinarians. The present work of ORP sits on a strong and scientifically robust collaborative plan. Current ORP research projects range from sea turtle population analyses, spatial ecology, rehabilitation of injured and sick individuals, epibiont parasite analyses, precise turtle identification through photo-ID research, linking ghost gear to responsible fisheries, and analyses of ghost gear drift patterns. The programme enhances community education and outreach by engaging schoolchildren, organizing workshops, promoting sustainable use of ghost gear waste, and training citizen scientists and local fishing communities. The ORP programme encompasses many principles of research engagement, effectively combining scientific knowledge, education and action. This article explores all stages of the process (from research planning and design, to knowledge exchange and inter- and trans-disciplinary impact assessments), describing the active engagement originated by the ORP initiative. A reflective insight into the learning, enrichment and challenges of engaging researchers and community actors is also included, considering the current social and scientific framework

    The Olive Ridley Project (ORP): a successful example of how to engage researchers, conservation practitioners and civil society

    Get PDF
    The Olive Ridley Project (ORP) was set up to protect sea turtles and their habitats. The project was formed in 2013, and it became a registered charity in the UK in 2016. From its inception, ORP took a multidisciplinary approach to achieve its goals. Part of its objectives, and the reason why the charity came to fruition, are related to the issue of olive ridley sea turtle (Lepidochelys olivacea) entanglement in abandoned, lost or discarded fishing gear (also known as ‘ghost gear’ or ‘ghost nets’), and the search for ghost gear and turtle entanglement ‘hot spots’ throughout the Indian Ocean. The initial ORP research questions were soon challenged by societal interests to develop inclusive educational programmes in local communities and tourist resorts that could raise awareness about the need for conservation of all sea turtle species. In February 2017, ORP opened the first veterinarian-run, fully equipped Marine Turtle Rescue Centre in the Maldives, bringing together the work of researchers, citizen scientists, volunteers, environmentalists, marine biologists and veterinarians. The present work of ORP sits on a strong and scientifically robust collaborative plan. Current ORP research projects range from sea turtle population analyses, spatial ecology, rehabilitation of injured and sick individuals, epibiont parasite analyses, precise turtle identification through photo-ID research, linking ghost gear to responsible fisheries, and analyses of ghost gear drift patterns. The programme enhances community education and outreach by engaging schoolchildren, organizing workshops, promoting sustainable use of ghost gear waste, and training citizen scientists and local fishing communities. The ORP programme encompasses many principles of research engagement, effectively combining scientific knowledge, education and action. This article explores all stages of the process (from research planning and design, to knowledge exchange and inter- and trans-disciplinary impact assessments), describing the active engagement originated by the ORP initiative. A reflective insight into the learning, enrichment and challenges of engaging researchers and community actors is also included, considering the current social and scientific framework

    Animal or Plant: Which Is the Better Fog Water Collector?

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    Occasional fog is a critical water source utilised by plants and animals in the Namib Desert. Fog basking beetles (Onymacris unguicularis, Tenebrionidae) and Namib dune bushman grass (Stipagrostris sabulicola, Poaceae) collect water directly from the fog. While the beetles position themselves optimally for fog water collection on dune ridges, the grass occurs predominantly at the dune base where less fog water is available. Differences in the fog-water collecting abilities in animals and plants have never been addressed. Here we place beetles and grass side-by-side in a fog chamber and measure the amount of water they collect over time. Based on the accumulated amount of water over a two hour period, grass is the better fog collector. However, in contrast to the episodic cascading water run-off from the grass, the beetles obtain water in a steady flow from their elytra. This steady trickle from the beetles' elytra to their mouth could ensure that even short periods of fog basking – while exposed to predators – will yield water. Up to now there is no indication of specialised surface properties on the grass leafs, but the steady run-off from the beetles could point to specific property adaptations of their elytra surface

    Ischemia-Reperfusion Injury and Pregnancy Initiate Time-Dependent and Robust Signs of Up-Regulation of Cardiac Progenitor Cells

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    To explore how cardiac regeneration and cell turnover adapts to disease, different forms of stress were studied for their effects on the cardiac progenitor cell markers c-Kit and Isl1, the early cardiomyocyte marker Nkx2.5, and mast cells. Adult female rats were examined during pregnancy, after myocardial infarction and ischemia-reperfusion injury with/out insulin like growth factor-1(IGF-1) and hepatocyte growth factor (HGF). Different cardiac sub-domains were analyzed at one and two weeks post-intervention, both at the mRNA and protein levels. While pregnancy and myocardial infarction up-regulated Nkx2.5 and c-Kit (adjusted for mast cell activation), ischemia-reperfusion injury induced the strongest up-regulation which occurred globally throughout the entire heart and not just around the site of injury. This response seems to be partly mediated by increased endogenous production of IGF-1 and HGF. Contrary to c-Kit, Isl1 was not up-regulated by pregnancy or myocardial infarction while ischemia-reperfusion injury induced not a global but a focal up-regulation in the outflow tract and also in the peri-ischemic region, correlating with the up-regulation of endogenous IGF-1. The addition of IGF-1 and HGF did boost the endogenous expression of IGF and HGF correlating to focal up-regulation of Isl1. c-Kit expression was not further influenced by the exogenous growth factors. This indicates that there is a spatial mismatch between on one hand c-Kit and Nkx2.5 expression and on the other hand Isl1 expression. In conclusion, ischemia-reperfusion injury was the strongest stimulus with both global and focal cardiomyocyte progenitor cell marker up-regulations, correlating to the endogenous up-regulation of the growth factors IGF-1 and HGF. Also pregnancy induced a general up-regulation of c-Kit and early Nkx2.5+ cardiomyocytes throughout the heart. Utilization of these pathways could provide new strategies for the treatment of cardiac disease

    A genome-wide association study in Europeans and South Asians identifies five new loci for coronary artery disease

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    The genetics of blood pressure regulation and its target organs from association studies in 342,415 individuals

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    To dissect the genetic architecture of blood pressure and assess effects on target-organ damage, we analyzed 128,272 SNPs from targeted and genome-wide arrays in 201,529 individuals of European ancestry and genotypes from an additional 140,886 individuals were used for validation. We identified 66 blood pressure loci, of which 17 were novel and 15 harbored multiple distinct association signals. The 66 index SNPs were enriched for cis-regulatory elements, particularly in vascular endothelial cells, consistent with a primary role in blood pressure control through modulation of vascular tone across multiple tissues. The 66 index SNPs combined in a risk score showed comparable effects in 64,421 individuals of non-European descent. The 66-SNP blood pressure risk score was significantly associated with target-organ damage in multiple tissues, with minor effects in the kidney. Our findings expand current knowledge of blood pressure pathways and highlight tissues beyond the classic renal system in blood pressure regulation

    New genetic loci link adipose and insulin biology to body fat distribution.

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    Body fat distribution is a heritable trait and a well-established predictor of adverse metabolic outcomes, independent of overall adiposity. To increase our understanding of the genetic basis of body fat distribution and its molecular links to cardiometabolic traits, here we conduct genome-wide association meta-analyses of traits related to waist and hip circumferences in up to 224,459 individuals. We identify 49 loci (33 new) associated with waist-to-hip ratio adjusted for body mass index (BMI), and an additional 19 loci newly associated with related waist and hip circumference measures (P < 5 × 10(-8)). In total, 20 of the 49 waist-to-hip ratio adjusted for BMI loci show significant sexual dimorphism, 19 of which display a stronger effect in women. The identified loci were enriched for genes expressed in adipose tissue and for putative regulatory elements in adipocytes. Pathway analyses implicated adipogenesis, angiogenesis, transcriptional regulation and insulin resistance as processes affecting fat distribution, providing insight into potential pathophysiological mechanisms

    Abdominal aortic aneurysm is associated with a variant in low-density lipoprotein receptor-related protein 1

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    Abdominal aortic aneurysm (AAA) is a common cause of morbidity and mortality and has a significant heritability. We carried out a genome-wide association discovery study of 1866 patients with AAA and 5435 controls and replication of promising signals (lead SNP with a p value &lt; 1 × 10-5) in 2871 additional cases and 32,687 controls and performed further follow-up in 1491 AAA and 11,060 controls. In the discovery study, nine loci demonstrated association with AAA (p &lt; 1 × 10-5). In the replication sample, the lead SNP at one of these loci, rs1466535, located within intron 1 of low-density-lipoprotein receptor-related protein 1 (LRP1) demonstrated significant association (p = 0.0042). We confirmed the association of rs1466535 and AAA in our follow-up study (p = 0.035). In a combined analysis (6228 AAA and 49182 controls), rs1466535 had a consistent effect size and direction in all sample sets (combined p = 4.52 × 10-10, odds ratio 1.15 [1.10-1.21]). No associations were seen for either rs1466535 or the 12q13.3 locus in independent association studies of coronary artery disease, blood pressure, diabetes, or hyperlipidaemia, suggesting that this locus is specific to AAA. Gene-expression studies demonstrated a trend toward increased LRP1 expression for the rs1466535 CC genotype in arterial tissues; there was a significant (p = 0.029) 1.19-fold (1.04-1.36) increase in LRP1 expression in CC homozygotes compared to TT homozygotes in aortic adventitia. Functional studies demonstrated that rs1466535 might alter a SREBP-1 binding site and influence enhancer activity at the locus. In conclusion, this study has identified a biologically plausible genetic variant associated specifically with AAA, and we suggest that this variant has a possible functional role in LRP1 expression

    Causal effect of plasminogen activator inhibitor type 1 on coronary heart disease

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    Background--Plasminogen activator inhibitor type 1 (PAI-1) plays an essential role in the fibrinolysis system and thrombosis. Population studies have reported that blood PAI-1 levels are associated with increased risk of coronary heart disease (CHD). However, it is unclear whether the association reflects a causal influence of PAI-1 on CHD risk. Methods and Results--To evaluate the association between PAI-1 and CHD, we applied a 3-step strategy. First, we investigated the observational association between PAI-1 and CHD incidence using a systematic review based on a literature search for PAI-1 and CHD studies. Second, we explored the causal association between PAI-1 and CHD using a Mendelian randomization approach using summary statistics from large genome-wide association studies. Finally, we explored the causal effect of PAI-1 on cardiovascular risk factors including metabolic and subclinical atherosclerosis measures. In the systematic meta-analysis, the highest quantile of blood PAI-1 level was associated with higher CHD risk comparing with the lowest quantile (odds ratio=2.17; 95% CI: 1.53, 3.07) in an age- and sex-adjusted model. The effect size was reduced in studies using a multivariable-adjusted model (odds ratio=1.46; 95% CI: 1.13, 1.88). The Mendelian randomization analyses suggested a causal effect of increased PAI-1 level on CHD risk (odds ratio=1.22 per unit increase of log-transformed PAI-1; 95% CI: 1.01, 1.47). In addition, we also detected a causal effect of PAI-1 on elevating blood glucose and high-density lipoprotein cholesterol. Conclusions--Our study indicates a causal effect of elevated PAI-1 level on CHD risk, which may be mediated by glucose dysfunction
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