214 research outputs found

    Dually noted: the effects of a pressure headcollar on compliance, discomfort and stress in horses during handling

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    Horse handlers often encounter problem behaviour resulting from a lack of stimulus control. Handlers are often only 15% of the weight of horses, which evolved strong flight responses. Therefore, many riders and handlers resort to the use of "aids" to maintain control of their animals. However, there are increasing concerns about the efficacy and welfare implication of such devices, particularly when applied to sensitive facial structures. One such device is a Dually® headcollar which aims to increase compliance. Despite its popularity, little is known about the effects of this aid on behaviour or stress. The aim of the current study was to determine whether the use of a Dually headcollar improves compliance during handling and, if so, whether this might be achieved with concomitant increases in stress or discomfort. Subjects completed two novel handling tests, one wearing a Dually with a line attached to the pressure mechanism and one attached to the standard ring as a Control. Crossing time and proactive behaviour were recorded as indicators of compliance. Core temperature and the discrepancy between eye temperatures were measured using IRT before and after testing as an indicator of stress. The Horse Grimace Scale (HGS) was used to measure discomfort caused by each configuration of the device. The Dually did not result in more compliant behaviour, compared to the Control (p=0.935; p=0.538). However, the Dually configuration did result in a significantly higher HGS scores (p=0.034). This may indicate that there is an impact on animal welfare by using this device that is not justified by improved behaviour. However, IRT readings of core temperature (p=0.186) and discrepancy between the eyes (p=0.972) did not indicate the Dually increased stress in subjects. Taken together, this suggests the Dually is ineffective in naïve horses but causes increased discomfort

    On the Use of Variance per Genotype as a Tool to Identify Quantitative Trait Interaction Effects: A Report from the Women's Genome Health Study

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    Testing for genetic effects on mean values of a quantitative trait has been a very successful strategy. However, most studies to date have not explored genetic effects on the variance of quantitative traits as a relevant consequence of genetic variation. In this report, we demonstrate that, under plausible scenarios of genetic interaction, the variance of a quantitative trait is expected to differ among the three possible genotypes of a biallelic SNP. Leveraging this observation with Levene's test of equality of variance, we propose a novel method to prioritize SNPs for subsequent gene–gene and gene–environment testing. This method has the advantageous characteristic that the interacting covariate need not be known or measured for a SNP to be prioritized. Using simulations, we show that this method has increased power over exhaustive search under certain conditions. We further investigate the utility of variance per genotype by examining data from the Women's Genome Health Study. Using this dataset, we identify new interactions between the LEPR SNP rs12753193 and body mass index in the prediction of C-reactive protein levels, between the ICAM1 SNP rs1799969 and smoking in the prediction of soluble ICAM-1 levels, and between the PNPLA3 SNP rs738409 and body mass index in the prediction of soluble ICAM-1 levels. These results demonstrate the utility of our approach and provide novel genetic insight into the relationship among obesity, smoking, and inflammation

    Mechanistic origins of variability in phytoplankton dynamics. Part II: analysis of mesocosm blooms under climate change scenarios

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    Driving factors of phytoplankton spring blooms have been discussed since long, but rarely analyzed quantitatively. Here, we use a mechanistic size-based ecosystem model to reconstruct observations made during the Kiel mesocosm experiments (2005–2006). The model accurately hindcasts highly variable bloom developments including community shifts in cell size. Under low light, phytoplankton dynamics was mostly controlled by selective mesozooplankton grazing. Selective grazing also explains initial dominance of large diatoms under high light conditions. All blooms were mainly terminated by aggregation and sedimentation. Allometries in nutrient uptake capabilities led to a delayed, post-bloom dominance of small species. In general, biomass and trait dynamics revealed many mutual dependencies, while growth factors decoupled from the respective selective forces. A size shift induced by one factor often changed the growth dependency on other factors. Within climate change scenarios, these indirect effects produced large sensitivities of ecosystem fluxes to the size distribution of winter phytoplankton. These sensitivities exceeded those found for changes in vertical mixing, whereas temperature changes only had minimal impacts

    Differences in MEF2 and NFAT Transcriptional Pathways According to Human Heart Failure Aetiology

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    BACKGROUND:Ca(2+) handling machinery modulates the activation of cardiac transcription pathways involved in heart failure (HF). The present study investigated the effect of HF aetiology on Ca(+2) handling proteins and NFAT1, MEF2C and GATA4 (transcription factors) in the same cardiac tissue. METHODOLOGY AND PRINCIPAL FINDINGS:A total of 83 hearts from ischemic (ICM, n = 43) and dilated (DCM, n = 31) patients undergoing heart transplantation and controls (CNT, n = 9) were analyzed by western blotting. Subcellular distribution was analyzed by fluorescence and electron microscopy. When we compared Ca(+2) handling proteins according to HF aetiology, ICM showed higher levels of calmodulin (24%, p<0.01), calcineurin (26%, p<0.01) and Ca(2+)/Calmodulin-dependent kinase II (CaMKIIδ(b) nuclear isoform 62%, p<0.001) than the CNT group. However, these proteins in DCM did not significantly increase. Furthermore, ICM showed a significant elevation in MEF2C (33%, p<0.01), and GATA4 (49%, p<0.05); also NFAT1 (66%, p<0.001) was increased, producing the resultant translocation of this transcriptional factor into the nuclei. These results were supported by fluorescence and electron microscopy analysis. Whereas, DCM only had a significant increase in GATA4 (52%, p<0.05). Correlations between NFAT1 and MEF2C in both groups (ICM r = 0.38 and DCM r = 0.59, p<0.05 and p<0.01, respectively) were found; only ICM showed a correlation between GATA4 and NFAT1 (r = 0.37, p<0.05). CONCLUSIONS/SIGNIFICANCE:This study shows an increase of Ca(2+) handling machinery synthesis and their cardiac transcription pathways in HF, being more markedly increased in ICM. Furthermore, there is a significant association between MEF2, NFAT1 and GATA4. These proteins could be therapeutic targets to improve myocardial function

    Estimating the Worldwide Extent of Illegal Fishing

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    Illegal and unreported fishing contributes to overexploitation of fish stocks and is a hindrance to the recovery of fish populations and ecosystems. This study is the first to undertake a world-wide analysis of illegal and unreported fishing. Reviewing the situation in 54 countries and on the high seas, we estimate that lower and upper estimates of the total value of current illegal and unreported fishing losses worldwide are between 10bnand10 bn and 23.5 bn annually, representing between 11 and 26 million tonnes. Our data are of sufficient resolution to detect regional differences in the level and trend of illegal fishing over the last 20 years, and we can report a significant correlation between governance and the level of illegal fishing. Developing countries are most at risk from illegal fishing, with total estimated catches in West Africa being 40% higher than reported catches. Such levels of exploitation severely hamper the sustainable management of marine ecosystems. Although there have been some successes in reducing the level of illegal fishing in some areas, these developments are relatively recent and follow growing international focus on the problem. This paper provides the baseline against which successful action to curb illegal fishing can be judged

    Secretory granule neuroendocrine protein 1 (SGNE1) genetic variation and glucose intolerance in severe childhood and adult obesity

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    <p>Abstract</p> <p>Background</p> <p>7B2 is a regulator/activator of the prohormone convertase 2 which is involved in the processing of numerous neuropeptides, including insulin, glucagon and pro-opiomelanocortin. We have previously described a suggestive genetic linkage peak with childhood obesity on chr15q12-q14, where the 7B2 encoding gene, <it>SGNE1 </it>is located. The aim of this study is to analyze associations of <it>SGNE1 </it>genetic variation with obesity and metabolism related quantitative traits.</p> <p>Methods</p> <p>We screened <it>SGNE1 </it>for genetic variants in obese children and genotyped 12 frequent single nucleotide polymorphisms (SNPs). Case control analyses were performed in 1,229 obese (534 children and 695 adults), 1,535 individuals with type 2 diabetes and 1,363 controls, all French Caucasians. We also studied 4,922 participants from the D.E.S.I.R prospective population-based cohort.</p> <p>Results</p> <p>We did not find any association between <it>SGNE1 </it>SNPs and childhood or adult obesity. However, the 5' region SNP -1,701A>G associated with higher area under glucose curve after oral glucose tolerance test (p = 0.0005), higher HOMA-IR (p = 0.005) and lower insulinogenic index (p = 0.0003) in obese children. Similar trends were found in obese adults. SNP -1,701A>G did not associate with risk of T2D but tends to associate with incidence of type 2 diabetes (HR = 0.75 95%CI [0.55–1.01]; p = 0.06) in the prospective cohort.</p> <p>Conclusion</p> <p><it>SGNE1 </it>genetic variation does not contribute to obesity and common forms of T2D but may worsen glucose intolerance and insulin resistance, especially in the background of severe and early onset obesity. Further molecular studies are required to understand the molecular bases involved in this process.</p

    Effect of food concentration and type of diet on Acartia survival and naupliar development

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    We have performed life table experiments to investigate the effects of different food types and concentrations on the larval development and survival up to adulthood of Acartia tonsa. The food species offered comprised a wide taxonomic spectrum: the pigmented flagellates Isochrysis galbana, Emiliania huxleyi, Rhodomonas sp., Prorocentrum minimum, the diatom Thalassiosira weissflogii, grown on medium offering enriched macronutrient concentrations and the ciliate Euplotes sp. initially cultured on Rhodomonas. For the ciliate species, also the functional response was studied. In order to avoid limitation by mineral nutrients, food algae have been taken from the exponential growth phase of the nutrient replete cultures. The suitability of Rhodomonas as a food source throughout the entire life cycle was not a surprise. However, in contrast to much of the recent literature about the inadequacy or even toxicity of diatoms, we found that also Thalassiosira could support Acartia-development through the entire life cycle. On the other hand, Acartia could not complete its life cycle when fed with the other food items, Prorocentrum having adverse effects even when mixed with Rhodomonas and Thalassiosira. Isochrysis well supported naupliar survival and development, but was insufficient to support further development until reproduction. With Emiliania and Euplotes, nauplii died off before most of them could reach the first copepodite stages. Acartia-nauplii showed a behavioral preference for Euplotes-feeding over diatom feeding, but nevertheless Euplotes was an insufficient diet to complete development beyond the naupliar stages

    A Systems Genetics Approach Implicates USF1, FADS3, and Other Causal Candidate Genes for Familial Combined Hyperlipidemia

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    We hypothesized that a common SNP in the 3' untranslated region of the upstream transcription factor 1 (USF1), rs3737787, may affect lipid traits by influencing gene expression levels, and we investigated this possibility utilizing the Mexican population, which has a high predisposition to dyslipidemia. We first associated rs3737787 genotypes in Mexican Familial Combined Hyperlipidemia (FCHL) case/control fat biopsies, with global expression patterns. To identify sets of co-expressed genes co-regulated by similar factors such as transcription factors, genetic variants, or environmental effects, we utilized weighted gene co-expression network analysis (WGCNA). Through WGCNA in the Mexican FCHL fat biopsies we identified two significant Triglyceride (TG)-associated co-expression modules. One of these modules was also associated with FCHL, the other FCHL component traits, and rs3737787 genotypes. This USF1-regulated FCHL-associated (URFA) module was enriched for genes involved in lipid metabolic processes. Using systems genetics procedures we identified 18 causal candidate genes in the URFA module. The FCHL causal candidate gene fatty acid desaturase 3 (FADS3) was associated with TGs in a recent Caucasian genome-wide significant association study and we replicated this association in Mexican FCHL families. Based on a USF1-regulated FCHL-associated co-expression module and SNP rs3737787, we identify a set of causal candidate genes for FCHL-related traits. We then provide evidence from two independent datasets supporting FADS3 as a causal gene for FCHL and elevated TGs in Mexicans
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