14 research outputs found

    SAFEDOR – the implementation of risk-based ship design and approval

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    The integrated project SAFEDOR has been completed in spring 2009 and this paper summarizes the achievements. SAFEDOR has been focusing work on the development of a risk-based regulatory framework, a risk-based design framework, advanced probabilistic simulation tools and their integration as well as a series of application examples. The paper outlines the elements of the risk-based regulatory framework incl. approval process, risk evaluation criteria, requirements for documentation and key personnel as well as onboard documentation. Novel risk-based simulation tools and their integration into a design environment are discussed. The paper also highlights the innovative ship designs developed within SAFEDOR and points towards possible future applications. Eventually, future research on risk-based approaches is outlined

    Model-independent search for the presence of new physics in events including H → γγ with s \sqrt{s} = 13 TeV pp data recorded by the ATLAS detector at the LHC

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    Abstract A model-independent search for new physics leading to final states containing a Higgs boson, with a mass of 125.09 GeV, decaying to a pair of photons is performed with 139 fb−1 of s s \sqrt{s} = 13 TeV pp collision data recorded by the ATLAS detector at the Large Hadron Collider at CERN. This search examines 22 final states categorized by the objects that are produced in association with the Higgs boson. These objects include isolated electrons or muons, hadronically decaying τ-leptons, additional photons, missing transverse momentum, and hadronic jets, as well as jets that are tagged as containing a b-hadron. No significant excesses above Standard Model expectations are observed and limits on the production cross section at 95% confidence level are set. Detector efficiencies are reported for all 22 signal regions, which can be used to convert detector-level cross-section limits reported in this paper to particle-level cross-section constraints

    Multiple Antenatal Dexamethasone Treatment Alters Brain Vessel Differentiation in Newborn Mouse Pups

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    Antenatal steroid treatment decreases morbidity and mortality in premature infants through the maturation of lung tissue, which enables sufficient breathing performance. However, clinical and animal studies have shown that repeated doses of glucocorticoids such as dexamethasone and betamethasone lead to long-term adverse effects on brain development. Therefore, we established a mouse model for antenatal dexamethasone treatment to investigate the effects of dexamethasone on brain vessel differentiation towards the blood-brain barrier (BBB) phenotype, focusing on molecular marker analysis. The major findings were that in total brains on postnatal day (PN) 4 triple antenatal dexamethasone treatment significantly downregulated the tight junction protein claudin-5, the endothelial marker Pecam-1/CD31, the glucocorticoid receptor, the NR1 subunit of the N-methyl-D-aspartate receptor, and Abc transporters (Abcb1a, Abcg2 Abcc4). Less pronounced effects were found after single antenatal dexamethasone treatment and in PN10 samples. Comparisons of total brain samples with isolated brain endothelial cells together with the stainings for Pecam-1/CD31 and claudin-5 led to the assumption that the morphology of brain vessels is affected by antenatal dexamethasone treatment at PN4. On the mRNA level markers for angiogenesis, the sonic hedgehog and the Wnt pathway were downregulated in PN4 samples, suggesting fundamental changes in brain vascularization and/or differentiation. In conclusion, we provided a first comprehensive molecular basis for the adverse effects of multiple antenatal dexamethasone treatment on brain vessel differentiation

    Effects of antenatal DEX treatment on claudin-5 expression in total brains and brain endothelial fractions at PN4 and PN10 pups.

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    <p>Data are presented as the means ± SEM. For mRNA data: n = 5–6 biological samples. At PN4, 2–3 brains from one litter were pooled to one biological sample; at PN10, one brain represented one biological sample. For western blotting: n = 6; at PN4 and PN10, one brain represented one biological sample. Biological samples were collected from at least three different litters; claudin-5 data were normalized to the expression of the endogenous control GAPDH, samples from antenatally dexamethasone treated mice were compared to corresponding samples from NaCl treated mice, *: p<0.05 (two-tailed Student’s <i>t-test</i>).</p

    Effects of triple antenatal DEX-treatment on vessel morphology of PN4 pups.

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    <p>Representative immunofluorescence images of brain slices obtained from PN4 pups treated antenatally either with 3x NaCl or 3x DEX. Merged images of claudin-5 (Cldn5) (red), Pecam-1/CD31 (green) and DAPI (blue) were presented. The bar indicates a length of 50 μm. Images were magnified 20x (A); the average vessel length was measured, and the number of vessel per field of view was counted, revealing that antenatal 3x DEX treatment led to more, but shorter, brain vessels in comparison with brains of 3x NaCl-treated control animals (B), n = 6 per treatment, *: p<0.05 (two-tailed Student’s <i>t-test</i>).</p

    Effects of antenatal DEX-treatment on receptor and transporter expression in total brains and brain endothelial fractions of PN4 pups.

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    <p>Data are presented as the means ± SEM. For mRNA data, n = 5–6 biological samples; at PN4 2–3, brains from one litter were pooled to one biological sample. For western blotting, n = 6; at PN4, one brain represented one biological sample. Biological samples were collected from at least three different litters; claudin-5 data were normalized to the expression of the endogenous control GAPDH, samples from antenatally dexamethasone treated mice were compared to corresponding samples from NaCl treated mice, $: p<0.05 (two-tailed Student’s <i>t-test</i>).</p

    Changes of mRNA expression of mechanistic brain markers of PN4 mouse pups by triple antenatal DEX-treatments.

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    <p>mRNA expression of mechanistic brain markers of PN4 mouse pups changed by triple antenatal DEX-treatments. Data are presented as the means ± SEM; n = 5–6 biological samples, at PN4 2–3 brains from one litter were pooled to one biological sample, biological samples were collected from at least three different litters</p><p>$: p<0.05 after two-tailed Student’s <i>t-test</i>.</p><p>Changes of mRNA expression of mechanistic brain markers of PN4 mouse pups by triple antenatal DEX-treatments.</p

    Effects of antenatal DEX-treatment on occludin expression in total brains and brain endothelial fractions of PN4 and PN10 pups.

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    <p>Data are presented as the means ± SEM. For mRNA data: n = 5–6 biological samples; at PN4, 2–3 brains from one litter were pooled to one biological sample; at PN10, one brain represented one biological sample. For western blotting, n = 6; at PN4 and PN10, one brain represented one biological sample. Biological samples were collected from at least three different litters; data were normalized to the expression of the endogenous control GAPDH, samples from antenatally dexamethasone treated mice were compared to corresponding samples from NaCl treated mice, *: p<0.05 (two-tailed Student’s <i>t-test</i>).</p

    Effects of antenatal DEX-treatment on claudin-3 (black bars) and ZO-1 (white bars) expression in total brains and brain endothelial fractions of PN4 and PN10 pups.

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    <p>Data are presented as the means ± SEM. For mRNA data, n = 5–6 biological samples; at PN4, 2–3 brains from one litter were pooled to one biological sample; at PN10, one brain represented one biological sample. For western blotting, n = 6; at PN4 and PN10, one brain represented one biological sample. Biological samples were collected from at least three different litters; data were normalized to the expression of the endogenous control GAPDH, samples from antenatally dexamethasone treated mice were compared to corresponding samples from NaCl treated mice, *: p<0.05 (two-tailed Student’s <i>t-test</i>).</p

    Habitat preferences of male Corn Buntings Emberiza calandra in north-eastern Germany

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    Agricultural ecosystems have faced dramatic changes during past decades, resulting in a dramatic loss of farmland biodiversity. The Corn Bunting Emberiza calandra is considered a suitable indicator for the conservation value of farmland habitats, and has recently suffered strong declines throughout much of its European range. As a basis for targeted conservation measures, we investigated the habitat preferences of this species in north-eastern Germany by comparing the composition of male territories with randomly chosen control sites. A territory was defined as the area within a radius of 150 meters around the assumed centre of the territory, as the majority of nests is found within this radius. To assess food availability for nestlings, arthropod abundance within the most abundant land use types i.e. crop fields, fallows, grassland as well as within unploughed strips was investigated. In total we found 102 male Corn Bunting territories, which were mainly composed of crop fields (50%), grassland (28%), and fallows (12%). Territories compared with control sites were characterized by a lower proportion of crop fields, a higher proportion of fallows, more diverse land use types, more abundant field boundaries, unploughed strips, and tracks, and a higher availability of song posts. However, neither the number of larger (>= 1 cm), smaller ( 10%) and song posts (> 70 m 'linear song posts' or > 1 solitary post per ha) for the habitat selection of male Corn Buntings. We conclude that measures to halt population declines of Corn Buntings seem to be relatively easy to implement, provided that farmers are granted a fair compensation
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