Mooring line fatigue damage evaluation for floating marine energy converters: Field measurements and prediction

publication-status: Publishedtypes: ArticleThe vision of large-scale commercial arrays of floating marine energy converters (MECs) necessitates the robust, yet cost-effective engineering of devices. Given the continuous environmental loading, fatigue has been iden- tified as one of the key engineering challenges. In particular the mooring sys- tem which warrants the station-keeping of such devices is subject to highly cyclic, non-linear load conditions, mainly induced by the incident waves. To ensure the integrity of the mooring system the lifecycle fatigue spec- trum must be predicted in order to compare the expected fatigue damage against the design limits. The fatigue design of components is commonly as- sessed through numerical modelling of representative load cases. However, for new applications such as floating marine energy converters numerical models are often scantily validated. This paper describes an approach where load measurements from large- scale field trials at the South West Mooring Testing Facility (SWMTF) are used to calculate and predict the fatigue damage. The described procedure employs a Rainflow cycle analysis in conjunction with the Palmgren-Miner rule to estimate the accumulated damage for the deployment periods and individual sea states. This approach allows an accurate fatigue assessment and prediction of mooring lines at a design stage, where field trial load measurements and wave climate information of potential installation sites are available. The mooring design can thus be optimised regarding its fatigue life and costly safety factors can be reduced. The proposed method also assists in monitoring and assessing the fatigue life during deployment periods

Heritage Futures - Comparative Approaches to Natural and Cultural Heritage Practices

This is the final version. Available on open access from UCL Press via the DOI in this recordWe present the book as a co-authored monograph because we acknowledge the collective contributions to the arguments developed within it, and the collaborative nature of the work. This has in itself been an experiment in finding a format in which diverse voices and views could productively speak to one another, while also acknowledging and foregrounding the diversity and range of different views, academic traditions and writing styles of contributors. As principal investigator, Harrison acted as the lead and coordinating author of the book, taking overall responsibilities for its editing and production. The co-investigators (DeSilvey, Holtorf, Macdonald) shared with Harrison editorial responsibilities for the individual thematic parts they each led, and for shaping the intellectual agenda of the book as a whole. However, we also felt it important to indicate the main authors of individual chapters within the book, to make clear specific contributions to the text and its arguments, and to highlight which named individuals were responsible for the empirical work that underpins them. Preservation of natural and cultural heritage is often said to be something that is done for the future, or on behalf of future generations, but the precise relationship of such practices to the future is rarely reflected upon. Heritage Futures draws on research undertaken over four years by an interdisciplinary, international team of 16 researchers and more than 25 partner organisations to explore the role of heritage and heritage-like practices in building future worlds. Engaging broad themes such as diversity, transformation, profusion and uncertainty, Heritage Futures aims to understand how a range of conservation and preservation practices across a number of countries assemble and resource different kinds of futures, and the possibilities that emerge from such collaborative research for alternative approaches to heritage in the Anthropocene. Case studies include the cryopreservation of endangered DNA in frozen zoos, nuclear waste management, seed biobanking, landscape rewilding, social history collecting, space messaging, endangered language documentation, built and natural heritage management, domestic keeping and discarding practices, and world heritage site management.Arts and Humanities Research Council (AHRC

The PTPN22 C1858T gene variant is associated with proinsulin in new-onset type 1 diabetes

<p>Abstract</p> <p>Background</p> <p>The protein tyrosine phosphatase nonreceptor type 2 (<it>PTPN22</it>) has been established as a type 1 diabetes susceptibility gene. A recent study found the C1858T variant of this gene to be associated with lower residual fasting C-peptide levels and poorer glycemic control in patients with type 1 diabetes. We investigated the association of the C1858T variant with residual beta-cell function (as assessed by stimulated C-peptide, proinsulin and insulin dose-adjusted HbA_1c), glycemic control, daily insulin requirements, diabetic ketoacidosis (DKA) and diabetes-related autoantibodies (IA-2A, GADA, ICA, ZnT8Ab) in children during the first year after diagnosis of type 1 diabetes.</p> <p>Methods</p> <p>The C1858T variant was genotyped in an international cohort of children (n = 257 patients) with newly diagnosed type 1 diabetes during 12 months after onset. We investigated the association of this variant with liquid-meal stimulated beta-cell function (proinsulin and C-peptide) and antibody status 1, 6 and 12 months after onset. In addition HbA_1cand daily insulin requirements were determined 1, 3, 6, 9 and 12 months after diagnosis. DKA was defined at disease onset.</p> <p>Results</p> <p>A repeated measurement model of all time points showed the stimulated proinsulin level is significantly higher (22%, p = 0.03) for the T allele carriers the first year after onset. We also found a significant positive association between proinsulin and IA levels (est.: 1.12, p = 0.002), which did not influence the association between <it>PTPN22 </it>and proinsulin (est.: 1.28, p = 0.03).</p> <p>Conclusions</p> <p>The T allele of the C1858T variant is positively associated with proinsulin levels during the first 12 months in newly diagnosed type 1 diabetes children.</p

Fructooligosacharides Reduce Pseudomonas aeruginosa PAO1 Pathogenicity through Distinct Mechanisms

Pseudomonas aeruginosa is ubiquitously present in the environment and acts as an opportunistic pathogen on humans, animals and plants. We report here the effects of the prebiotic polysaccharide inulin and its hydrolysed form FOS on this bacterium. FOS was found to inhibit bacterial growth of strain PAO1, while inulin did not affect growth rate or yield in a significant manner. Inulin stimulated biofilm formation, whereas a dramatic reduction of the biofilm formation was observed in the presence of FOS. Similar opposing effects were observed for bacterial motility, where FOS inhibited the swarming and twitching behaviour whereas inulin caused its stimulation. In co-cultures with eukaryotic cells (macrophages) FOS and, to a lesser extent, inulin reduced the secretion of the inflammatory cytokines IL-6, IL-10 and TNF- a . Western blot experiments indicated that the effects mediated by FOS in macrophages are associated with a decreased activation of the NF- k B pathway. Since FOS and inulin stimulate pathway activation in the absence of bacteria, the FOS mediated effect is likely to be of indirect nature, such as via a reduction of bacterial virulence. Further, this modulatory effect is observed also with the highly virulent ptxS mutated strain. Co-culture experiments of P. aeruginosa with IEC18 eukaryotic cells showed that FOS reduces the concentration of the major virulence factor, exotoxin A, suggesting that this is a possible mechanism for the reduction of pathogenicity. The potential of these compounds as components of antibacterial and anti-inflammatory cocktails is discussed.The authors acknowledge financial support from FEDER funds and Fondo Social Europeo through grants from the Spanish Ministry of Economy and Competitiveness (grants SAF2011-22922, SAF2011-22812) the Andalusian regional government Junta de Andalucía (grant CVI-7335) and the Centre of Networked Biomedical Research on Hepatic and Digestive Diseases (CIBERehd) which is funded by the Carlos III Health Institute and the Ramón Areces Foundation, Spain