28 research outputs found

    Aluminum and stainless steel tubes joined by simple ring and welding process

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    Duranel ring is used to join aluminum and stainless steel tubing. Duranel is a bimetal made up of roll-bonded aluminum and stainless steel. This method of joining the tubing requires only two welding operations

    Precision metal molding

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    Method provides precise alignment for metal-forming dies while permitting minimal thermal expansion without die warpage or cavity space restriction. The interfacing dowel bars and die side facings are arranged so the dies are restrained in one orthogonal angle and permitted to thermally expand in the opposite orthogonal angle

    Diets of the Barents Sea cod (Gadus morhua) from the 1930s to 2018

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    A new dataset on the diet of Atlantic cod in the Barents Sea from the 1930s to the present day has been compiled to produce one of the largest fish diet datasets available globally. Atlantic cod is one of the most ecologically and commercially important fish species in the North Atlantic. The stock in the Barents Sea is by far the largest, as a result of both successful management and favourable environmental conditions since the early 2000s. As a top predator, cod plays a key role in the Barents Sea ecosystem. The species has a broad diet consisting mainly of crustaceans and teleost fish, and both the amount and type of prey vary in space and time. The data – from Russia, Norway and the United Kingdom – represent quantitative stomach content records from more than 400 000 fish and qualitative data from 2.5 million fish. Many of the data are from joint collaborative surveys between Norway and Russia. The sampling was conducted throughout each year, allowing for seasonal, annual and decadal comparisons to be made. Visual analysis shows cod diets have changed considerably from the start of the dataset in the 1930s to the present day. There was a large proportion of herring in the diets in the 1930s, whereas in more recent decades capelin, invertebrates and other fish dominate. There are also significant interannual asynchronous fluctuations in prey, particularly capelin and euphausiids. Combining these datasets can help us understand how the environment and ecosystems are responding to climatic changes, and what influences the diet and prey switching of cod. Trends in temperature and variability indices can be tested against the occurrence of different prey items, and the effects of fishing pressure on cod and prey stocks on diet composition could be investigated. The dataset will also enable us to improve parametrization of food web models and to forecast how Barents Sea fisheries may respond in the future to management and to climate change. The Russian data are available through joint projects with the Polar Branch of the Russian Federal Research Institute of Fisheries and Oceanography (VNIRO).publishedVersio

    Harmful algal blooms and climate change: exploring future distribution changes

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    Harmful algae can cause death in fish, shellfish, marine mammals, and humans, via their toxins or from effects associated with their sheer quantity. There are many species, which cause a variety of problems around north-west Europe, and the frequency and distribution of algal blooms have altered in the recent past. Species distribution modelling was used to understand how harmful algal species may respond in the future to climate change, by considering environmental preferences and how these may shift. Most distribution studies to date use low resolution global model outputs. In this study, high resolution, downscaled shelf seas climate projections for the north-west European shelf were nested within lower resolution global projections, to understand how the distribution of harmful algae may change by the mid to end of century. Projections suggest that the habitat of most species (defined by temperature, salinity, depth, and stratification) will shift north this century, with suitability increasing in the central and northern North Sea. An increase in occurrence here might lead to more frequent detrimental blooms if wind, irradiance and nutrient levels are also suitable. Prioritizing monitoring of species in these susceptible areas could help in establishing early-warning systems for aquaculture and health protection schemes

    The V471A polymorphism in autophagy-related gene ATG7 modifies age at onset specifically in Italian Huntington disease patients

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    The cause of Huntington disease (HD) is a polyglutamine repeat expansion of more than 36 units in the huntingtin protein, which is inversely correlated with the age at onset of the disease. However, additional genetic factors are believed to modify the course and the age at onset of HD. Recently, we identified the V471A polymorphism in the autophagy-related gene ATG7, a key component of the autophagy pathway that plays an important role in HD pathogenesis, to be associated with the age at onset in a large group of European Huntington disease patients. To confirm this association in a second independent patient cohort, we analysed the ATG7 V471A polymorphism in additional 1,464 European HD patients of the “REGISTRY” cohort from the European Huntington Disease Network (EHDN). In the entire REGISTRY cohort we could not confirm a modifying effect of the ATG7 V471A polymorphism. However, analysing a modifying effect of ATG7 in these REGISTRY patients and in patients of our previous HD cohort according to their ethnic origin, we identified a significant effect of the ATG7 V471A polymorphism on the HD age at onset only in the Italian population (327 patients). In these Italian patients, the polymorphism is associated with a 6-years earlier disease onset and thus seems to have an aggravating effect. We could specify the role of ATG7 as a genetic modifier for HD particularly in the Italian population. This result affirms the modifying influence of the autophagic pathway on the course of HD, but also suggests population-specific modifying mechanisms in HD pathogenesis

    Identification of genetic variants associated with Huntington's disease progression: a genome-wide association study

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    Background Huntington's disease is caused by a CAG repeat expansion in the huntingtin gene, HTT. Age at onset has been used as a quantitative phenotype in genetic analysis looking for Huntington's disease modifiers, but is hard to define and not always available. Therefore, we aimed to generate a novel measure of disease progression and to identify genetic markers associated with this progression measure. Methods We generated a progression score on the basis of principal component analysis of prospectively acquired longitudinal changes in motor, cognitive, and imaging measures in the 218 indivduals in the TRACK-HD cohort of Huntington's disease gene mutation carriers (data collected 2008–11). We generated a parallel progression score using data from 1773 previously genotyped participants from the European Huntington's Disease Network REGISTRY study of Huntington's disease mutation carriers (data collected 2003–13). We did a genome-wide association analyses in terms of progression for 216 TRACK-HD participants and 1773 REGISTRY participants, then a meta-analysis of these results was undertaken. Findings Longitudinal motor, cognitive, and imaging scores were correlated with each other in TRACK-HD participants, justifying use of a single, cross-domain measure of disease progression in both studies. The TRACK-HD and REGISTRY progression measures were correlated with each other (r=0·674), and with age at onset (TRACK-HD, r=0·315; REGISTRY, r=0·234). The meta-analysis of progression in TRACK-HD and REGISTRY gave a genome-wide significant signal (p=1·12 × 10−10) on chromosome 5 spanning three genes: MSH3, DHFR, and MTRNR2L2. The genes in this locus were associated with progression in TRACK-HD (MSH3 p=2·94 × 10−8 DHFR p=8·37 × 10−7 MTRNR2L2 p=2·15 × 10−9) and to a lesser extent in REGISTRY (MSH3 p=9·36 × 10−4 DHFR p=8·45 × 10−4 MTRNR2L2 p=1·20 × 10−3). The lead single nucleotide polymorphism (SNP) in TRACK-HD (rs557874766) was genome-wide significant in the meta-analysis (p=1·58 × 10−8), and encodes an aminoacid change (Pro67Ala) in MSH3. In TRACK-HD, each copy of the minor allele at this SNP was associated with a 0·4 units per year (95% CI 0·16–0·66) reduction in the rate of change of the Unified Huntington's Disease Rating Scale (UHDRS) Total Motor Score, and a reduction of 0·12 units per year (95% CI 0·06–0·18) in the rate of change of UHDRS Total Functional Capacity score. These associations remained significant after adjusting for age of onset. Interpretation The multidomain progression measure in TRACK-HD was associated with a functional variant that was genome-wide significant in our meta-analysis. The association in only 216 participants implies that the progression measure is a sensitive reflection of disease burden, that the effect size at this locus is large, or both. Knockout of Msh3 reduces somatic expansion in Huntington's disease mouse models, suggesting this mechanism as an area for future therapeutic investigation
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