The control of seed-borne fungi by fumigation

Imperial Users onl

Measurement of residual stresses in a dissimilar metal welded pipe

Dissimilar metal welds (DMW) are used in light water reactor power plants to join ferritic and austenitic steel piping components. High residual stresses remaining in this type of welded joint can significantly increase its susceptibility to stress corrosion cracking (SCC) under water reactor chemistry conditions. This degradation mechanism has compromised the integrity of many nuclear power plants throughout the world over the past 10 years. The Open University (OU) is undertaking a programme of research aimed at improving the reliability of residual stress measurements in DMWs using neutron diffraction. AREVA, the French nuclear power plant constructor, has developed an improved narrow gap DMW weld using a nickel-based corrosion resistant filler (alloy-52) to eliminate the risk of SCC in next generation nuclear plant. Through-wall neutron measurements have been carried out on a full-size DMW mock-up (352 mm OD, 40 mm thick) using the ENGIN-X instrument at the ISIS Facility in the UK. The results have shown that the largest tensile stress components in the welded component lie in the hoop direction, and have values of around 250 MPa and 225 MPa in the austenitic and alloy-52 materials respectively. These measured stresses were in reasonable agreement with those obtained from deep-hole drilling and numerical simulations. A notable finding in the experimental work was a wide scatter in the measured unstressed lattice parameters within a range equivalent to micro-strains of ≈ 430, 400 and 600 for austenitic stainless steel, ferritic steel and alloy-52 respectively. This scatter was reduced by two orders of magnitude through making additional measurements whilst slowly rotating the stress-free reference cubes. The OU is undertaking systematic studies to identify the origins of the observed measurement scatter in order to improve the reliability of measurements

Electron backscatter diffraction (EBSD) measurement of accumulated strain

Reliable life prediction depends on a sound knowledge of the accumulated strain in components subject to creep. Electron backscatter diffraction (EBSD) is now well-established for estimating/measuring plastic strain and there have been a number of different EBSD metrics proposed for this. Microstructure has a strong effect on the calibration of most of these, limiting their use in critical areas such as around welds where microstructure is inhomogeneous. During the service life of materials such as 316 steel there is extensive precipitation but most published applications of EBSD are on precipitate-free materials. A systematic study has been made on the applicability of different EBSD metrics to both solution-annealed and service-aged 316H stainless steel subject to a range of plastic and creep strains between 0 and 35% to determine the conditions for maximum strain sensitivity of each. A simple new method of assessing cumulative strain, ‘deformed grain fraction’ (DGF) is presented and DGF has been compared with more conventional EBSD strain metrics. In 316H steel with a range of microstructures the effects of plastic and creep strains are additive for all metrics. DGF is relatively insensitive to changes in microstructure and its use is demonstrated in measuring total plastic strain in ex-service welded components

Natural Products Studies of Marine Organisms of the South Pacific

This thesis describes the NMR-guided isolation and structural elucidation of one novel and several known compounds from marine organisms collected from Tonga and New Zealand. In the process of this work, 11 Tongan algal specimens were subjected to preliminary NMR-guided investigation, as the study of Tongan marine algae is poorly represented. The HMBC spectra of crude fractions generated by the first chromatographic purification of the crude extracts were analysed for perceived structural novelty, providing three specimens that warranted further investigation. Investigation of unknown algae PTN4_17G afforded substructure 76, observed in the known compound avrainvilloside, which included the rare 6-deoxy-6-aminoglucose moiety. This aminoglucose moiety has been reported from marine sources only twice in literature, both in algae specimens. An investigation of unknown brown algae PTN4_18E afforded substructure 83, a methacrylic acid containing moiety. Methacrylic acid moieties are also uncommon in marine organisms, with 27 reported structures containing the moiety, of which only two occur from algae. In each case suitable, mass spectrometry data was not obtainable therefore full structural elucidation of the compounds was not achieved. Further analysis of the unknown algae PTN3_38C afforded the known compound fistularin-3 86, although further studies revealed that a sponge contaminant was responsible for the presence of the compound. The results of this algae study provided interesting correlations between secondary metabolite concentrations of algae in temperate and sub-tropical environments, contrary to the observed correlations of marine sponges. An investigation into an unknown New Zealand Raspailia sponge was conducted as previous studies had suggested the presence of novel resonances. Further analysis of the specimen yielded the known clerodane raspailodane A 126 and the unexpected novel steroidal glycoside raspailoside A 135. Biological activity studies conducted on raspailoside A showed inactivity towards the mammalian cell line HL-60 and Saccharomyces cerevisiae assays

An EBSD study of the deformation of service-aged 316 austenitic steel

Electron backscatter diffraction (EBSD) has been used to examine the plastic deformation of an ex-service 316 austenitic stainless steel at 297K and 823K (24 °C and 550 °C)at strain rates 3.5x10-3 to 4 x 10-7 s-1. The distribution of local misorientations was found to depend on the imposed plastic strain following a lognormal distribution at true strains 0.1. At 823 K (550 °C), the distribution of misorientations depended on the applied strain rate. The evolution of lattice misorientations with increasing plastic strain up to 0.23 was quantified using the metrics kernel average misorientation, average intragrain misorientation, and low angle misorientation fraction. For strain rate down to 10-5 s-1 all metrics were insensitive to deformation temperature, mode (tension vs. compression) and orientation of the measurement plane. The strain sensitivity of the different metrics was found to depend on the misorientation ranges considered in their calculation. A simple new metric, proportion of undeformed grains, is proposed for assessing strain in both aged and unaged material. Lattice misorientations build up with strain faster in aged steel than in un-aged material and most of the metrics were sensitive to the effects of thermal aging. Ignoring aging effects leads to significant overestimation of the strains around welds. The EBSD results were compared with nanohardness measurements and good agreement established between the two techniques of assessing plastic strain in aged 316 steel

Gastroesophageal reflux GWAS identifies risk loci that also associate with subsequent severe esophageal diseases

Funder: The Swedish Esophageal Cancer Study was funded by grants (R01 CA57947-03) from the National Cancer Institute he California Tobacco Related Research Program (3RT-0122; and; 10RT-0251) Marit Peterson Fund for Melanoma Research. CIDR is supported by contract HHSN268200782096CAbstract: Gastroesophageal reflux disease (GERD) is caused by gastric acid entering the esophagus. GERD has high prevalence and is the major risk factor for Barrett’s esophagus (BE) and esophageal adenocarcinoma (EA). We conduct a large GERD GWAS meta-analysis (80,265 cases, 305,011 controls), identifying 25 independent genome-wide significant loci for GERD. Several of the implicated genes are existing or putative drug targets. Loci discovery is greatest with a broad GERD definition (including cases defined by self-report or medication data). Further, 91% of the GERD risk-increasing alleles also increase BE and/or EA risk, greatly expanding gene discovery for these traits. Our results map genes for GERD and related traits and uncover potential new drug targets for these conditions

Association studies of up to 1.2 million individuals yield new insights into the genetic etiology of tobacco and alcohol use

Tobacco and alcohol use are leading causes of mortality that influence risk for many complex diseases and disorders 1 . They are heritable 2,3 and etiologically related 4,5 behaviors that have been resistant to gene discovery efforts 6–11 . In sample sizes up to 1.2 million individuals, we discovered 566 genetic variants in 406 loci associated with multiple stages of tobacco use (initiation, cessation, and heaviness) as well as alcohol use, with 150 loci evidencing pleiotropic association. Smoking phenotypes were positively genetically correlated with many health conditions, whereas alcohol use was negatively correlated with these conditions, such that increased genetic risk for alcohol use is associated with lower disease risk. We report evidence for the involvement of many systems in tobacco and alcohol use, including genes involved in nicotinic, dopaminergic, and glutamatergic neurotransmission. The results provide a solid starting point to evaluate the effects of these loci in model organisms and more precise substance use measures

Identification of novel risk loci, causal insights, and heritable risk for Parkinson's disease: a meta-analysis of genome-wide association studies

Background Genome-wide association studies (GWAS) in Parkinson's disease have increased the scope of biological knowledge about the disease over the past decade. We aimed to use the largest aggregate of GWAS data to identify novel risk loci and gain further insight into the causes of Parkinson's disease. Methods We did a meta-analysis of 17 datasets from Parkinson's disease GWAS available from European ancestry samples to nominate novel loci for disease risk. These datasets incorporated all available data. We then used these data to estimate heritable risk and develop predictive models of this heritability. We also used large gene expression and methylation resources to examine possible functional consequences as well as tissue, cell type, and biological pathway enrichments for the identified risk factors. Additionally, we examined shared genetic risk between Parkinson's disease and other phenotypes of interest via genetic correlations followed by Mendelian randomisation. Findings Between Oct 1, 2017, and Aug 9, 2018, we analysed 7·8 million single nucleotide polymorphisms in 37 688 cases, 18 618 UK Biobank proxy-cases (ie, individuals who do not have Parkinson's disease but have a first degree relative that does), and 1·4 million controls. We identified 90 independent genome-wide significant risk signals across 78 genomic regions, including 38 novel independent risk signals in 37 loci. These 90 variants explained 16–36% of the heritable risk of Parkinson's disease depending on prevalence. Integrating methylation and expression data within a Mendelian randomisation framework identified putatively associated genes at 70 risk signals underlying GWAS loci for follow-up functional studies. Tissue-specific expression enrichment analyses suggested Parkinson's disease loci were heavily brain-enriched, with specific neuronal cell types being implicated from single cell data. We found significant genetic correlations with brain volumes (false discovery rate-adjusted p=0·0035 for intracranial volume, p=0·024 for putamen volume), smoking status (p=0·024), and educational attainment (p=0·038). Mendelian randomisation between cognitive performance and Parkinson's disease risk showed a robust association (p=8·00 × 10−7). Interpretation These data provide the most comprehensive survey of genetic risk within Parkinson's disease to date, to the best of our knowledge, by revealing many additional Parkinson's disease risk loci, providing a biological context for these risk factors, and showing that a considerable genetic component of this disease remains unidentified. These associations derived from European ancestry datasets will need to be followed-up with more diverse data. Funding The National Institute on Aging at the National Institutes of Health (USA), The Michael J Fox Foundation, and The Parkinson's Foundation (see appendix for full list of funding sources)