Small ring testing of a creep resistant material

Many components in conventional and nuclear power plant, aero-engines, chemical plant etc., operate at temperatures which are high enough for creep to occur. These include steam pipes, pipe branches, gas and steam turbine blades, etc. The manufacture of such components may also require welds to be part of them. In most cases, only nominal operating conditions (i.e. pressure, temperatures, system load, etc.) are known and hence precise life predictions for these components are not possible. Also, the proportion of life consumed will vary from position to position within a component. Hence, non-destructive techniques are adopted to assist in making decisions on whether to repair, continue operating or replace certain components. One such approach is to test a small sample removed from the component to make small creep test specimens which can be tested to give information on the remaining creep life of the component. When such a small sample cannot be removed from the operating component, e.g. in the case of small components, the component can be taken out of operation in order to make small creep test specimens, the results from which can then be used to assist with making decisions regarding similar or future components. This paper presents a small creep test specimen which can be used for the testing of particularly strong and creep resistant materials, such as nickel-based superalloys

ECCC TEST PROGRAMME AND DATA ASSESSMENT ON GTD111 CREEP RUPTURE, STRAIN AND DUCTILITY

GTD111, a creep resistant Ni-based superalloy developed by GE, is widely used in land-based gas turbine first stage blades. However, there is little published information on its creep properties and microstructure. The European Creep Collaborative Committee (ECCC) Working Group 3C consequently selected GTD111 as a model material for testing and complementary data assessment. The aim of this paper is to present the results from the ECCC test program and data assessment, and to compare equiaxed (EA) and directionally solidified (DS) material performance. Testing and metallographic laboratories from six European nations collaborated to produce strain monitored creep rupture data on four EA and DS materials out to beyond 10,000 hours within a wide range of temperatures, 850-950°C, and stresses, 293-99 MPa. Available (generally short term) results from other sources were also included in the compiled, small but viable, 51-test data set. Assessment was carried out by three different assessors using different tools and adopting different prediction models. Conventional ECCC post-assessment techniques and novel “back-fitting” methods were used to identify a preferred model. It was shown that assessing all the EA and DS data together can lead to non-conservative predictions for EA materials, but separating the two classes creates small data subsets which cannot be modelled effectively. As a pragmatic compromise, the DS data and those EA data which also showed good ductility were included in a final "ductile GTD111" assessment. The resulting creep rupture material models and rupture strength predictions are presented up to 3 times the longest test duration. It was then shown that the performance of lower ductility EA materials can also be predicted effectively with the "ductile" model by truncating the rupture time at the measured fracture strain. For this exercise, a creep strain model based on rupture and time to strain data was fitted. In parallel, microstructural examination was performed to characterize the damage modes involved in the low ductility failures. It was thereby shown that the creep rupture strength shortfall of an EA material compared to its DS equivalent is not a constant factor, but is primarily governed by the reduced creep ductility. Hence, the shortfall varies between different EA casts, and tends to become greater in the longer term.JRC.F.4-Innovative Technologies for Nuclear Reactor Safet

Geographical Detector-Based Risk Assessment of the Under-Five Mortality in the 2008 Wenchuan Earthquake, China

On 12 May, 2008, a devastating earthquake registering 8.0 on the Richter scale occurred in Sichuan Province, China, taking tens of thousands of lives and destroying the homes of millions of people. Many of the deceased were children, particular children less than five years old who were more vulnerable to such a huge disaster than the adult. In order to obtain information specifically relevant to further researches and future preventive measures, potential risk factors associated with earthquake-related child mortality need to be identified. We used four geographical detectors (risk detector, factor detector, ecological detector, and interaction detector) based on spatial variation analysis of some potential factors to assess their effects on the under-five mortality. It was found that three factors are responsible for child mortality: earthquake intensity, collapsed house, and slope. The study, despite some limitations, has important implications for both researchers and policy makers

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

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

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