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- Babu, Prasath, et al.
(författare)
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On the formation and stability of precipitate phases in a near lamellar γ-TiAl based alloy during creep
- 2018
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Ingår i: Intermetallics (Barking). - : Elsevier. - 0966-9795 .- 1879-0216. ; 98, s. 115-125
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Tidskriftsartikel (refereegranskat)abstract
- The formation, evolution and stability of metastable phases observed in the γ-TiAl based alloy Ti-47Al-2Cr-2Nb was studied under creep deformation with stress applied at two different hard orientations in a highly textured as-cast + HIPed material. Previously we have reported that the metastable phase Ti(Al,Cr)2 with C14 Laves phase structure forms at the γ-α2 interface which acts as sink for the alloying elements ejected from the dissolving α2 phase and also expected to effectively control the interface stresses through short range diffusion and modifications in the chemical composition [1]. Ab initio density functional theory based calculations were carried out to evaluate the effect of choice of lattice position and site occupancy of aluminium atoms in the Ti(Al,Cr)2 structure on the lattice parameter variation and thermodynamic stability. C14 with the composition 25 at. % Al was found to have lattice parameter values close to the inter-planar spacing of <110>γ and <10-10>α2 which would have a lower misfit with C14 across the interface. From the cohesive energy calculations, Laves phase C14 with a constrained lattice parameter due to the adjoining phases, exhibits higher stability than the B2 and L10 structures across a range of compositions studied. Electron diffraction simulations of C14 with a composition of 25% Al compared with the experimental data suggest that the structure C14 has taken up either a random site occupancy compared to a specific choice of ordering to minimize the interfacial stress. Though the experimental evidences do not strongly support a long-range ordering theory in C14, short-range ordering could be a tangible choice for alleviating interface misfits. The ability of C14 to assume different lattice parameters at and far from the α2-γ interface also suggest that the C14 acts as buffer layer between α2 and γ phases in the presence of local stresses, although this is not the thermodynamically expected phase at the temperature of creep experiment.
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| 2. |
- Segre, Ayellet V., et al.
(författare)
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Common Inherited Variation in Mitochondrial Genes Is Not Enriched for Associations with Type 2 Diabetes or Related Glycemic Traits
- 2010
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Ingår i: PLoS Genetics. - : Public Library of Science (PLoS). - 1553-7404. ; 6:8
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Tidskriftsartikel (refereegranskat)abstract
- Mitochondrial dysfunction has been observed in skeletal muscle of people with diabetes and insulin-resistant individuals. Furthermore, inherited mutations in mitochondrial DNA can cause a rare form of diabetes. However, it is unclear whether mitochondrial dysfunction is a primary cause of the common form of diabetes. To date, common genetic variants robustly associated with type 2 diabetes (T2D) are not known to affect mitochondrial function. One possibility is that multiple mitochondrial genes contain modest genetic effects that collectively influence T2D risk. To test this hypothesis we developed a method named Meta-Analysis Gene-set Enrichment of variaNT Associations (MAGENTA; http://www.broadinstitute.org/mpg/magenta). MAGENTA, in analogy to Gene Set Enrichment Analysis, tests whether sets of functionally related genes are enriched for associations with a polygenic disease or trait. MAGENTA was specifically designed to exploit the statistical power of large genome-wide association (GWA) study meta-analyses whose individual genotypes are not available. This is achieved by combining variant association p-values into gene scores and then correcting for confounders, such as gene size, variant number, and linkage disequilibrium properties. Using simulations, we determined the range of parameters for which MAGENTA can detect associations likely missed by single-marker analysis. We verified MAGENTA's performance on empirical data by identifying known relevant pathways in lipid and lipoprotein GWA meta-analyses. We then tested our mitochondrial hypothesis by applying MAGENTA to three gene sets: nuclear regulators of mitochondrial genes, oxidative phosphorylation genes, and,1,000 nuclear-encoded mitochondrial genes. The analysis was performed using the most recent T2D GWA meta-analysis of 47,117 people and meta-analyses of seven diabetes-related glycemic traits (up to 46,186 non-diabetic individuals). This well-powered analysis found no significant enrichment of associations to T2D or any of the glycemic traits in any of the gene sets tested. These results suggest that common variants affecting nuclear-encoded mitochondrial genes have at most a small genetic contribution to T2D susceptibility.
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