A Re-examination of the Portevin-Le Chatelier Effect in Alloy 718 in Connection with Oxidation-Assisted Intergranular Cracking

In Alloy 718, a sharp transition exists in the fracture path changing from an intergranular brittle mode to a transgranular ductile mode which is associated with a transition of flow behavior from smooth in the dynamic strain aging regime to a serrated one in the Portevin-Le Chatelier (PLC) regime. In order to better understand both deformation and rupture behavior, PLC phenomenon in a precipitation-hardened nickel-base superalloy was carefully investigated in a wide range of temperatures [573 K to 973 K (300°C to 700°C)] and strain rates (109^-5 to 3.2910^-2 s^-1 ). Distinction was made between two PLC domains characterized by different evolutions of the critical strain to the onset of the first serration namely normal and inverse behavior. The apparent activation energies associated with both domains were determined using different methods. Results showed that normal and inverse behavior domains are related to dynamic interaction of dislocations with, respectively, interstitial and substitutional solutes atoms. This analysis confirms that normal PLC regime may be associated to the diffusion of carbon atoms, whereas the substitutional species involves in the inverse regime is discussed with an emphasis on the role of Nb and Mo

Atomic Species Associated with the Portevin–Le Chatelier Effect in Superalloy 718 Studied by Mechanical Spectroscopy

In many Ni-based superalloys, dynamic strain aging (DSA) generates an inhomogeneous plastic deformation resulting in jerky flow known as the Portevin--Le Chatelier (PLC) effect. This phenomenon has a deleterious effect on the mechanical properties and, at high temperature, is related to the diffusion of substitutional solute atoms toward the core of dislocations. However, the question about the nature of the atomic species responsible for the PLC effect at high temperature still remains open. The goal of the present work is to answer this important question; to this purpose, three different 718-type and a 625 superalloy were studied through a nonconventional approach by mechanical spectroscopy. The internal friction (IF) spectra of all the studied alloys show a relaxation peak P718 (at 885 K for 0.1 Hz) in the same temperature range, 700 K to 950 K, as the observed PLC effect. The activation parameters of this relaxation peak have been measured, Ea(P718){\thinspace}={\thinspace}2.68{\thinspace}{\textpm}{\thinspace}0.05 eV, $\tau$0{\thinspace}={\thinspace}2{\textperiodcentered}10-15 {\textpm} 1 s as well as its broadening factor $\beta${\thinspace}={\thinspace}1.1. Experiments on different alloys and the dependence of the relaxation strength on the amount of Mo attribute this relaxation to the stress-induced reorientation of Mo-Mo dipoles due to the short distance diffusion of one Mo atom by exchange with a vacancy. Then, it is concluded that Mo is the atomic species responsible for the high-temperature PLC effect in 718 superallo

Distinct iron architecture in SF3B1-mutant myelodysplastic syndrome patients is linked to an SLC25A37 splice variant with a retained intron

Perturbation in iron homeostasis is a hallmark of some hematologic diseases. Abnormal sideroblasts with accumulation of iron in the mitochondria are named ring sideroblasts (RS). RS is a cardinal feature of refractory anemia with RS (RARS) and RARS with marked thrombocytosis (RARS/-T). Mutations in SF3B1, a member of the RNA splicing machinery are frequent in RARS/-T and defects of this gene were linked to RS formation. Here we showcase the differences in iron architecture of SF3B1-mutant and wild-type (WT) RARS/-T and provide new mechanistic insights by which SF3B1 mutations lead to differences in iron. We found higher iron levels in SF3B1 mutant vs WT RARS/-T by transmission electron microscopy/spectroscopy/flow cytometry. SF3B1 mutations led to increased iron without changing the valence as shown by the presence of Fe2+ in mutant and WT. Reactive oxygen species and DNA damage were not increased in SF3B1-mutant patients. RNA-sequencing and Reverse transcriptase PCR showed higher expression of a specific isoform of SLC25A37 in SF3B1-mutant patients, a crucial importer of Fe2+ into the mitochondria. Our studies suggest that SF3B1 mutations contribute to cellular iron overload in RARS/-T by deregulating SLC25A37

Differences in Iron Distribution in Patients with Myelodysplastic Syndromes Carrying SF3B1 Mutations Using Energy-dispersive X-ray Spectroscopy (XEDS) and Electron-Energy Loss Spectroscopy (EELS)

Extended abstract of a paper presented at Microscopy and Microanalysis 2013 in Indianapolis, Indiana, USA, August 4 – August 8, 2013