Reaction kinetic analysis of damage rate effects on defect structural evolution in Fe–Cu

In Fe–Cu alloys, Cu precipitates are formed during high-energy particle irradiation. If there exists energetic binding between vacancies and Cu atoms, vacancy clusters (voids) are formed in precipitates at an initial stage of irradiation, separate from voids in the matrix, because of the migration of Cu atoms with vacancies. In this paper, the damage rate dependence on the formation and annihilation of voids in the precipitates and in the matrix is simulated by reaction kinetic analysis. The initial formation of voids at precipitates, the annihilation of them with an increased dosage and new formation of voids in the matrix are simulated, and the results are compared with the experiments. In a high damage rate of 3.3 × 10^[−7] dpa/s, the formation of voids in Cu precipitates is not significant, but the formation of voids in the matrix is dominant, different from those in a low damage rate of 1.5 × 10^[−10] dpa/s

Reaction kinetic analysis of reactor surveillance data

Available online 30 January 2015In reactor pressure vessel surveillance data, it was found that the concentration of matrix defects was very low even after nearly 40 years of operation, though a large number of precipitates existed. In this paper, defect structures obtained from surveillance data of A533B (high Cu concentration) were simulated using reaction kinetic analysis with 11 rate equations. The coefficients used in the equations were quite different from those obtained by fitting a Fe-0.6 wt%Cu alloy irradiated by the Kyoto University Reactor. The difference was mainly caused by alloying elements in A533B, and the effect of alloying elements was extracted. The same code was applied to low-Cu A533B irradiated with high irradiation damage rate, and the formation of voids was correctly simulated

Wettability Modification of Nanomaterials by Low-Energy Electron Flux

Controllable modification of surface free energy and related properties (wettability, hygroscopicity, agglomeration, etc.) of powders allows both understanding of fine physical mechanism acting on nanoparticle surfaces and improvement of their key characteristics in a number of nanotechnology applications. In this work, we report on the method we developed for electron-induced surface energy and modification of basic, related properties of powders of quite different physical origins such as diamond and ZnO. The applied technique has afforded gradual tuning of the surface free energy, resulting in a wide range of wettability modulation. In ZnO nanomaterial, the wettability has been strongly modified, while for the diamond particles identical electron treatment leads to a weak variation of the same property. Detailed investigation into electron-modified wettability properties has been performed by the use of capillary rise method using a few probing liquids. Basic thermodynamic approaches have been applied to calculations of components of solid–liquid interaction energy. We show that defect-free, low-energy electron treatment technique strongly varies elementary interface interactions and may be used for the development of new technology in the field of nanomaterials

Anaplasma phagocytophilum Ats-1 Is Imported into Host Cell Mitochondria and Interferes with Apoptosis Induction

Anaplasma phagocytophilum, the causative agent of human granulocytic anaplasmosis, infects human neutrophils and inhibits mitochondria-mediated apoptosis. Bacterial factors involved in this process are unknown. In the present study, we screened a genomic DNA library of A. phagocytophilum for effectors of the type IV secretion system by a bacterial two-hybrid system, using A. phagocytophilum VirD4 as bait. A hypothetical protein was identified as a putative effector, hereby named Anaplasma translocated substrate 1 (Ats-1). Using triple immunofluorescence labeling and Western blot analysis of infected cells, including human neutrophils, we determined that Ats-1 is abundantly expressed by A. phagocytophilum, translocated across the inclusion membrane, localized in the host cell mitochondria, and cleaved. Ectopically expressed Ats-1 targeted mitochondria in an N-terminal 17 residue-dependent manner, localized in matrix or at the inner membrane, and was cleaved as native protein, which required residues 55–57. In vitro-translated Ats-1 was imported in a receptor-dependent manner into isolated mitochondria. Ats-1 inhibited etoposide-induced cytochrome c release from mitochondria, PARP cleavage, and apoptosis in mammalian cells, as well as Bax-induced yeast apoptosis. Ats-1(55–57) had significantly reduced anti-apoptotic activity. Bax redistribution was inhibited in both etoposide-induced and Bax-induced apoptosis by Ats-1. Taken together, Ats-1 is the first example of a bacterial protein that traverses five membranes and prevents apoptosis at the mitochondria