Three dimensional (3D) microstructure-based modeling of interfacial decohesion in particle reinforced metal matrix composites

Modeling and prediction of the overall elastic–plastic response and local damage mechanisms in heterogeneous materials, in particular particle reinforced composites, is a very complex problem. Microstructural complexities such as the inhomogeneous spatial distribution of particles, irregular morphology of the particles, and anisotropy in particle orientation after secondary processing, such as extrusion, significantly affect deformation behavior. We have studied the effect of particle/matrix interface debonding in SiC particle reinforced Al alloy matrix composites with (a) actual microstructure consisting of angular SiC particles and (b) idealized ellipsoidal SiC particles. Tensile deformation in SiC particle reinforced Al matrix composites was modeled using actual microstructures reconstructed from serial sectioning approach. Interfacial debonding was modeled using user-defined cohesive zone elements. Modeling with the actual microstructure (versus idealized ellipsoids) has a significant influence on: (a) localized stresses and strains in particle and matrix, and (b) far-field strain at which localized debonding takes place. The angular particles exhibited higher degree of load transfer and are more sensitive to interfacial debonding. Larger decreases in stress are observed in the angular particles, because of the flat surfaces, normal to the loading axis, which bear load. Furthermore, simplification of particle morphology may lead to erroneous results

Interpretation of Fracture Toughness and R-Curve Behavior by Direct Observation of Microfracture Process in Ti-Based Dendrite-Containing Amorphous Alloys

Fracture properties of Ti-based amorphous alloys containing ductile beta dendrites were explained by directly observing microfracture processes. Three Ti-based amorphous alloys were fabricated by adding Ti, Zr, V, Ni, Al, and Be into a Ti-6Al-4V alloy by a vacuum arc melting method. The effective sizes of dendrites varied from 63 to 104 mu m, while their volume fractions were almost constant within the range from 74 to 76 pct. The observation of the microfracture of the alloy containing coarse dendrites revealed that a microcrack initiated at the amorphous matrix of the notch tip and propagated along the amorphous matrix. In the alloy containing fine dendrites, the crack propagation was frequently blocked by dendrites, and many deformation bands were formed near or in front of the propagating crack, thereby resulting in a zig-zag fracture path. Crack initiation toughness was almost the same at 35 to 36 MPaaem within error ranges in the three alloys because it was heavily affected by the stress applied to the specimen at the time of crack initiation at the crack tip as well as strength levels of the alloys. According to the R-curve behavior, however, the best overall fracture properties in the alloy containing fine dendrites were explained by mechanisms of blocking of the crack growth and crack blunting and deformation band formation at dendrites. (C) The Minerals, Metals & Materials Society and ASM International 2015ope

Type I Interferons Induce T Regulatory 1 Responses and Restrict Humoral Immunity during Experimental Malaria

We thank Christopher Hunter and Bob Axtell for critical feedback, and the Flow Cytometry Laboratory at OUHSC for technical assistance.Author Summary Humoral immunity is essential for host resistance to pathogens that trigger highly inflammatory immune responses, including Plasmodium parasites, the causative agents of malaria. Long-lived, secreted antibody responses depend on a specialized subset of CD4 T cells called T follicular helper (Tfh) cells. However, anti-Plasmodium humoral immunity is often short-lived, non-sterilizing, and immunity rapidly wanes, leaving individuals susceptible to repeated bouts of malaria. Here we explored the relationship between inflammatory type I interferons, the regulation of pathogen-specific CD4 T cell responses, and humoral immunity using models of experimental malaria and systemic virus infection. We identified that type I interferons promote the formation and accumulation of pathogen-specific CD4 T regulatory 1 cells that co-express interferon-gamma and interleukin-10. Moreover, we show that the combined activity of interferon-gamma and interleukin-10 limits the magnitude of infection-induced Tfh responses, the secretion of parasite-specific secreted antibody, and parasite control. Our study provides new insight into the regulation of T regulatory 1 responses and humoral immunity during inflammatory immune reactions against systemic infections.Yeshttp://www.plospathogens.org/static/editorial#pee