Publications by authors named "William A Curtin"

Mo-Ti alloys form solid solutions over a wide range of compositions, with lattice misfit parameters increasing significantly with titanium content. This indicates a strong increase in the critical stress for edge dislocation motion. Here, we probe the transition from screw to edge dislocation-dominated strengthening in Mo-Ti solid solutions with titanium content up to 80 at%.

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The urgent need for clean energy coupled with the exceptional promise of hydrogen (H) as a clean fuel is driving development of new metals resistant to hydrogen embrittlement. Experiments on new fcc high entropy alloys present a paradox: these alloys absorb more H than Ni or SS304 (austenitic 304 stainless steel) while being more resistant to embrittlement. Here, a new theory of embrittlement in fcc metals is presented based on the role of H in driving an intrinsic ductile-to-brittle transition at a crack tip.

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Osteoporosis is associated with systemic bone loss, leading to a significant deterioration of bone microarchitecture and an increased fracture risk. Although recent studies have shown that the distribution of bone mineral becomes more heterogeneous because of estrogen deficiency in animal models of osteoporosis, it is not known whether osteoporosis alters mineral distribution in human bone. Type 2 diabetes mellitus (T2DM) can also increase bone fracture risk and is associated with impaired bone cell function, compromised collagen structure, and reduced mechanical properties.

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Fracture in metals is controlled by material behavior around the crack tip where size-dependent plasticity, now widely demonstrated at the micron scale, should play a key role. Here, a physical origin of the controlling length scales in fracture is identified using discrete-dislocation plasticity simulations. Results clearly demonstrate that the spacing between obstacles to dislocation motion controls fracture toughness.

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Despite significant advances in computational materials science, a quantitative, parameter-free prediction of the mechanical properties of alloys has been difficult to achieve from first principles. Here, we present a new analytic theory that, with input from first-principles calculations, is able to predict the strengthening of aluminium by substitutional solute atoms. Solute-dislocation interaction energies in and around the dislocation core are first calculated using density functional theory and a flexible-boundary-condition method.

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Background: Hypertonic saline (HTS) reduces the severity of lung injury in ischemia-reperfusion, endotoxin-induced and ventilation-induced lung injury. However, the potential for HTS to modulate the resolution of lung injury is not known. We investigated the potential for hypertonic saline to modulate the evolution and resolution of oleic acid induced lung injury.

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Dynamic strain ageing (DSA) is the phenomenon in which solute atoms diffuse around dislocations and retard dislocation motion, leading to negative strain-rate sensitivity (nSRS) and thus to material instabilities during processing, an important issue in commercial metal alloys. Here, we show the mechanism of DSA and nSRS on experimental strain-rate, temperature and stress scales for Al-Mg to be single-atomic-hop motion of solutes from the compression to the tension side of a dislocation core. We derive an analytic expression for the strengthening versus strain rate and temperature that justifies widely used phenomenological forms, provides specific dependences of the parameters on material properties and is supported by atomistic kinetic Monte Carlo simulations.

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Three different anti-inflammatory agents--diclofenac, dexamethasone, and N-acetylcysteine--were compared to evaluate their effectiveness in suppressing monocyte-macrophage cell culture activation and mediator release (tumor necrosis factor-alpha [TNF-alpha] and interleukin-1beta [IL-1beta]) in response to polymethylmethacrylate particulate debris. N-acetylcysteine and diclofenac were most effective in suppressing TNF-alpha and IL-1beta expression by the monocyte-macrophages. Dexamethasone reduced TNF-alpha expression but was not as effective suppressing IL-1beta expression.

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We investigated the effectiveness of an antioxidant agent, N-acetylcysteine (NAC), in suppressing macrophage activation and mediator release in response to particulate debris. Polymethylmethacrylate (PMMA) particle-stimulated monocyte-macrophages were cultured alone and with varying concentrations of NAC. Tumor necrosis factor alpha (TNFalpha) and interleukin-1beta (IL-1beta) expression in the resultant cultures were measured using enzyme-linked immunosorbant assays.

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