Mechanism and Prediction of Hydrogen Embrittlement in fcc Stainless Steels and High Entropy Alloys.

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. The theory quantitatively predicts the H concentration at which a transition to embrittlement occurs in good agreement with experiments for SS304, SS316L, CoCrNi, CoNiV, CoCrFeNi, and CoCrFeMnNi. The theory rationalizes why CoNiV is the alloy most resistant to embrittlement and why SS316L is more resistant than the high entropy alloys CoCrFeNi and CoCrFeMnNi, which opens a path for the computationally guided discovery of new embrittlement-resistant alloys.

Bone Mineral Is More Heterogeneously Distributed in the Femoral Heads of Osteoporotic and Diabetic Patients: A Pilot Study.

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. However, it is not known whether alterations in mineral distribution arise in diabetic (DB) patients' bone. In this study, we quantify mineral content distribution and tissue microarchitecture (by µCT) and mechanical properties (by compression testing) of cancellous bone from femoral heads of osteoporotic (OP; n = 10), DB (n = 7), and osteoarthritic (OA; n = 7) patients. We report that though OP cancellous bone has significantly deteriorated compressive mechanical properties and significantly compromised microarchitecture compared with OA controls, there is also a significant increase in the mean mineral content. Moreover, the heterogeneity of the mineral content in OP bone is significantly higher than controls (+25%) and is explained by a significant increase in bone volume at high mineral levels. We propose that these mineral alterations act to exacerbate the already reduced bone quality caused by reduced cancellous bone volume during osteoporosis. We show for the first time that cancellous bone mineralization is significantly more heterogeneous (+26%) in patients presenting with T2DM compared with OA (non-DB) controls, and that this heterogeneity is characterized by a significant increase in bone volume at low mineral levels. Despite these mineralization changes, bone microarchitecture and mechanical properties are not significantly different between OA groups with and without T2DM. Nonetheless, the observed alterations in mineral heterogeneity may play an important tissue-level role in bone fragility associated with OP and DB bone. © 2019 The Authors. JBMR Plus published by Wiley Periodicals, Inc. on behalf of American Society for Bone and Mineral Research.

Origin of plasticity length-scale effects in fracture.

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. The simulations support a continuum strain-gradient plasticity model and provide a physical interpretation for that model's phenomenological length scale. Analysis of a dislocation pileup under a stress gradient predicts the yield stress to increase with increasing obstacle spacing, physically rationalizing the simulations.

Quantitative prediction of solute strengthening in aluminium alloys.

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. An analytic model for the strength, or stress to move a dislocation, owing to the random field of solutes, is then presented. The theory, which has no adjustable parameters and is extendable to other metallic alloys, predicts both the energy barriers to dislocation motion and the zero-temperature flow stress, allowing for predictions of finite-temperature flow stresses. Quantitative comparisons with experimental flow stresses at temperature T=78 K are made for Al-X alloys (X=Mg, Si, Cu, Cr) and good agreement is obtained.

Hypertonic saline reduces inflammation and enhances the resolution of oleic acid induced acute lung injury.

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. METHODS: Adult male Sprague Dawley rats were used in all experiments. Series 1 examined the potential for HTS to reduce the severity of evolving oleic acid (OA) induced acute lung injury. Following intravenous OA administration, animals were randomized to receive isotonic (Control, n = 12) or hypertonic saline (HTS, n = 12), and the extent of lung injury assessed after 6 hours. Series 2 examined the potential for HTS to enhance the resolution of oleic acid (OA) induced acute lung injury. Following intravenous OA administration, animals were randomized to receive isotonic (Control, n = 6) or hypertonic saline (HTS, n = 6), and the extent of lung injury assessed after 6 hours. RESULTS: In Series I, HTS significantly reduced bronchoalveolar lavage (BAL) neutrophil count compared to Control [61.5 +/- 9.08 versus 102.6 +/- 11.89 x 10(3) cells.ml-1]. However, there were no between group differences with regard to: A-a O2 gradient [11.9 +/- 0.5 vs. 12.0 +/- 0.5 KPa]; arterial PO2; static lung compliance, or histologic injury. In contrast, in Series 2, hypertonic saline significantly reduced histologic injury and reduced BAL neutrophil count [24.5 +/- 5.9 versus 46.8 +/- 4.4 x 10(3) cells.ml-1], and interleukin-6 levels [681.9 +/- 190.4 versus 1365.7 +/- 246.8 pg.ml-1]. CONCLUSION: These findings demonstrate, for the first time, the potential for HTS to reduce pulmonary inflammation and enhance the resolution of oleic acid induced lung injury.

A predictive mechanism for dynamic strain ageing in aluminium-magnesium alloys.

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. Using literature material properties, the predicted strengthening quantitatively agrees with the experimentally derived behaviour of Al-2.5% Mg at 300 K, and qualitatively agrees with the strain rate and temperature ranges of DSA and nSRS in Al-Mg alloys. The analyses herein show a clear path for multiscale design, from quantum to continuum mechanics, of solute strengthening in face-centred-cubic metal alloys.

Comparison of different anti-inflammatory agents in suppressing the monocyte response to orthopedic particles.

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. N-acetylcysteine and dexamethasone had no effect on cell viability whereas diclofenac at the highest concentrations decreased cell viabilities. N-acetylcysteine and diclofenac, but less so dexamethasone, are effective in suppressing wear debris-related cell activation and mediator release and thus potentially represent therapeutic or preventive modalities for periprosthetic osteolysis.

Inhibition of polymethylmethacrylate particle-induced monocyte activation and IL-1beta and TNF-alpha expression by the antioxidant agent N-acetylcysteine.

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. The ultrastructural effect of treatment was also assessed by electron microscopy. Cell viability in the various cultures was measured to rule out an effect of cytotoxicity. NAC treatment reduced TNFalpha and IL-1beta expression by the monocyte-macrophages. Culturing with NAC was also associated with less ultrastructural activation of the monocytes. Furthermore, NAC was not associated with any adverse effect on cell viability in the concentrations used. Our findings demonstrate the effectiveness of the antioxidant N-acetylcysteine in suppressing the cell activation and TNFalpha release seen on exposure to wear debris. This represents a novel potential therapeutic method in the prevention or treatment of periprosthetic osteolysis.