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Structural material development for lightweight applications aims at improving the key parameters strength, stiffness and ductility at low density, but these properties are typically mutually exclusive. Here we present how we overcome this trade-off with a new class of nano-structured steel – TiB 2 composites synthesised in-situ via bulk metallurgical spray-forming. Owing to the nano-sized dispersion of the TiB 2 particles of extreme stiffness and low density – obtained by the in-situ formation with rapid solidification kinetics – the new material has the mechanical performance of advanced high strength steels, and a 25% higher stiffness/density ratio than any of the currently used high strength steels, aluminium, magnesium and titanium alloys. This renders this High Modulus Steel the first density-reduced, high stiffness, high strength and yet ductile material which can be produced on an industrial scale. Also ideally suited for 3D printing technology, this material addresses all key requirements for high performance and cost effective lightweight design.

Out of the multitude of researched processing routes for sustainable ironmaking, hydrogen-based direct reduction and hydrogen plasma smelting reduction (HyPSR) are currently the most promising candidates for a successful industrial application. Both processes operate under gaseous atmospheres, which turn the partial and absolute pressure of hydrogen into a relevant process parameter. Here, we present first insights into the influence of total pressure and concentration of hydrogen on the reduction of hematite, focusing on the more pressure-sensitive route (HyPSR). The effect of pressure on the dissociation of H 2 molecules into metastable H atoms or H + ions,- and the overall hydrogen utilization is discussed using a thermodynamic approach. Validation experiments were conducted to testify the practical feasibility of adjusting these parameters. A decrease in the total pressure of the system from 900 mbar to 450 mbar resulted in an improved hydrogen utilization, thus suggesting that a larger population of H atoms can exist in the plasma arcs ignited under 450 mbar. An increase in the hydrogen concentration to 20 vol.% lead to undesired evaporation, likely because of a parallel increase in plasma temperature. Possibilities and challenges for exploiting these pressure-related phenomena for the industrial production of green steel are outlined and discussed.

The proposal of configurational entropy maximization to produce massive solid-solution (SS)-strengthened, single-phase high-entropy alloy (HEA) systems has gained much scientific interest. Although most of this interest focuses on the basic role of configurational entropy in SS formability, setting future research directions also requires the overall property benefits of massive SS strengthening to be carefully investigated. To this end, taking the most promising CoCrFeMnNi HEA system as the starting point, we investigate SS formability, deformation mechanisms, and the achievable mechanical property ranges of different compositions and microstructural states. A comparative assessment of the results with respect to room temperature behavior of binary Fe-Mn alloys reveals only limited benefits of massive SS formation. Nevertheless, the results also clarify that the compositional requirements in this alloy system to stabilize the face-centered cubic (fcc) SS are sufficiently relaxed to allow considering nonequiatomic compositions and exploring improved strength–ductility combinations at reduced alloying costs.

Understanding the mechanisms of shock-induced pore collapse is of great interest in various disciplines in sciences and engineering, including materials science, biological sciences, and geophysics. However, numerical modeling of the complex pore collapse processes can be costly. To this end, a strong need exists to develop surrogate models for generating economic predictions of pore collapse processes. In this work, we study the use of a data-driven reduced-order model, namely dynamic mode decomposition, and a deep generative model, namely conditional generative adversarial networks, to resemble the numerical simulations of the pore collapse process at representative training shock pressures. Since the simulations are expensive, the training data are scarce, which makes training an accurate surrogate model challenging. To overcome the difficulties posed by the complex physics phenomena, we make several crucial treatments to the plain original form of the methods to increase the capability of approximating and predicting the dynamics. In particular, physics information is used as indicators or conditional inputs to guide the prediction. In realizing these methods, the training of each dynamic mode composition model takes only around 30 s on CPU. In contrast, training a generative adversarial network model takes 8 h on GPU. Moreover, using dynamic mode decomposition, the final-time relative error is around 0.3% in the reproductive cases. We also demonstrate the predictive power of the methods at unseen testing shock pressures, where the error ranges from 1.3 to 5% in the interpolatory cases and 8 to 9% in extrapolatory cases.

Many genetically encoded biosensors use Förster resonance energy transfer (FRET) between fluorescent proteins to report biochemical phenomena in living cells. Most commonly, the enhanced cyan fluorescent protein (ECFP) is used as the donor fluorophore, coupled with one of several yellow fluorescent protein (YFP) variants as the acceptor. ECFP is used despite several spectroscopic disadvantages, namely a low quantum yield, a low extinction coefficient and a fluorescence lifetime that is best fit by a double exponential. To improve the characteristics of ECFP for FRET measurements, we used a site-directed mutagenesis approach to overcome these disadvantages. The resulting variant, which we named Cerulean (ECFP/S72A/Y145A/H148D), has a greatly improved quantum yield, a higher extinction coefficient and a fluorescence lifetime that is best fit by a single exponential. Cerulean is 2.5-fold brighter than ECFP and replacement of ECFP with Cerulean substantially improves the signal-to-noise ratio of a FRET-based sensor for glucokinase activation.

Mechanical unloading during microgravity causes skeletal muscle atrophy and impairs mitochondrial energetics. The elevated production of reactive oxygen species (ROS) by mitochondria and Nox2, coupled with impairment of stress protection (e.g., SIRT1, antioxidant enzymes), contribute to atrophy. We tested the hypothesis that the SIRT1 activator, SRT2104 would rescue unloading-induced mitochondrial dysfunction. Mitochondrial function in rat gastrocnemius and soleus muscles were evaluated under three conditions (10 days): ambulatory control (CON), hindlimb unloaded (HU), and hindlimb-unloaded-treated with SRT2104 (SIRT). Oxidative phosphorylation, electron transfer capacities, H2O2 production, and oxidative and antioxidant enzymes were quantified using high-resolution respirometry and colorimetry. In the gastrocnemius, (1) integrative (per mg tissue) proton LEAK was lesser in SIRT than in HU or CON; (2) intrinsic (relative to citrate synthase) maximal noncoupled electron transfer capacity (ECI+II) was lesser, while complex I-supported oxidative phosphorylation to ECI+II was greater in HU than CON; (3) the contribution of LEAK to ECI+II was greatest, but cytochrome c oxidase activity was lowest in HU. In both muscles, H2O2 production and concentration was greatest in SIRT, as was gastrocnemius superoxide dismutase activity. In the soleus, H2O2 concentration was greater in HU compared to CON. These results indicate that SRT2104 preserves mitochondrial function in unloaded skeletal muscle, suggesting its potential to support healthy muscle cells in microgravity by promoting necessary energy production in mitochondria.

We present recent developments in the field of austenitic steels with up to 18% reduced mass density. The alloys are based on the Fe-Mn-Al-C system. Here, two steel types are addressed. The first one is a class of low-density twinning-induced plasticity or single phase austenitic TWIP (SIMPLEX) steels with 25–30 wt.% Mn and <4–5 wt.% Al or even <8 wt.% Al when naturally aged. The second one is a class of κ-carbide strengthened austenitic steels with even higher Al content. Here, κ-carbides form either at 500–600°C or even during quenching for >10 wt.% Al. Three topics are addressed in more detail, namely, the combinatorial bulk high-throughput design of a wide range of corresponding alloy variants, the development of microstructure–property relations for such steels, and their susceptibility to hydrogen embrittlement.

Anorexia nervosa (AN) is a psychiatric disorder characterized by prolonged caloric restriction and skeletal muscle atrophy. Mitochondrial health is a key mediator of muscle function, yet the role of mitochondria during AN and following weight regain has not been investigated. The objective of this study was to evaluate mitochondrial capacities and quality control mechanisms in a rodent model of AN, spanning the acute underweight phase and multiple recovery periods. Through a series of experiments, 8‐week‐old female Sprague–Dawley rats underwent a 30‐day simulated AN protocol, followed by different durations of weight recovery via ad libitum feeding. Following designated interventions, muscle performance on a submaximal fatiguing protocol and components of mitochondrial function were evaluated. AN resulted in 23%–25% lower muscle performance compared to healthy controls, and these alterations remained even after short‐term weight gain. AN rats had 23% lower contribution of complex I to maximal mitochondrial electron transfer as well as alterations to genes important for mitochondrial translation and dynamics, many of which were not resolved with short‐term recovery. With long‐term recovery, muscle performance and mRNA content of genes related to mitochondrial translation were similar to healthy controls. However, genes related to mitochondrial fission were greater than healthy controls. AN results in reduced muscle performance during a fatiguing protocol, reliance on mitochondrial complex I and genes related to mitochondrial quality control. Many alterations persist with short‐term weight recovery; however, given sufficient time, many facets of mitochondrial health appear to normalize following AN, though there still may be long‐term consequences to mitochondrial dynamics. What is the central question of this study? How does simulated anorexia nervosa (AN) affect skeletal muscle function and mitochondrial health during AN and following different durations of weight gain in a rodent model of AN? What is the main finding and its importance? Simulated AN in female rats leads to reduced muscle and mitochondrial respiratory capacities. Short‐term weight gain does not recover muscle function nor many aspects of mitochondrial health. Long‐term weight gain restores many aspects of muscle function and mitochondrial health, but some alterations to mitochondrial dynamics appear to remain.

The element, Selenium (Se), has an essential nutritive and biological role as a trace mineral known primarily for its vital antioxidant functions as a constituent of the selenoenzyme, glutathione peroxidase. However, Se also has a much more global biological impact beyond antioxidant function. The objective of this review is to present an overview of prior research on the extra-antioxidant effects of Se with a key focus on skeletal muscle mitochondrial energetics. Cognizance of these additional functions of Se is requisite when formulating and recommending dietary supplementation of Se in humans or animals. Chief amongst its myriad of biological contributions, Se influences mitochondrial capacity and function and, subsequently, muscular health. Dietary Se supplementation has been shown to increase skeletal muscle mitochondrial volume density and within some cell lines, Se treatment increases mitochondrial biogenesis and respiratory capacity. In addition, the selenoproteins H, N, W, and O and deiodinases exhibit varying effects on mitochondrial and/or skeletal muscle function. Selenoprotein H enhances mitochondrial biogenesis whereas selenoproteins N and W appear to influence muscle calcium homeostasis which impacts mitochondrial function. Moreover, selenoprotein O's intramitochondrial residence facilitates Se's redox function. Deiodinases regulate thyroid hormone activation which impacts muscle cell regeneration, metabolism, and reactive oxygen species production. Although the precise relationships between dietary Se and skeletal muscle mitochondria remain unclear, previous research constitutes a firm foundation that portends promising new discoveries by future investigations.