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The effects of particulate fraction, rolling thickness reduction, and heat treatment on the microstructure and mechanical properties of an Al-Cu-Mg-Sc/TiB 2  composite (TiB 2  /Al2618) are analyzed. The yield strength (YS), ultimate tensile strength (UTS), and elongation of both the matrix alloy and TiB 2 /Al2618 composite are increased with the increase of rolling reduction. The YS and UTS reach 250 MPa and 300 MPa, respectively, after a 70% rolling reduction, which are 16.3% and 7.4% higher than the unreinforced matrix alloy of an identical amount of rolling reduction. After solid solution and artificial aging treatment, both YS and UTS are further increased for both the matrix alloy and the composites with a 35% rolling reduction. While for those with 70% rolling reduction, the improvement is alleviated. The effects of hot rolling, heat treatment, and TiB 2 particulates on the microstructure and mechanical properties are discussed to understand the underlying mechanisms. Graphical abstract

A micromechanical simulation has been performed to study the effect of particle distribution on the mechanical properties and damage behaviors of particle reinforced metal matrix composites (PRMMCs). Two-dimensional (2D) representative volume elements with variable particle size, volume fraction and particle distribution were generated and subjected to finite element simulation. An enhanced continuum model, which incorporates dislocation punching effect at particle-matrix interfaces and Taylor-based nonlocal theory of plasticity in matrix, was used to simulate the mismatch in coefficients of thermal expansion strengthening and particle size-dependent strengthening. Additionally, constitutive damage behaviors were involved in simulating the crack initiation and evolution, considering the ductile damage in matrix and dislocation punching zone, as well as the particle cracking. Simulation results indicate that refining the particle size is helpful to improve the tensile strength and fracture resistance of PRMMCs, whereas the increase of particle clustering volume fraction or severity facilitates damage evolution and deteriorates the mechanical properties. Statistical analysis indicates a negative linear dependence between particle distribution homogeneity and the ductility, given a constant particle size and volume fraction.

Understanding cellular metabolism holds immense potential for developing new classes of therapeutics that target metabolic pathways in cancer. Metabolic pathways are altered in bulk neoplastic cells in comparison to normal tissues. However, carcinoma cells within tumors are heterogeneous, and tumor-initiating cells (TICs) are important therapeutic targets that have remained metabolically uncharacterized. To understand their metabolic alterations, we performed metabolomics and metabolite tracing analyses, which revealed that TICs have highly elevated methionine cycle activity and transmethylation rates that are driven by MAT2A. High methionine cycle activity causes methionine consumption to far outstrip its regeneration, leading to addiction to exogenous methionine. Pharmacological inhibition of the methionine cycle, even transiently, is sufficient to cripple the tumor-initiating capability of these cells. Methionine cycle flux specifically influences the epigenetic state of cancer cells and drives tumor initiation. Methionine cycle enzymes are also enriched in other tumor types, and MAT2A expression impinges upon the sensitivity of certain cancer cells to therapeutic inhibition.Elevated activity of the methionine cycle is essential for cancer stem cell tumorigenesis and represents a therapeutic vulnerability.

Since the first discovery of the fatigue phenomenon in the late 1830s, efforts to fight against fatigue failure have continued. Here we report a fatigue resistance phenomenon in nano-TiB2-decorated AlSi10Mg enabled by additive manufacturing. This fatigue resistance mechanism benefits from the three-dimensional dual-phase cellular nanostructure, which acts as a strong volumetric nanocage to prevent localized damage accumulation, thus inhibiting fatigue crack initiation. The intrinsic fatigue strength limit of nano-TiB2-decorated AlSi10Mg was proven to be close to its tensile strength through the in situ fatigue tests of a defect-free microsample. To demonstrate the practical applicability of this mechanism, printed bulk nano-TiB2-decorated AlSi10Mg achieved fatigue resistance more than double those of other additive manufacturing Al alloys and surpassed those of high-strength wrought Al alloys. This strategy of additive-manufacturing-assisted nanostructure engineering can be extended to the development of other dual-phase fatigue-resistant metals.An ultrahigh fatigue-resistant AlSi10Mg alloy is achieved by additive manufacturing, with its three-dimensional dual-phase cellular nanostructure acting as a strong volumetric nanocage to inhibit fatigue damage accumulation.

A large amount of low-grade waste heat (flue gas waste heat) cannot be fully utilized in thermal power plants in non-heating seasons; therefore, this study combines cross-seasonal heat storage technology with the cross-seasonal storage of low-grade waste heat in power plants. We propose a cross-seasonal underground heat storage and gas turbine co-generation coupling system to recover low-grade waste heat and large-scale cross-seasonal space–time migration and utilization. The basic law of soil heat storage and release was elucidated through a geotechnical thermal response experiment. The results show that the initial average temperature of the rock and soil mass within a depth range of 0–300 m in the study area was 16.7 °C, λ was 1.97 W/(m∙K), Cv was 2655 kJ/(m3∙K), and R was 0.353 (m∙K)/W. An increase in the operating share decreases unit heat transfer per linear meter of buried pipe heat exchanger. The heat release per unit linear meter increases with the average temperature of the circulating medium in the heat release mode. Similarly, the heat absorption per unit linear meter increases with the rock and soil temperature in the heat absorption mode.

Reduced methionine (Met) intake can extend lifespan of rodents; however, whether this regimen represents a general strategy for regulating aging has been controversial. Here we report that Met restriction extends lifespan in both fruit flies and yeast, and that this effect requires low amino-acid status. Met restriction in Drosophila mimicks the effect of dietary restriction and is associated with decreased reproduction. However, under conditions of high amino-acid status, Met restriction is ineffective and the trade-off between longevity and reproduction is not observed. Overexpression of InRDN or Tsc2 inhibits lifespan extension by Met restriction, suggesting the role of TOR signalling in the Met control of longevity. Overall, this study defines the specific roles of Met and amino-acid imbalance in aging and suggests that Met restiction is a general strategy for lifespan extension. Dietary restriction of the amino acid methionine extends the lifespan of rodents. Here the authors systematically test diets with varying amino-acid content and show that methionine restriction extends the lifespan of yeast and flies only when the content of other amino acids in the diet is also low.

Alteration of normal ploidy (aneuploidy) can have a number of opposing effects, such as unbalancing protein abundances and inhibiting cell growth but also accelerating genetic diversification and rapid adaptation. The interplay of these detrimental and beneficial effects remains puzzling. Here, to understand how cells develop tolerance to aneuploidy, we subject disomic (i.e. with an extra chromosome copy) strains of yeast to long-term experimental evolution under strong selection, by forcing disomy maintenance and daily population dilution. We characterize mutations, karyotype alterations and gene expression changes, and dissect the associated molecular strategies. Cells with different extra chromosomes accumulated mutations at distinct rates and displayed diverse adaptive events. They tended to evolve towards normal ploidy through chromosomal DNA loss and gene expression changes. We identify genes with recurrent mutations and altered expression in multiple lines, revealing a variant that improves growth under genotoxic stresses. These findings support rapid evolvability of disomic strains that can be used to characterize fitness effects of mutations under different stress conditions. Aneuploidy (abnormal chromosome number) can enable rapid adaptation to stress conditions, but it also entails fitness costs from gene imbalance. Here, the authors experimentally evolve yeast while forcing maintenance of aneuploidy to identify the mechanisms that promote tolerance of aneuploidy.

Metallic materials typically experience significant strength degradation at elevated temperatures. Traditional strengthening methods, which rely on thermally stable particle dispersion, exhibit limited effectiveness owing to the challenges in suppressing thermally activated dislocation motion. This work introduces a strategy for achieving exceptional high-temperature strength through a thermally stable nanoscale eutectic cellular network (ECN) enabled by additive manufacturing. A near-eutectic AlLaScZr alloy is developed for laser powder bed fusion, incorporating an Al-La nanoscale ECN and dense intracellular nanoprecipitates. This alloy demonstrates excellent printability and remarkable high-temperature yield strength above 0.6 T m (~250 MPa at 300 °C), outperforming conventional aluminium alloys by 2–5 times with minimal degradation after prolonged annealing. Compared with the conventional configuration of particle dispersion, the nanoscale ECN architecture enhances load-bearing capacity and strengthens aluminium by caging dislocation motion within ultrafine cells (~200 nm), effectively mitigating intrinsic high-temperature softening. Metallic materials suffer severe strength degradation at elevated temperatures. The authors report exceptional high-temperature strength in an additive manufactured aluminum alloy with a thermally stable nanoscale eutectic cellular network.

Mammalian lifespan differs by >100 fold, but the mechanisms associated with such longevity differences are not understood. Here, we conducted a study on primary skin fibroblasts isolated from 16 species of mammals and maintained under identical cell culture conditions. We developed a pipeline for obtaining species-specific ortholog sequences, profiled gene expression by RNA-seq and small molecules by metabolite profiling, and identified genes and metabolites correlating with species longevity. Cells from longer lived species up-regulated genes involved in DNA repair and glucose metabolism, down-regulated proteolysis and protein transport, and showed high levels of amino acids but low levels of lysophosphatidylcholine and lysophosphatidylethanolamine. The amino acid patterns were recapitulated by further analyses of primate and bird fibroblasts. The study suggests that fibroblast profiling captures differences in longevity across mammals at the level of global gene expression and metabolite levels and reveals pathways that define these differences.

To understand the genetic basis and selective forces acting on longevity, it is useful to examine lifespan variation among closely related species, or ecologically diverse isolates of the same species, within a controlled environment. In particular, this approach may lead to understanding mechanisms underlying natural variation in lifespan. Here, we analyzed 76 ecologically diverse wild yeast isolates and discovered a wide diversity of replicative lifespan (RLS). Phylogenetic analyses pointed to genes and environmental factors that strongly interact to modulate the observed aging patterns. We then identified genetic networks causally associated with natural variation in RLS across wild yeast isolates, as well as genes, metabolites, and pathways, many of which have never been associated with yeast lifespan in laboratory settings. In addition, a combined analysis of lifespan-associated metabolic and transcriptomic changes revealed unique adaptations to interconnected amino acid biosynthesis, glutamate metabolism, and mitochondrial function in long-lived strains. Overall, our multiomic and lifespan analyses across diverse isolates of the same species shows how gene–environment interactions shape cellular processes involved in phenotypic variation such as lifespan.