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C250 steel, renowned for its remarkable strength and toughness, is extensively utilized in the aerospace industry for manufacturing critical components. This research investigates the microstructure and properties of forgings produced through different heat treatment temperatures, aging durations, and thermal cycling intervals. The results demonstrate that the samples were compressed at 1050 °C followed by air-cooling using the conventional maraging treatment. For the cycle heat treatment, temperature was maintained at 1050 °C and cycled 1–2 times, with a heat preservation period of 1 h and subsequent water-cooling. Solution heat treatment at a temperature of 1050 °C, aging for 5 h, and then air hardening were performed to achieve the best forging hardness. Interestingly, the solution time under age hardening conditions had no significant effect on the grain size but had a significant effect on the hardness of martensitic aged steel. [ABSTRACT FROM AUTHOR]

A new kind of low-carbon bainite steel with excellent strength and toughness was developed, serving as the bogie of the next-generation high-speed train. However, the softening of the heat-affected zone (HAZ) in laser-arc hybrid welding (LAHW) needs to be overcome. In this study, the effect of the cooling rate of the LAHW process on the microstructure and mechanical properties in the HAZ was explored via thermal simulation. The results showed that with increased cooling rate, the grain size increased, the content of lath martensite decreased, and the lath bainite gradually changed to a granular shape in the thermal simulation specimen. With the decrease in the cooling rate, i.e., with the increase of t8/5, the strength–toughness matching of the material showed a downward trend. The thermal simulation specimen with a t8/5 of 6~8 s had higher strength and good toughness, which can be considered a potential welding parameter reference. The content of martensitic austenite (M-A) constituents was the main factor that determined the strength and toughness of the joint. During the tensile test, the axial force caused the material to tighten, and the transverse stress as obvious in the part of the M-A constituents that are prone to microcracks and many defects, resulting in cracks, paths, and multi-component layers in the center. As a result, the thermal cycle specimens had mixed fracture characteristics. [ABSTRACT FROM AUTHOR]

Wnt/β-catenin is a crucial repressor of adipogenesis. We have shown that E2 promoter binding factor 1 (E2F1) suppresses Wnt/β-catenin activity through transactivation of β-catenin interacting protein 1 (CTNNBIP1), also known as inhibitor of β-catenin and TCF4 (ICAT) in human colorectal cancers. However, it remains unknown whether ICAT is required for E2F1 to promote differentiation by inhibiting β-catenin activity in pre-adipocytes. In the present study, we found that 1-methyl-3-isobutylxanthine, dexamethasone, and insulin (MDI)-induced differentiation and lipid accumulation in 3T3-L1 pre-adipocytes was reversed by activation of β-catenin triggered by CHIR99021, a GSK3β inhibitor. Intriguingly, we observed a reduced protein level of E2F1 and ICAT at a later stage of pre-adipocytes differentiation. Importantly, overexpression of ICAT in 3T3-L1 pre-adipocytes markedly promote the adipogenesis and partially reversed the inhibitory effect of CHIR99021 on MDI-induced adipogenesis and lipid accumulation by regulating adipogenic regulators and Wnt/β-catenin targets. Moreover, pre-adipocytes differentiation induced by MDI were markedly inhibited in siE2F1 or siICAT transfected 3T3-L1 cells. Gene silencing of ICAT in the E2F1 overexpressed adipocytes also inhibited the adipogenesis. These data indicated that E2F1 is a metabolic regulator with an ability to promote pre-adipocyte differentiation by activating ICAT, therefore represses Wnt/β-catenin activity in 3T3-L1 cells. We also demonstrated that ICAT overexpression did not affect oleic acid-induced lipid accumulation at the surface of Hela and HepG2 cells. In conclusion, we show that E2F1 is a critical regulator with an ability to promote differentiation and adipogenesis by activating ICAT in pre-adipocytes. [ABSTRACT FROM AUTHOR]

Apoptosis of intestinal epithelial cells following oxidative stress is a major cause of mucosal barrier dysfunction and is associated with the pathogenesis of various gastrointestinal diseases. Although L-tryptophan (Trp) is known to improve intestinal integrity and function, a beneficial effect of N-acetyl serotonin (NAS), a metabolite of Trp, on the apoptosis of enterocytes and the underlying mechanisms remain largely unknown. In the present study, we showed that porcine enterocytes treated with 4-hydroxy-2-nonenal (4-HNE), a metabolite of lipid peroxidation, led to upregulation of apoptotic proteins, including Bax and cleaved caspase-3, and reduction of tight junction proteins. These effects of 4-HNE were significantly abrogated by NAS. In addition, NAS reduced ROS accumulation while increasing the intracellular concentration of glutathione (GSH), and the abundance of the Nrf2 protein in the nucleus and its downstream target proteins. Importantly, these protective effects of NAS were abrogated by Atra, an inhibitor of Nrf2, indicating a dependence on Nrf2 signaling. Taken together, we demonstrated that NAS attenuated oxidative stress-induced cellular injury in porcine enterocytes by regulating Nrf2 signaling. These findings provide new insights into a functional role of NAS in maintaining intestinal homeostasis. [ABSTRACT FROM AUTHOR]

Preheating and compression tests of Inconel 718 superalloy double cone specimens were carried out to investigate the microstructure heredity during hot working. Optical microscopy, scanning electron microscopy (SEM), electron backscatter diffraction (EBSD), and transmission electron microscopy (TEM) were used to characterize the microstructure evolution. The results show that intense microstructure heredity can be found at the temperature 960~990 °C. During the preheating process, δ phase precipitation or grain growth could increase the fraction of high angle grain boundary (HAGBs) and Σ3n boundaries. Otherwise, the generation or spread of annealing twin could increase the fraction of LAGBs, Volume fraction of recrystallized grains was evaluated at the whole hot working process. At the temperature of 960~990 °C, the volume fraction of recrystallized grains increases with effective strain increasing. At the super solution temperature of δ phase, the volume fraction of recrystallized grains decreases and then increases with the increase of the effective strain. The unimodal grain size distribution and fully recrystallized grains can be obtained at low strains at 960~990 °C. The twin boundary length fraction of deformed specimens is always lower than that of preheated ones. Discontinuous dynamic recrystallization (DDRX) was considered as the dominant nucleation mechanism, and continuous dynamic recrystallization (CDRX) was strengthened with the increasing grain size. Twin introduced deformation will be the main deformation mode for alloy 718 with larger grain. [ABSTRACT FROM AUTHOR]

Glycine supplementation has been reported to alleviate lipopolysaccharide (LPS)-induced lung injury in mice. However, the underlying mechanisms responsible for this beneficial effect remain unknown. In the present study, male C57BL/6 mice were treated with aerosolized glycine (1000 mg in 5 mL of 0.9% saline) or vehicle (0.9% saline) once daily for 7 continuous days, and then were exposed to aerosolized LPS (5 mg in 5 mL of 0.9% saline) for 30 min to induce lung injury. Sera and lung tissues were collected 24 h post LPS challenge. Results showed that glycine pretreatment attenuated LPS-induced decreases of mucin at both protein and mRNA levels, reduced LPS-triggered upregulation of pro-inflammatory cytokines, such as tumor necrosis factor-α (TNF-α), interferons, granulocyte-macrophage colony-stimulating factor (GM-CSF), and interleukins. Further study showed that glycine-reduced LPS challenge resulted in the upregulation of nuclear factor κB (NF-κB), nucleotide binding domain (NOD)-like receptor protein 3 (NLRP3) inflammasome. In addition, LPS exposure led to the downregulation of NRF2 and downstream targets, which were significantly improved by glycine administration in the lung tissues. Our findings indicated that glycine pretreatment prevented LPS-induced lung injury by regulating both NLRP3 inflammasome and NRF2 signaling. [ABSTRACT FROM AUTHOR]

l-Tryptophan (Trp) is known to play an important role in the health of the large intestine. However, a role of dietary Trp in the small-intestinal mucosal barrier and microbiota remains poorly understood. The present study was conducted with weaned piglets to address this issue. Postweaning piglets were fed for 4 weeks a corn- and soybean meal-based diet supplemented with 0 (Control), 0.1, 0.2, or 0.4% Trp. The small-intestinal microbiota and serum amino acids were analyzed by bacterial 16S rRNA gene-based high-throughput sequencing methods and high-performance liquid chromatography, respectively. The mRNA levels for genes involved in host defense and the abundances of tight-junction proteins in jejunum and duodenum were measured by real time-PCR and Western blot techniques, respectively. The concentrations of Trp in the serum of Trp-supplemented piglets increased in a dose-dependent manner. Compared with the control group, dietary supplementation with 0.2–0.4% Trp reduced the abundances of Clostridium sensu stricto and Streptococcus in the jejunum, increased the abundances of Lactobacillus and Clostridium XI (two species of bacteria that can metabolize Trp) in the jejunum, and augmented the concentrations of secretory immunoglobulin A (sIgA) as well as mRNA levels for porcine β-defensins 2 and 3 in jejunal tissues. Moreover, dietary Trp supplementation activated the mammalian target of rapamycin signaling and increased the abundances of tight-junction proteins (zonula occludens (ZO)-1, ZO-3, and claudin-1) in jejunum and duodenum. We suggested that Trp-metabolizing bacteria in the small intestine of weaned pigs primarily mediated the beneficial effects of dietary Trp on its mucosal integrity, health, and function. [ABSTRACT FROM AUTHOR]