12 research outputs found

    Synthesis and characterization of high entropy (TiVNbTaM)2AlC (M = Zr, Hf) ceramics

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    The high-entropy design of MAX phases is expected to confer superior properties, but its study was hindered by the complex synthesis method and limited purity of samples. In this work, two noteworthy types of high-entropy MAX phase structural ceramics, high-entropy (TiVNbTaM)2AlC (M = Zr, Hf), were designed and prepared by the in-situ synthesis using spark plasma sintering (SPS). The microstructure and lattice parameters of sintered samples were determined. Compared with the single-component MAX phases, the highly pure high-entropy (TiVNbTaZr)2AlC sample had good physical and mechanical properties, including electrical conductivity of 0.96×106 Ω−1·m−1, thermal expansion coefficient of 3.65×10−6 K−1, thermal conductivity of 8.98 W·m−1·K−1, Vickers hardness of 9.80 GPa, flexural strength of 507 MPa, fracture toughness of 5.62 MPa·m1/2, and compressive strength of 1364 MPa, which exhibited the remarkable hardening-strengthening effect

    MACHINABILITY AND REMOVAL MECHANISM OF METAL-BASED SUPPORT STRUCTURES IN SELECTIVE LASER MELTING

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    Ph.DDOCTOR OF PHILOSOPHY (CDE-ENG

    Molluscicidal activity and physiological toxicity of quaternary benzo[c]phenanthridine alkaloids (QBAs) from Macleaya cordata fruits on Oncomelania hupensis.

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    Schistosomiasis is a serious worldwide parasitic disease. One of the best ways to control schistosomiasis is to control the population of Oncomelania hupensis snails. We sought to identify a high-efficiency biogenic molluscicide against Oncomelania with low toxicity, to avoid chemical molluscicide contamination and toxicity in aquatic organisms. We extracted quaternary benzo[c]phenanthridine alkaloids (QBAs) from Macleaya cordata fruits. Molluscicidal activity of the QBAs against Oncomelania was determined using bioassay. Our results showed that the extracted QBAs had a strong molluscicidal effect. In treatment of O. hupensis with QBAs for 48 h and 72 h, the lethal concentration (LC50) was 2.89 mg/L and 1.29 mg/L, respectively. The molluscicidal activity of QBAs was close to that of niclosamide (ethanolamine salt), indicating that QBAs have potential development value as novel biogenic molluscicides. We also analyzed physiological toxicity mechanisms by examining the activity of several important detoxification enzymes. We measured the effect of the extracted QBAs on the activities of glutathione S-transferase (GST), carboxylesterase (CarE), acid phosphatase (ACP), and alkaline phosphatase (AKP) in the liver of O. hupensis. We found that the effects of QBAs on detoxification metabolism in O. hupensis were time and concentration dependent. The activities of GST, CarE, AKP, and ACP in the liver of snails increased significantly in the early stage of treatment (24 h), but decreased sharply in later stages (120 h), compared with these activities in controls. GST, CarE, AKP, and ACP activity in the liver of snails treated with LC50 QBAs for 120 h decreased by 62.3%, 78.1%, 59.2%, and 68.6%, respectively. Our results indicate that these enzymes were seriously inhibited by the extracted QBAs and the detoxification and metabolic functions of the liver gradually weakened, leading to poisoning, which could be the main cause of death in O. hupensis snails

    Support Removal on Thin-Walled Parts Produced by Laser Powder Bed Fusion

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    10.1089/3dp.2021.02683D PRINTING AND ADDITIVE MANUFACTURIN

    A novel role for the ROS-ATM-Chk2 axis mediated metabolic and cell cycle reprogramming in the M1 macrophage polarization

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    Reactive oxygen species (ROS) play a pivotal role in macrophage-mediated acute inflammation. However, the precise molecular mechanism by which ROS regulate macrophage polarization remains unclear. Here, we show that ROS function as signaling molecules that regulate M1 macrophage polarization through ataxia-telangiectasia mutated (ATM) and cell cycle checkpoint kinase 2 (Chk2), vital effector kinases in the DNA damage response (DDR) signaling pathway. We further demonstrate that Chk2 phosphorylates PKM2 at the T95 and T195 sites, promoting glycolysis and facilitating macrophage M1 polarization. In addition, Chk2 activation increases the Chk2-dependent expression of p21, inducing cell cycle arrest for subsequent macrophage M1 polarization. Finally, Chk2-deficient mice infected with lipopolysaccharides (LPS) display a significant decrease in lung inflammation and M1 macrophage counts. Taken together, these results suggest that inhibiting the ROS-Chk2 axis can prevent the excessive inflammatory activation of macrophages, and this pathway can be targeted to develop a novel therapy for inflammation-associated diseases and expand our understanding of the pathophysiological functions of DDR in innate immunity
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