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The magmatic diagenetic environment was simulated by high-temperature melting and natural cooling. A series of glass-ceramics with different Nd2O3 contents were prepared by using complex component granite (aluminosilicate material). The phase evolution of the matrix at different temperatures was studied by X-ray diffraction (XRD). The structure of glass-ceramics was analyzed by infrared spectroscopy (IR) and scanning electron microscopy (SEM). The mechanical properties of glass-ceramics were also evaluated. The results showed that the glass transition of pure matrix begins at 1200 °C, and the sample with the highest degree of vitrification is obtained at 1500 °C. The addition of Nd2O3 promoted the melting of Fe3O4 crystal, resulting in the complete amorphous matrix when the Nd2O3 amount is in the range of 20–26 wt.%. With the further increase of Nd2O3 content, Nd-bearing feldspar first appeared. No raw material Nd2O3 was found, indicating that the formation of Nd-bearing feldspar may increase the carrying capacity of the material. The Gaussian fitting results showed that the glass-ceramic samples with Nd2O3 content of 29 wt.% are mainly composed of Q2 and Q3 structural units. In the EDS result, part of neodymium was clustered with small bright spots, while the spots were uniformly distributed on the sample surface as a whole. Meanwhile, the addition of Nd2O3 increased the mechanical properties of the samples (3.20 g/cm3, 8.33 GPa for the sample with 29 wt.% of Nd2O3). The results provide a strategy for the treatment of solid waste with radioactive residual actinides. [ABSTRACT FROM AUTHOR]

Background: Acute lung injury (ALI) is a complex disease with a high mortality. Src homology 2 (SH2)-containing protein tyrosine phosphatase 2 (SHP2) is a protein tyrosine phosphatase that participates in pathogenesis of multiple diseases. Nevertheless, the role of SHP2 in ALI remains unknown., Methods: The in vivo and in vitro lipopolysaccharide (LPS)-induced ALI models were successfully established. The histopathological changes were evaluated by hematoxylin and eosin staining. The vascular permeability of lungs was assessed by Evans blue assay. The expression of ACSL4 and SHP2 was detected by western blot and qRT-PCR assay. The lactate dehydrogenase (LDH) activity, malondialdehyde (MDA), iron, and glutathione (GSH) levels were measured by commercial kits., Results: The SHP2 was upregulated in LPS-induced ALI mice and LPS-stimulated MLE-12 cells. In loss-of function experiment, the knockdown of SHP2 attenuated LPS-induced lung injury, microvessels damage, pulmonary edema, and increase of lung vascular permeability in vivo . Mechanically, shSHP2-rescued LPS induced increase in LDH activity, MDA, and iron levels, and decrease in GSH levels, as well as the accumulation of reactive oxygen species in vivo and in vitro , leading to an alleviation of LPS-induced ferroptosis. Notably, shSHP2 reduced the expression of Acyl-CoA synthetase long-chain 4 (ACSL4). In the rescued experiments, overexpression of ACSL4 abolished the shSHP2-induced reduction of LDH activity, MDA, and iron levels, and increase in GSH levels, thereby aggravating the LPS-induced ferroptosis., Conclusion: These findings concluded that the knockdown of SHP2 attenuated LPS-induced ferroptosis via downregulation of ACSL4 expression in ALI, providing a novel sight for ALI treatment., Competing Interests: The authors state that there are no conflicts of interest to disclose.