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Herein, Ti3C2Tx (MXene) was synthesized and mixed with polyvinyl alcohol (PVA) to fabricate PVA/MXene nanocomposites. The results confirmed that delaminated MXene was successfully synthesized. The nanocomposites were obtained via casting/evaporation method. The thermal stability was evaluated by thermogravimetric analysis (TGA). For the PVA composites with content of 2 wt% MXene (PVA‐MXene2), the thermal decomposition was retarded by approximately 20°C when the temperature was lower than 350°C compared with that of pure PVA. Moreover, the evolved gas products of the PVA/MXene composite were lower than those of pure PVA. For the first time, the flame retardancy of PVA/MXene nanocomposite was investigated using a microscale combustion calorimeter. The peak heat release rate (PHRR) and total heat release of the PVA composite were reduced by 25.7% and 25.5%, respectively, with 1 wt% of MXene. The temperatures at PHRR of PVA/MXene composites were improved with the addition of MXene. Moreover, the addition of MXene resulted in PVA composites with a higher tensile strength and elongation at break than those of a pure PVA film. The improvements in the flame retardancy, thermal and mechanical properties of PVA/MXene composites should enable a wide range of potential applications of MXenes in polymer matrices.

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MicroRNAs are emerging as critical regulators in cerebral ischemia/reperfusion injury; however, their exact roles remain poorly understood. miR-153 is reported to be a neuron-related miRNA involved in neuroprotection. In this study, we aimed to investigate the precise role of miR-153 in regulating neuron survival during cerebral ischemia/reperfusion injury using an oxygen-glucose deprivation and reoxygenation (OGD/R) cellular model. We found that miR-153 was significantly upregulated in neurons subjected to OGD/R treatment. Inhibition of miR-153 significantly attenuated OGD/R-induced injury and oxidative stress in neurons. Nuclear factor erythroid 2-related factor 2 (Nrf2) was identified as a target gene of miR-153. Inhibition of miR-153 significantly promoted the expression of Nrf2 and heme oxygenase-1 (HO-1). However, silencing of Nrf2 significantly blocked the protective effects of miR-153 inhibition. Our study indicates that the inhibition of miR-153 protects neurons against OGD/R-induced injury by regulating Nrf2/HO-1 signaling and suggests a potential therapeutic target for cerebral ischemia/reperfusion injury.

A large volume of Early Cretaceous volcanic rocks are exposed in the central Lhasa subterrane, which are essential for models developed for understanding the evolution of Lhasa Terrane. However, the petrogenesis and geodynamic background of these rocks are still in debate. In this paper, we carried out a detailed study on the volcanic rocks of the Zenong Group, including andesite, dacite, and rhyolite from the Coqen area in the central Lhasa subterrane. Zircons from one dacitic tuff yields an age of 115.3 ± 1.1 Ma. All the rocks are enriched in light rare earth elements (LREEs), Th, U, and Pb and depleted in high field strength elements (HFSEs, e.g. Nb, Ta, P, and Ti). The dacite and rhyolite samples are high‐K calc‐alkaline to shoshonitic and are metaluminous to peraluminous. These felsic samples are characterized by negative ƐNd(t) (−8.9 to −2.1) and ƐHf(t) (−8.1 to −5.6) and have high radiogenic Pb isotopic composition (206Pb/204Pb = 18.6287–19.5578, 207Pb/204Pb = 15.7161–15.7720, and 208Pb/204Pb = 39.1440–40.6253). Particularly, a negative correlation between the ƐNd(t) values and SiO2 contents can be observed in these dacites and rhyolites. Meanwhile, the andesites exhibit similar Sr–Nd–Pb isotopic compositions to dacites and rhyolites (ƐNd(t) = −4.3; 206Pb/204Pb = 18.7119–18.8575, 207Pb/204Pb = 15.7159–15.7203, and 208Pb/204Pb = 39.2944–39.6036). Our new data indicate that different geochemical reservoirs are involved in generating the ca. 115 Ma magmatism in the central Lhasa subterrane. It is likely that dacites and rhyolites are derived from the magma mixing between the ancient basement‐derived melts and mantle‐derived melts with varying degrees of partial melting. The andesites might originate from partial melting of an ancient lithospheric mantle that have been metasomatized by fluids and/or melts derived from the Tethyan oceanic slab. Our results, together with recent studies, suggest that the Zenong Group volcanic rocks in the Coqen area may represent the magmatic responses to the break‐off of the southward subduction of the Bangong–Nujiang Tethyan oceanic slab.

The cerebrospinal fluid-contacting nucleus (CSF-CN) has been demonstrated to be involved in neuropathic pain, but the underlying molecular mechanisms remain unclear. Previous work has shown that mTOR and ERK1/2 are important signaling pathways regulating neuropathic pain. However, studies on the interactions between these major pathways in neuropathic pain are very rare. Therefore, the purpose of this study is to determine whether mTOR and ERK1/2 exist in the CSF-CN and elucidate their alterations in neuropathic pain, especially, the crosstalk between them. Our results showed that mTOR and ERK1/2 were distributed in the CSF-CN, and their expression levels were increased in chronic constriction injury (CCI)-induced neuropathic pain. Furthermore, the injection of both the mTOR antagonist rapamycin and the ERK1/2 antagonist U0126 into the lateral ventricle of the brain attenuated CCI-induced neuropathic pain. Inhibition of the ERK1/2 pathway had little impact on mTOR signaling, but inhibition of the mTOR pathway significantly increased ERK/2 signaling. The coadministration of rapamycin and U0126 inhibited the rapamycin-induced upregulation of ERK, and had a greater effect on pain behaviors than did the single-drug administrations. These data extend our understanding of the relationship between mTOR and ERK in the supraspinal site and demonstrate that the CSF-CN participates in neuropathic pain via the regulation of mTOR and ERK1/2.

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