3 research outputs found

    Dynamical Approach to Realize Room-Temperature Superconductivity in LaH10_{10}

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    Metallic hydrogen and hydride materials stand as promising avenues to achieve room-temperature superconductivity. Characterized by their high phonon frequencies and moderate coupling strengths, several high-pressure hydrides were theoretically predicted to exhibit transition temperatures (TcT_c) exceeding 250\,K, a claim further substantiated by experimental evidence. In an effort to push TcT_c beyond room temperature, we introduce a dynamical method that involves stimulating hydrides with mid-infrared lasers. Employing Floquet first-principles simulations, we observe that in a nonequilibrium state induced by light, both the electronic density of states and the coupling to high-energy phonons see notable enhancements. These simultaneous improvements collectively result in an estimated 20\%-30\% rise in TcT_c in practical pump conditions. Our theoretical investigation, therefore, offers a novel strategy to potentially raise the TcT_c of hydrides above room temperature.Comment: 11 pages, 6 figure

    Structure and transition behavior of crosslinked poly(2-(2-methoxyethoxy) ethylmethacrylate-co-(ethyleneglycol) methacrylate) gel film on cellulosic-based flat substrate

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    The structure and transition behavior of crosslinked thermo-responsive poly(2-(2-methoxyethoxy) ethylmethacrylate-co-(ethyleneglycol) methacrylate) (P(MEO2MA-co-EGMA360)) gel film on a flat cellulosic-based substrate were investigated. The regenerated cellulose (RC) film was prepared by spin-coating with trimethylsilyl cellulose (TMSC), followed by etching with hydrochloric acid vapor on a treated silicon wafer, then crosslinked polymer gel film was obtained by spin-coating, drying, and baking with a pre-crosslinked solution containing polymers. Fourier transform infrared spectroscopy, X-ray photoelectron spectrometer, and atomic force microscopy results show that a RC film with a thickness of 25 nm is generated in the upper layer of TMSC film on the silicon wafer. The cross-linking induces closer arrangement and hinders the extension of chain segments, leading to less prominent phase transition behaviors of polymer gel films. By quartz crystal microbalance measurement and 3D microscopes, a phase transition hysteresis is discovered, the hydrated and loose structure of crosslinked polymer gel film switches to dehydrated and compact structure in initial heating process, which subsequently recovers during the following cooling process. However, the degrees of rehydration and flexibility of film could not reach the initial value because of the insufficient transition time and steric hindrance caused by crosslinking

    Preclinical Studies of Chiauranib Show It Inhibits Transformed Follicular Lymphoma through the VEGFR2/ERK/STAT3 Signaling Pathway

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    Transformed follicular lymphoma (t-FL), for which there is no efficient treatment strategy, has a rapid progression, treatment resistance, and poor prognosis, which are the main reasons for FL treatment failure. In this study, we identified a promising therapeutic approach with chiauranib, a novel orally developed multitarget inhibitor targeting VEGFR/Aurora B/CSF-1R. We first determined the cytotoxicity of chiauranib in t-FL cell lines through CCK-8, EdU staining, flow cytometry, and transwell assays. We also determined the killing effect of chiauranib in a xenograft model. More importantly, we identified the underlying mechanism of chiauranib in t-FL tumorigenesis by immunofluorescence and Western blotting. Treatment with chiauranib significantly inhibited cell growth and migration, promoted apoptosis, induced cell cycle arrest in G2/M phase, and resulted in significant killing in vivo. Mechanistically, chiauranib suppresses the phosphorylation level of VEGFR2, which has an anti-t-FL effect by inhibiting the downstream MEK/ERK/STAT3 signaling cascade. In conclusion, chiauranib may be a potential therapy to treat t-FL, since it inhibits tumor growth and migration and induces apoptosis by altering the VEGFR2/ERK/STAT3 signaling pathway
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