Electrically Triggered Domain Wall Movement in Cu2Se Semiconductor.

The ion-conductive α-Cu2Se is found to possess antipolar dipoles, and the movement of the domain boundary under the applied voltage causes change of resistance, showing promising application in memristors. However, due to the complex ordering of Cu ions in the α-Cu2Se, there are multiple types of domain wall structure. Here, we show that two typical domain walls in α-Cu2Se can be formed, by controlling the voltage during phase transition from high-temperature cubic ß-Cu2Se to α-Cu2Se. We also show by in situ transmission electron microscopy that the formed [01̅0]/[101̅] domain wall performs a reversible movement under the applied external voltage, while the [010]/[01̅0] domain wall does not move. We further demonstrate that pinning of the [010]/[01̅0] domain wall could be due to the formed dislocations in the interface. This study shows that applying preprocess conditions is important to obtain the designed microstructure and resistive properties of α-Cu2Se.

Stabilized Li-Rich Layered Oxide Cathode by a Spontaneously Formed Yb and Oxygen-Vacancy Rich Layer on the Surface.

Li-rich layered oxides (LLOs) are among the most promising cathode materials with high theoretical specific capacity (>250 mAh g-1 ). However, capacity decay and voltage hysteresis due tostructural degradation during cycling impede the commercial application of LLOs. Surface engineering and element doping are two methods widely applied tomitigate the structural degradation. Here, it is found that trace amount lanthanide element Yb doping can spontaneously form a surficial Yb-rich layer with high density of oxygen vacancy on the LLO-0.3% Yb (Li1.2 Mn0.54 Co0.13-x Ybx Ni0.13 O2 where x = 0.003) cathodes, which mitigating lattice oxygen loss and the non-preferred layered-to-spinel-to-rock salt tri-phase transition. Meanwhile, there are also some Yb ions doped into the lattice of LLO, which enhance the binding energy with oxygen and stabilize the lattice in grain interior during cycling. The dual effects of Yb doping greatly mitigate the structure degradation during cycling, and facilitate fast diffusion of lithium ions. As a result, the LLO-0.3% Yb sample achieves significantly improved cycling stability, with a capacity retention of 84.69% after 100 cycles at 0.2 C and 84.3% after 200 cycles at 1 C. These finding shighlight the promising rare element doping strategy that can have both surface engineering and doping effects in preparing LLO cathodes with high stability.

Dealloying-Derived Porous Spinel Oxide for Bifunctional Oxygen Electrocatalysis and Rechargeable Zinc-Air Batteries: Promotion of Activity Via Hereditary Al-Doping.

The large-scale fabrication of highly efficient and low-cost bifunctional catalysts for oxygen reduction reaction (ORR) and oxygen evolution reaction (OER) is critical to the development of rechargeable zinc-air batteries (ZABs). Herein, a scalable dealloying strategy was proposed to obtain hierarchically porous spinel-type oxide with minor hereditary Al doping. Benefiting from the well-structured porosity and native dopant, O-np-Ni5 Co10 (Al), namely Al-NiCo2 O4 , exhibited excellent electrocatalytic ORR and OER activities, giving a small potential gap of 0.71 V. The rechargeable ZAB with O-np-Ni5 Co10 (Al) as cathode catalyst delivered a high specific capacity of 757 mAh g-1 , a competitive peak power density of 142 mW cm-2 , and a long-term discharge-charge cycling stability. Furthermore, density functional theory calculations evidenced that appropriate Al doping into NiCo2 O4 could significantly reduce the Gibbs free energy difference to 1.71 eV. This work is expected to inspire the design of performance-oriented bifunctional electrocatalysts for wider applications in renewable energy systems.

FBXO31 suppresses lipogenesis and tumor progression in glioma by promoting ubiquitination and degradation of CD147.

Glioma is the most frequent tumor occurred in brain and spinal cord with a high mortality and morbidity. This study aimed to explore the effects of FBXO31 on lipid synthesis and tumor progression in glioma. The expression of FBXO31 was low in glioma tissues and cell lines, which indicated poor prognosis in glioma patients. Overexpression of FBXO31 accelerated ubiquitination and degradation of CD147, which downregulated the expression of SREBP1c. In addition, overexpression of FBXO31 resulted in the reduction of lipogenesis through suppressing the activation of AKT/mTOR signaling axis, thus preventing the tumor growth and aggressiveness in glioma. These results provided a new cognition to pathology of glioma and new therapeutic targets for treating glioma in future.

Expression level of PD-L1 is involved in ALDH1A1-mediated poor prognosis in patients with head and neck squamous cell carcinoma.

OBJECTIVE: To evaluate the expression levels of ALDH1A1, PDL1, and PDL2 in head and neck squamous cell carcinoma (HNSCC) patients, and explore their clinical relevance in prognosis of patients with HNSCC. METHODS: Immunohistochemistry of ALDH1A1 and PD-L1/PD-L2 in 85 primary HNSCC patients was carried out. The expression level of PD-L2 was assessed with the modified Moratin's immune response scoring (IRS) system. tumor proportion score (TPS) was defined as the percentage of viable tumor cells showing partial or complete membrane staining at any intensity. The chi-square test and Fisher's exact test were used to analyze the associations between ALDH1A1 expression and clinicopathological features. The Spearman's correlation was applied to analyze the correlation of ALDH1A1 expression with PD-L1/PD-L2 expression. RESULTS: kaplan-Meier analysis showed that the expression levels of ALDH1A1 and PD-L1/PD-L2 were inversely associated with recurrence-free survival (RFS; P = 0.001, 0.014, and 0.023, respectively). Moreover, expression levels of ALDH1A1 and PD-L1 were correlated with poor overall survival (OS; P = 0.002 and 0.039, respectively). Furthermore, multivariate logistics regression analyses demonstrated that expression level of ALDH1A1 was independently associated with shorter RFS (P = 0.013) and poorer OS (P = 0.014) in HNSCC patients, and the expression level of PD-L2 was only negatively associated with RFS (P = 0.041), rather than PD-L1. Spearman's correlation analysis unveiled that expression levels of PD-L1 and PD-L2 were positively correlated with ALDH1A1 expression in HNSCC patients (P = 0.000 and 0.015, respectively). Especially, the patients with expression levels of ALDH1A1 and PD-L1 had the worst prognosis. CONCLUSIONS: Our results indicated that ALDH1A1 is an independent prognostic factor in patients with HNSCC, and the expression level of PDL-1 may be involved in ALDH1A1-mediated poor prognosis in patients with HNSCC.

Songorine suppresses cell growth and metastasis in epithelial ovarian cancer via the Bcl­2/Bax and GSK3ß/ß­catenin signaling pathways.

Epithelial ovarian cancer (EOC) is the most frequent cause of cancer­associated mortality among all types of gynecological cancer. The high recurrence rate and the poor 5­year survival rate indicate that more effective therapeutic strategies are required. The aim of the present study was to investigate the role and potential mechanisms of songorine in treating EOC. EOC cells were cultured with different concentrations of songorine, following which MTT and flow cytometric analyses were conducted to measure cell viability and apoptosis. Wound healing and Transwell assays were used to detect cell migration and invasion abilities. Furthermore, associated molecules in the glycogen synthase kinase (GSK)­3ß/ß­catenin and B­cell lymphoma 2 (Bcl­2)/Bcl­2­associated X (Bax) signaling pathways were semi­quantified by western blotting. Finally, tumor size measurements, pathological observations, western blot analysis and toxicological evaluations were performed in SKOV­3 tumor­bearing BALB/c nude mice to investigate the efficacy and safety of songorine. As expected, songorine inhibited EOC cell survival, invasion and migration, promoted EOC cell apoptosis and suppressed mammalian EOC tumorigenic behavior. In particular, GSK3ß inhibitor treatment restored the songorine­induced regulation of the GSK3ß/ß­catenin signaling pathway. Furthermore, in the in vitro and in vivo experiments, songorine consistently downregulated the expression of N­cadherin, vimentin, matrix metalloproteinase (MMP)­2, MMP­9, phosphorylated­GSK3ß, ß­catenin and Bcl­2, and upregulated the expression of E­cadherin, cleaved caspase­3, cleaved caspase­9 and Bax. In conclusion, songorine exerted its anticancer effect through the GSK3ß/ß­catenin and Bcl­2/Bax signaling pathways. These results highlight the potential use of songorine as a novel therapeutic agent for EOC.

CCNG1 (Cyclin G1) regulation by mutant-P53 via induction of Notch3 expression promotes high-grade serous ovarian cancer (HGSOC) tumorigenesis and progression.

TP53 mutation is considerably common in advanced high-grade serous ovarian cancer (HGSOC) and significantly associated with a poor prognosis. In this study, we investigated the role of Cyclin G1 (CCNG1), a target gene of wild-type TP53 (P53wt), in HGSOC and the possible regulatory mechanism between TP53 mutant (P53mt) and CCNG1 in the progression of HGSOC. High expression level of CCNG1 was found in 61.3% of HGSOC tissues and only 18.2% in fimbriae of fallopian tubes. Additionally, overexpression of CCNG1 was significantly associated with a shorter overall survival (P < 0.0001) and progression-free survival (P < 0.0004) in HGSOC patients. In vitro, CCNG1 promoted both tumor cell motility by inducing epithelial-mesenchymal transition (EMT) and resistance to cisplatin (CDDP). In vivo, knockdown expression of CCNG1 inhibited cancer metastasis. Furthermore, P53mt increased the expression of CCNG1 by regulating Notch3 expression, and a positive correlation between CCNG1 and Notch3 protein expression was observed by Immunohistochemistry (IHC) (r = 0.39, P: 0.01528). In conclusion, the activation of P53mt-Notch3-CCNG1 pathway was responsible for tumor progression to advanced disease with correlation with worse prognosis in patients with HGSOC. These data suggest a possible molecular mechanism of disease and highlights CCNG1's potential role as a therapeutic target in HGSOC.