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This paper focuses on the linguistic landscape (LL) of four towns along the rural-urban line in Liangshan Yi Autonomous Prefecture, which is located in southwest China and is the main residence of the Yi ethnic minority group. In recent years, the status of the Yi language has been challenged by Han (Chinese Mandarin) and English both in the field of education and general society in Liangshan. Recognising this, the local government has issued a range of policies to revitalise the Yi language, including ensuring its use on public signage. The aim of this study is to explore the LL of Liangshan, which has not been looked at before, and the actual implementation of these signage policies. 1497 language signs were analysed, including commercial signs, government signs and public signs in four schools. The findings indicate that the visibility of the Yi language on public signage is closely related to the intensity of policy support. However, in order to make signage policies effective, a holistic approach is in need at both prefectural and regional levels, and in 'micro spaces' such as education spheres and workplaces.

In this paper, we construct a GCCP multivariate datalink network for teaching and learning resource sharing through the Generalized Control Chaining Primary Protocol (GCCP) combined with mutual cooperative services among the physical, data link and network layers for resource sharing. The solution set is mapped to the distributed dynamic self-organizing network data links through Nash equilibrium. Attribute descriptions for the necessary digital teaching resources are provided in a P2P system for sharing resources in large-scale heterogeneous teaching environments. Finally, simulations are conducted under the Group Service Control Protocol (GCCP) for teaching resource sharing to verify the effectiveness of the scheduling and management model for digital teaching resources. According to the results, the system with a multivariate datalink network maintains an average cluster size of 5 nodes. The response time of the system increases significantly with the increase of scale when RP(k)C-Grid takes k as 10,20,30,40,50 respectively. This paper effectively manages and maintains the entire digital resource management system for teaching and learning in universities, making it more stable and efficient.

Mobilising urban early-career teachers to commonly perceived 'under-resourced' and 'challenging' rural schools has become an approach to address the rural teacher shortage and improve rural teacher quality. However, the demographic change often requires mobile rural-early career teachers (MR-ECTs) better prepare for a different educational environment. This qualitative case study explores the professional trajectories of four MR-ECTs in a rural primary school in Guangxi, China, regarding their process and outcome of adaptation during their first two years of teaching. Adopting semi-structured interviews, this study finds that the MR-ECTs were somehow under-prepared for the rural school and adopted a 'deficit' mindset in the first place to perceive their professional challenges in the rural school. Yet, they gradually became more resilient in overcoming the challenges and retaining in the rural school by harnessing and collecting available resources from their pre-service and in-service experiences to increase their place consciousness and rural readiness. This understanding will enable teachers, teacher educators, policymakers and school leaders to assist MR-ECTs' ruralisation and contribution to rural schools in more informed ways. [ABSTRACT FROM AUTHOR]

Lung cancer still remains the leading cause of cancer-related death worldwide. It is an urgent need for development of novel therapeutic agents to improve current treatment of this disease. Here we investigate whether the effective component formula of traditional Chinese Medicine could serve as new potential therapeutic drugs to treat lung cancer. We optimize the most effective component formula of Salvia miltiorrhiza and Panax Ginseng (FMG), which is composed of Salvianolic acid A, 20(S)-Ginsenoside and Ginseng polysaccharide. We discovered that FMG selectively inhibited lung cancer cell proliferation and induced apoptosis but had no any cytotoxic effects on normal lung epithelial BEAS-2B cells. Moreover, FMG inhibited lung cancer cell migration and invasion. Mechanistically, we found that FMG significantly promoted p-PTEN expression and subsequently inhibited PI3K/AKT signaling pathway. The phosphatase activity of PTEN protein was increased after FMG bound to PTEN protein, indicating that PTEN is one of the FMG targeted proteins. In addition, FMG regulated expression of some marker proteins relevant to cell apoptosis, migration and invasion. Collectively, these results provide mechanistic insight into the anti-NSCLC of FMG by enhancing the phosphatase activity of PTEN, and suggest that FMG could be as a potential option for lung cancer treatment.

Objective To investigate the significance of down-regulating the miR-4443/TIMP2 pathway on sorafenib sensitivity in HepG2 cells. Methods HepG2 cells were divided into control group (DMSO) and sorafenib treatment group (10 μmol/L). After treatment for 24 h, the mRNA level of miR-4443 was measured by RT-qPCR. CCK-8 assay was used to study the effects of transfection with miR-4443 mimics or pretreatment of its inhibitor on the cell viability of HepG2 cells treated with sorafenib for 24 h. Bioinformatics analysis was used to predict the downstream target gene of miR-4443. The expression of TIMP2 at mRNA and protein levels was assessed by RT-qPCR and Western blotting in the HepG2 cells treated with sorafenib for 24 h, transfected with miR-4443 mimics or pretreatment of its inhibitor followed by sorafenib treatment. Then TIMP2 siRNA was transfected into HepG2 cells by liposome transfection, the content of TIMP2 protein was detected by Western blotting, and the effect of TIMP2 knockdown combined with sorafenib treatment on the viability of HepG2 cells was measured with CCK-8 assay. Results Sorafenib treatment decreased the expression of miR-4443 in HepG2 cells (P < 0.05). Overexpression of miR-4443 (transfection of miR-4443 mimics) significantly decreased the inhibitory effect of sorafenib on cell viability (P < 0.05), while pretreatment of miR-4443 inhibitor could enhance the effect of the drug (P < 0.05). Bioinformatics analysis indicated that the downstream target gene of miR-4443 was TIMP2. The mRNA and protein levels of TIMP2 were obviously increased in HepG2 cells after sorafenib treatment (P < 0.05), but the transfection of miR-4443 mimics or pretreatment of its inhibitor would down- or up-regulate the mRNA level of TIMP2, and the transfection of miR-4443 mimics decreased the protein level of TIMP2, indicating the regulative relationship between the 2 molecules. The transfection of TIMP2 siRNA decreased the expression of TIMP2 and then enhanced the inhibitory effect of sorafenib on HepG2 viability (P < 0.05). Conclusion Down-regulation of the miR-4443/TIMP2 pathway enhances sorafenib sensitivity in HepG2 cells.

Objective To investigate the effect of activating the miR-101-3p/EZH2 pathway on sorafenib sensitivity of HepG2 cells. Methods HepG2 cells treated with sorafenib (10 μmol/L) for 24 h were examined for protein expression of enhancer of zeste homolog 2 (EZH2) using Western blotting and for mRNA expression of EZH2 and miR-101-3p using RT-qPCR. The interaction between miR-101-3p and EZH2 mRNA was analyzed through informatics analysis and verified using dual luciferase reporter assay. HepG2 cells were transfected with miR-101-3p mimic or treated with the EZH2 inhibitor EPZ-6438 followed by treatment with sorafenib for 24 h, and the change in cell proliferation was assessed using CCK-8 assay. Results Sorafenib obviously decreased the expression of miR-101-3p in HepG2 cells (P < 0.05). Informatics analysis showed that miR-101-3p could bind to the 3'-UTR of EZH2 mRNA, and transfection with miR-101-3p significantly inhibited the expression of EZH2 in HepG2 cells (P < 0.05). Sorafenib treatment significantly increased the expression of EZH2 in HepG2 cells (P < 0.05). Both miR-101-3p over-expression and EPZ-6438 treatment resulted in significantly increased sorafenib sensitivity of HepG2 cells (P < 0.05). Conclusion Activation of the miR-101-3p/EZH2 pathway can enhance sorafenib sensitivity of HepG2 cells.