In this study, an integrated gaming and multistage guiding approach was proposed for conducting in-field mobile learning activities. A mobile learning system was developed based on the proposed approach. To investigate the interaction between the gaming and guiding strategies on students' learning performance and motivation, a 2 × 2 experiment was conducted on an elementary school natural science course. Four groups of students were situated in a field trip to learn with different mobile learning approaches (ie, gaming or nongaming) and guiding mechanisms (ie, multistage or single-stage). The experimental results showed that both the gaming and multistage guiding mechanisms proposed in this study significantly enhanced the students' learning achievements. Moreover, the interaction between the two showed that the lead-in of the gaming strategy could significantly improve the learning motivation of the students who learned with the multistage guiding mechanism; on the contrary, their learning motivation could be significantly decreased without the gaming approach, although the multistage guiding mechanism was effective. The findings imply that "gamification" could be a good approach for helping students accept learning support or tools provided in mobile learning scenarios.
By differentiating into and the balance being regulated between M1 (proinflammatory) and M2 (anti-inflammatory) heterogeneous populations, macrophages play critical roles during the host immune response in various physiological contexts in both health and diseases. Besides regulating innate and adaptive immune capacity, macrophages are also decisively involved in K E Y W O R D S adipose tissue-derived mesenchymal stem cells, bone marrow-derived macrophages, cell polarity, differentiation
Traumatic osteonecrosis of femoral head (TONFH) is a common orthopedic disease caused by physical injury in hip. However, the unclear pathogenesis mechanism of TONFH and lacking of simple noninvasive early diagnosis method cause the necessity of hip replacement for most patients with TONFH. In this study, we aimed to identify circulating microRNAs (miRNAs) by integrated bioinformatics analyses as potential biomarker of TONFH. mRNA expression profiles were downloaded from the Gene Expression Omnibus database. Then we combined two miRNA screen methods: Weighted gene co‐expression network analysis and fold change based differentially expressed miRNAs analysis. As a result, we identified 14 key miRNAs as potential biomarkers for TONFH. Besides, 302 target genes of these miRNAs were obtained and the miRNA–mRNA interaction network was constructed. Furthermore, the results of Kyoto Encyclopedia of Gene and Genome pathway analysis, Gene Ontology function analysis, protein–protein interaction (PPI) network analysis and PPI network module analysis showed close correlation between these 14 key miRNAs and TONFH. Then we established receiver operating characteristic curves and identified 6‐miRNA signature with highly diagnosis value including miR‐93‐5p (area under the curve [AUC] = 0.93), miR‐1324 (AUC = 0.92), miR‐4666a‐3p (AUC = 0.92), miR‐5011‐3p (AUC = 0.92), and miR‐320a (AUC = 0.89), miR‐185‐5p (AUC = 0.89). Finally, the results of quantitative real‐time polymerase chain reaction confirmed the significantly higher expression of miR‐93‐5p and miR‐320a in the serum of patients with ONFH. These circulating miRNAs could serve as candidate early diagnosis markers and potential treatment targets of TONFH.
Tumor metastasis is the dominant cause of death in colorectal cancer (CRC) patients, and it often involves dysregulation of various cytoskeletal proteins. Plastin 1 (PLS1) is an actin‐bundling protein that has been implicated in the structure of intestinal epithelial microvilli; however, its role in CRC metastasis has not yet been determined. In this study, we demonstrated that PLS1 is highly expressed in 33.3% (45/135) of CRC patients and is correlated with lymph node metastasis and poor survival. In in vitro and in vivo experiments, PLS1 induced the migration and invasion of CRC cells and the metastases to the liver and lung in mice. Moreover, the expressions of key factors for CRC metastases, matrix metalloproteinase (MMP) 9 and 2, were enhanced by PLS1, which was dependent on phosphorylating ERK1/2 activated by IQGAP1/Rac1 signaling. The connection between these signals and PLS1 was further confirmed in CRC tissues of patients and the metastatic nodules from a mouse model. These findings suggest that PLS1 promotes CRC metastasis through the IQGAP1/Rac1/ERK pathway. Targeting PLS1 may provide a potential approach to inhibit the metastasis of CRC cells.
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