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Background. Chemokine (C-C motif) ligand 18 (CCL18) is a chemokine that plays a key role in immune and inflammatory responses. In recent years, CCL18 participates in the development and progression of various cancers, but its expression and role in thyroid cancer (TC) remain unclear. Methods. RT-qPCR assay and Western blot assay were used to explore the expression level of CCL18 in TC tissues and cells. Cell proliferation was measured by MTT assay. Transwell assay was adopted to detect cell migration in TC cells. Dual luciferase reporter assay was performed to assess the relationship between CCL18 and miR-149-5p. Results. There was an uptrend of CCL18 in TC tissues and cells. Our findings indicated that CCL18 overexpression facilitated lymph node metastasis in patients with TC. CCL18 silencing was found to inhibit cell migration, proliferation, and EMT progression in TC cells. CCL18 was proved to be a target gene of miR-149-5p. Additionally, miR-149-5p weakened the effect of CCL18 in the progression of TC. Conclusion. Therefore, our results indicated that CCL18 knockdown restrained TC progression and suggested that CCL18 might be a potential therapeutic target for TC.

Protective coatings are effective to prevent concrete from corrosion and improve its durability. In this study, we report a novel epoxy coating with cross-linkable solvent via Diels-Alder reaction. Such a coating has a low viscosity so it can permeate into the pores or defects of concrete up to 1.5 mm, whereas the solvents cross-link with epoxy resin in-situ at higher temperature, forming a robust root-like coating/concrete composite. The concrete is significantly reinforced in the mechanical strength and corrosion resistance. Moreover, the cross-linkable solvents allow the coating to have a low content of volatile organic compound (VOC) (

BACKGROUND The aim of this study was to compare the transcriptome between impaired fasting glucose (IFG) and type 2 diabetes mellitus (T2DM), and further research their molecular mechanisms. MATERIAL AND METHODS The original microarray GSE21321, including miRNA and mRNA expression profiles, was downloaded from the GEO database. Data preprocessing was processed by limma package, and differentially expressed genes (DGs) and miRNA (DMs) were screened. Then, the regulatory relationships among miRNA, TF, and genes were screened and the regulatory network was constructed. Finally, DAVID was used for KEGG enrichment analysis. RESULTS There were 11 upregulated IFG-related DMs and five upregulated T2DM-related DMs. Three of the DMs overlapped. In addition, there were eight downregulated IFG-related DMs and two downregulated T2DM-related DMs. Only one downregulated DM overlapped. Similarly, there were 264 upregulated IFG-related DGs and 331 upregulated T2DM-related DGs; and 196 overlapping genes were obtained. In addition, there were 400 downregulated IFG-related DMs and 568 downregulated T2DM-related DMs. A total of 326 downregulated DMs were overlapped. The overlapped DGs were enriched in various pathways, including hematopoietic cell lineage, Fc gamma R-mediated phagocytosis, and MAPK signaling pathway. TAF1 (upregulated gene) and MAFK (downregulated gene) were hub nodes both in IFG- and T2DM-related miRNA-TF-gene regulatory network. In addition, miRNAs, including hsa-miR-29a, hsa-miR-192, and hsa-miR-144, were upregulated hub nodes in the two regulatory networks. CONCLUSIONS Genes including TAF1 and MAFK, and miRNAs including hsa-miR-29a, hsa-miR-192, and hsa-miR-144 might be potential target genes and important miRNAs for IFG and T2DM.

Objective Diabetes mellitus type 2 (T2DM) is a metabolic disease that has become a pressing issue, with potential adverse impact on mental health. We aimed to explore the potential molecular mechanism of T2DM. Material and methods GSE38642 microarray data downloaded from gene expression omnibus was used to identify the differentially expressed genes (DEGs). Profiling of complex functionality (ProfCom) was used to analyze the complex function and mine T2DM signature genes. Finally, the differential expression network (DEN) was constructed. Results We identified 147 DEGs including 59 up- and 88 down-regulated genes. With increasing of degree, the specificity of functional description of DEGs was higher. GO term of “integral to membrane and immune response (not receptor activity) not regulation of immune response” in degree 4 was enriched by 6 DEGs, while the GO term of “immune response” in degree 1 was enriched by 12 DEGs. Two complex functions of integral to membrane an immune response and response to glucose stimulus were enriched by 11 T2DM signature genes including ARG2, GLP1R, PFKFB2, PTPRN, ACSL5, CCR7, IL2RA, IL7R, IL1R2, IL1RL1 and CHST4 . Finally, DEN including 11 signature genes and 491 edges was obtained. Conclusion The identified DEGs especially 11 signature genes such as PTPRN, GLP1R, CCR7 and IL2RA may play important roles in the pathogenesis of T2DM.