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05). The changes of IMA, D-D and MCP-1 levels were positively correlated with the levels of CTT and hs-CRP (P less then 0.05). The AUC, specificity and sensitivity of patients with AMI diagnosed with MCP-1 alone were 0.8084, 81.61 and 69.51%, respectively. Those of patients diagnosed by D-D were 0.7302, 59.77 and 81.71%, those of patients diagnosed by IMA alone were 0.7289, 58.62 and 80.49%, and those of patients detected by the combination of MCP-1, D-D and IMA were 0.9047, 58.62 and 93.90%. In conclusion, the levels of IMA, D-D and MCP-1 in AMI patients are higher than those in the control group. The levels of IMA, D-D and MCP-1 were positively correlated with CTnT and hs-CRP levels in AMI patients. Combined detection of IMA, D-D, and MCP-1 can improve the accuracy.Numerous studies have reported the critical roles of long non-coding RNAs (lncRNAs) in the regulation of osteoarthritis (OA) development. The present study aimed to assess the function and regulatory mechanism of a lncRNA, KCNQ1 opposite strand/antisense transcript 1 (KCNQ1OT1), in OA in vitro. C28/I2 cells were treated with lipopolysaccharide (LPS) to generate an in vitro OA model. The relative expression levels of KCNQ1OT1, microRNA (miR)-211-5p and transcription factor 4 (TCF4) were determined via reverse transcription-quantitative polymerase chain reaction. The associations between KCNQ1OT1, miR-211-5p and TCF4 were confirmed using a dual-luciferase reporter assay. Furthermore, cell viability was assessed using the MTT assay. Inflammatory cytokine levels were measured using ELISA. The protein expression levels of matrix metalloproteinase-3/13, collagen II/X and TCF4 were detected by western blotting. KCNQ1OT1 and TCF4 were highly expressed in the cartilage tissues of patients with OA and C28/I2 cells treated with LPS (OA cells), whereas miR-211-5p was downregulated concomitantly in OA tissues and cells. Knockdown of KCNQ1OT1 stimulated cell viability, and suppressed the inflammation and degradation of the extracellular matrix (ECM) in OA cells. In addition, overexpression of miR-211-5p stimulated cell viability, and inhibited inflammation and degradation of the ECM in OA cells. Notably, miR-211-5p was revealed to be the target of, and was negatively regulated by, KCNQ1OT1. TCF4 was targeted and negatively modulated by miR-211-5p. Transfection of cells with the miR-211-5p inhibitor or pcDNA-TCF4 reversed the suppressive effects of short hairpin RNA (sh)-KCNQ1OT1 on inflammation and ECM degradation, as well as the promotive effect of sh-KCNQ1OT1 on viability in OA in vitro. Therefore, KCNQ1OT1 may regulate the miR-211-5p/TCF4 axis to ameliorate OA in vitro.Hepatocellular carcinoma (HCC) is a common type of tumor with high mortality worldwide. Investigations associated with the molecular etiology of HCC and screening novel therapeutic targets are still urgently in need. Anillin (ANLN), as a type of evolutionarily conserved actin-binding protein, is involved in multiple cellular processes. ANLN widely affected the progression and metastasis of several types of cancer, and its overexpression was frequently demonstrated in previous studies. The present study demonstrated high expression of ANLN in human HCC tissues, which was also associated the prognosis of patients with HCC. The associations between ANLN expression and the clinicopathological features were determined, including the number of tumor nodes (P=0.011) and tumor size (P=0.003) of patients with HCC. It was found that ANLN promoted cell proliferation, invasion and migration of HCC cells in vitro, and affected tumor growth in vivo. Therefore, ANLN is suggested as a promising therapeutic target for the treatment of HCC.Transplantation of cell-based material is a promising approach for the treatment of critical bone defects. However, it is still limited by the lack of suitable scaffold material or abundant seeding cell sources. The present study aimed to establish a novel composite of an adipose-derived stem cell (ADSC) sheet and a synthetic porous β-tricalcium phosphate/collagen-I fiber (β-TCP/COL-I) scaffold to enhance osteogenic activity. ADSCs were isolated from 3-week-old female Sprague Dawley rats and the ADSC sheets were prepared in an osteoinductive medium. The study groups included the ADSC sheets/scaffold, scattered ADSCs/scaffold, ADSC sheet alone and scaffold alone. Scanning electron microscopy and energy-dispersive spectrometry were used to observe cell-scaffold interactions and analyze the relative calcium content on the composites' surface. Alizarin red S staining was used to examine the calcium deposition. ELISA and reverse transcription-quantitative PCR were used to detect the expression levels of alkaline phosphatase (ALP), osteocalcin (OCN) and osteopontin (OPN). The results revealed that ADSCs were able to tightly adhere to the β-TCP/COL-I scaffold with no cytotoxicity. selleck kinase inhibitor The calcifying nodules reaction was positive on ADSC sheets and gradually increased after osteogenic induction. In addition, the β-TCP/COL-I scaffold combined with ADSC sheets was able to significantly enhance the expression levels of ALP, OCN and OPN and increase the superficial relative calcium content compared to scattered ADSCs/scaffold or the ADSC sheet alone (P less then 0.05). The results indicated that ADSCs possess a strong osteogenic potential, particularly in the cell-sheet form and when compounded with the β-TCP/COL-I scaffold, compared to scattered ADSCs with a β-TCP/COL-I scaffold or an ADSC sheet alone. This novel composite may be a promising candidate for bone engineering.Excitotoxic neuronal injury is associated with numerous acute and chronic neurological disorders, such as Alzheimer's disease and glaucoma. Neuroprotection is a direct and effective therapeutic approach, with small-molecule bioactive peptides displaying certain advantages, including high membrane permeability, low immunogenicity and convenient synthesis and modification. FK18 is a novel peptide derived from basic fibroblast growth factor, which is a protein with neuroprotective effects. The present study aims to evaluate the neuroprotective effect of FK18 against excitotoxic injury. For this purpose, cell viability was determined by the MTS assay, cell apoptosis was assessed by flow cytometry and the TUNEL assay; expression of antiapoptotic proteins Bcl-2, proapoptotic protein Bax and caspase-3 as well as the phosphorylation of Akt and Erk was estimated by western blotting. The results of the present study demonstrated that FK18 effectively increased the viability of, and attenuated glutamate-induced apoptosis of SH-SY5Y cells.