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OBJECTIVE: To explore the role of microRNA-409 in spinal cord injury (SCI) recovery and its underlying mechanism. MATERIALS AND METHODS: The mouse SCI model was first established, and the difference in recovery of grip strength was detected. MicroRNA-409 expressions in mice tissues from sham operation group and SCI group were detected by quantitative Real-Time Polymerase Chain Reaction (qRT-PCR). We further increased microRNA-409 level in mice spinal cord by plasmids transfection. Luciferase activity was detected to verify the direct binding of microRNA-409 and ZNF366. RESULTS: The grip strength in both groups was temporarily decreased after surgery, while the grip strength in SCI group was always remarkably lower than that of the sham operation group since the first week after the surgery, suggesting the successful construction of mouse SCI model. MicroRNA-409 expression in the SCI group was gradually decreased from the postoperative 3rd day, which was remarkably lower than that of the sham group. Additionally, ZNF366 expression in the SCI group began to increase from the first day after the surgery, which was markedly higher than that of the sham group. After injection of exogenous microRNA-409, ZNF366 expression in the SCI group showed a remarkable decrease compared to that of the sham operation group. We also confirmed that ZNF366 was the target gene of microRNA-409 by bioinformatics analysis and luciferase activity assay. CONCLUSIONS: MicroRNA-409 is downregulated after spinal cord injury. Overexpression of microRNA-409 directly targets ZNF366 and promotes the recovery of spinal cord injury. [ABSTRACT FROM AUTHOR]

OBJECTIVE: Ankylosing spondylitis (AS) is a common clinical autoimmune disease, the pathogenesis of which, however, is not yet elucidated. In this study, we aim to explore the effect of B cells in the development and progression of AS and its underlying mechanism. PATIENTS AND METHODS: B cells were isolated from peripheral blood of AS patients and normal controls. Surface expression of CD40 in B cells was detected by flow cytometry. Expressions of downstream genes in MAPK pathway were detected by Western blot. Moreover, IL-10 expressions in peripheral blood of AS patients and normal controls were detected by ELISA. RESULTS: No difference was found in the surface expression of CD40 in B cells between AS patients and normal controls. However, CD40 expression was inhibited after B cells in peripheral blood were specifically stimulated by lipopolysaccharide (LPS) in vitro. Abnormal activated B cells, dysregulated p38 expressions and decreased serum expressions of IL-10 were also observed in AS patients. CONCLUSIONS: Abnormal surface expres- sion of CD40 inn B cells of AS patients may lead to abnormal activation of B cells, thereby interfering the p38 MAPK pathway and reducing the IL-10 secretion. [ABSTRACT FROM AUTHOR]

The microstructure, magnetic and magnetocaloric properties are investigated in the melt-spun and annealed Ni42.9Co6.9Mn38.3Sn11.9 ribbons. The columnar grains grow perpendicular to ribbon surfaces. After annealing, the grain size increases greatly. Meanwhile, the parent phase is suppressed and therefore L10 martensite predominates, indicating obvious shift of martensitic transformation to high temperature. More interestingly, the martensite variants are distinctly observed on the fractured cross-section of annealed ribbons, not just on the free surface in general. The significant enhancement of magnetic entropy change and effective refrigerant capacities with relatively smaller thermal hysteresis make annealed ribbons potential candidate in magnetic refrigeration around room temperature. [ABSTRACT FROM AUTHOR]

OBJECTIVE: To investigate the role of long noncoding RNA (lncRNA) UCA1 in the multiple myeloma (MM) development. PATIENTS AND METHODS: In samples of MM, the expression of UCA1 and TGF-β was investigated using real-time PCR. UCA1 lentiviral small hairpin RNA (shRNA) was transfected in MM cell lines. CCK-8 and colony formation assay were used to detect cell lines proliferation. The cell apoptosis assay was conducted to detect cell apoptosis. Western blot was utilized to detect the protein level of TGF-β. RESULTS: The expression level of UCA1 increased in MM samples and cell lines, and its high expression was associated with poor MM prognosis. Downregulation of UCA1 significantly inhibited cell lines proliferation and promoted cell apoptosis. UCA1 could positively regulate TGF-β in MM. Overexpression of TGF-β partially reversed the effect of UCA1 knockdown. CONCLUSIONS: UCA1 promotes MM cell lines proliferation b y targeting TGF-β. [ABSTRACT FROM AUTHOR]

OBJECTIVE: This study aimed at exploring the expression and prognostic values of a novel long noncoding RNA RUSC1-AS-N in hepatocellular carcinoma (HCC), and to investigate the biological roles of RUSC1-AS-N in HCC cells. PATIENTS AND METHODS: RUSC1-AS-N expression in public available microarray data was analyzed. The expression of RUSC1-AS-N in our cohort containing 66 HCC tissues and paired adjacent non-cancerous hepatic tissues was measured by qRT-PCR. The correlation between RUSC1-AS-N expression and clinicopathological characteristics was evaluated by Pearson χ2- test. The prognostic value of RUSC1-AS-N was analyzed by Kaplan-Meier survival analysis. The biological roles of RUSC1-AS-N on HCC cell viability were evaluated by Glo cell viability assays and Ethynyl deoxyuridine incorporation assays. The effects of RUSC1-AS-N on HCC cell cycle were evaluated by fluorescence-activated cell sorting (FACS) analyses of propidium-iodide (PI) stained cells. The effects of RUSC1-AS-N on HCC cell apoptosis were evaluated by TdT-mediated dUTP nick end-labeling (TUNEL) assays. RESULTS: RUSC1-AS-N is upregulated in HCC tissues and associated with poor prognosis of HCC patients from GSE54238 and GSE40144. In our cohort, we further confirmed the upregulation of RUSC1-AS-N in HCC tissues. High expression of RUSC1-AS-N associates with large tumor size, vein invasion, encapsulation incompletion, advanced BCLC stage, and poor recurrence-free survival and overall survival. Functional assays revealed that RUSC1-AS-N knockdown markedly decreases cell viability, induces cell-cycle arrest and apoptosis of HCC cells. CONCLUSIONS: RUSC1-AS-N is upregulated and acts as an oncogene in HCC. RUSC1-AS-N may be a promising prognostic biomarker and therapeutic target for HCC. [ABSTRACT FROM AUTHOR]

Investigates the effects of sputtering characteristics on the magnetic properties of FeNiMo sputtered films. Preparation of the thin films; Data on the argon pressure dependence of frequency characteristics.