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Background: Circular RNAs (circRNAs) play a crucial regulatory role in human diseases. However, the roles of circRNAs in ankylosing spondylitis (AS) are barely known. In this study, the functions of circ_0018168 in AS were investigated. Methods: Quantitative real-time polymerase chain reaction (qRT-PCR) and western blot assay were used for circ_0018168, microRNA-330-3p (miR-330-3p), dickkopf-1 (DKK1), alkaline phosphatase (ALP), osteocalcin (OCN), Runt-related transcription factor 2 (Runx2) levels. Cell Counting Kit-8 (CCK-8) assay and 5'-ethynyl-2'-deoxyuridine (EdU) assay were conducted to analyze cell proliferation ability. Flow cytometry analysis was manipulated for cell cycle process. ALP activity was examined with a commercial kit. RNA immunoprecipitation (RIP) assay, RNA pull-down assay and dual-luciferase reporter assay were used to analyze the relationships of circ_0018168, miR-330-3p and DKK1. Results: Circ_0018168 and DKK1 levels were lowly expressed in AS hip capsule specimens. Circ_0018168 overexpression repressed cell proliferation, cell cycle process as well as reduced ALP activity and ALP, OCN and Runx2 protein levels in AS fibroblasts. DKK1 silencing ameliorated the impact of circ_0018168 on AS progression. In addition, circ_0018168 served as the sponge for miR-330-3p, which could target DKK1. MiR-330-3p inhibition suppressed the proliferation, cell cycle and osteogenic differentiation in AS fibroblasts, but DKK1 silencing reversed the impacts. Besides, the effect of circ_0018168 on AS development was abolished by miR-330-3p upregulation. Conclusion: Circ_0018168 overexpression restrained fibroblast proliferation and osteogenic differentiation in AS by elevating DKK1 through adsorbing miR-330-3p.

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Vascular remodeling caused by essential hypertension is a leading cause of death in patients, and vascular smooth muscle cell (VSMC) dysfunction and phenotypic switching result in vascular remodeling. Therefore, inhibiting cell dysfunction and phenotypic switching in VSMCs may be a new treatment strategy for essential hypertension. The aim of the current study is to explore the roles of long non-coding RNA (lncRNA) MRAK048635_P1 in VSMC function and phenotypic switching. The MRAK048635_P1 level was determined in spontaneously hypertensive rats (SHRs) and VSMCs isolated from SHRs. MRAK048635_P1 was knocked down using a specific siRNA in VSMCs isolated from the thoracic aorta of SHRs and Wistar-Kyoto rats. Then, the proliferation and migration of VSMCs were determined using a cell counting kit-8 (CCK-8), a 3H labeling method, a transwell assay, and a wound healing assay. Flow cytometry was used to test the effect of MRAK048635_P1 on VSMC apoptosis. The protein and mRNA levels of associated genes were measured through Western blotting, immunofluorescence, and Quantitative Reverse Transcription-Polymerase Chain Reaction (qRT-PCR). MRAK048635_P1 showed low expression during hypertension in vivo and in vitro Down-regulation of lncRNA MRAK048635_P1 promoted proliferation and migration and inhibited apoptosis in VSMCs isolated from healthy rat vascular tissue and SHR-derived VSMCs. Importantly, we also found that down-regulation of MRAK048635_P1 could induce VSMC phenotypic switching from a contractile to a secretory phenotype. In conclusion, our findings reveal that decreased MRAK048635_P1 is probably an important factor for vascular remodeling by affecting VSMC cell function and phenotypic switching in essential hypertension.

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OBJECTIVE: To investigate the clinical significance of applicating posterior internal fixation for regulating spinal curvature in thoracolumbar compression fractures. METHODS: Between May 2006 and May 2009, 63 patients with thoracolumbar compression fractures were treated, and the clinical data were retrospectively analyzed. Among them, 33 patients received traditional posterior internal fixation in control group; 30 patients underwent posterior internal fixation with spinal curvature correction under C-arm X-ray device in trial group. There was no significant difference in age, gender, cause of injury, injured segment, grade of fracture, and time from injury to operation between 2 groups (P > 0.05). The Cobb angle, height of injured vertebral body, and disc height were measured by X-ray examination; loosening and breakage of internal fixation were observed and compared between 2 groups. The recovery rate was calculated according to pre- and post-operative visual analogue scale (VAS) and Oswestry disability index (ODI) scores for each patient. RESULTS: All cases were followed up 20-45 months (mean, 31 months). The postoperative VAS score, ODI, Cobb angle, height of injured vertebral body, and disc height were improved significantly when compared with preoperative values in 2 groups (P < 0.05). At last follow-up, VAS and ODI scores of trial group were significantly better than those of control group (P < 0.05); loss of Cobb angle was (2.1 +/- 1.7) degrees in trial group and (4.2 +/- 3.2) degrees in control group, showing significant difference (t=1.457, P=0.000); loss of disc height was (1.4 +/- 1.2) mm in trial group and (3.4 +/- 2.3) mm in control group, showing significant difference (t=9.336, P= 0.000); loss of height of injured vertebral body was 1.8% +/- 0.6% in trial group and 5.4% +/- 2.1% in control group, showing significant difference (t=3.435, P=0.000). Broken screw and loosening screw occurred in 1 case of control group, respectively (6.1%), but no broken or loosening screw in trial group, showing significant difference (P=0.000). CONCLUSION: Application of posterior internal fixation for regulating spinal curvature has a good clinical effectiveness. The postoperative spinal curvature, the height of injured vertebral body, and disc height can be improved significantly and low back pain can be recovered satisfactorily. The modified technique is also effective in reducing broken and loosening incidence of the fixation system.

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