Background Traditional tension band wiring and plate fixation represent the commonest methods for treating olecranon fractures. However, there is no agreement on which method provides the best outcome. The aim of this retrospective study is to compare the outcomes of tension band wiring (TBW) and plate fixation (PF) for treating displaced olecranon fractures. This is the first study to use propensity score matching analysis to compare treatment methods for olecranon fracture. Method A total of 107 patients aged between 18 and 85 had acute isolated and displaced olecranon fractures. The patients were divided into either TBW (n = 49) or PF (n = 58) groups. To conduct propensity score matching for the treatment method (TBW versus PF), 58 patients were analyzed by logistic regression (29 patients in each group). Various demographic and treatment-related variables were examined and analyzed to determine their correlation. Results Functional effects between two groups are similar (in terms of Mayo Elbow Performance Score (MEPS), the patients’ range of elbow motion (ROM) and forearm rotation (RFR), the time return to work (RTW)). The total adverse events rate and metalwork removal events rate are higher in TBW than that in PF. After propensity score matching analysis, similar primary treatment efficacy (indicated by MEPS> 90) in 2 groups and more primary adverse events (indicated by metalwork removal) were perceived in TBW than that in PF. Logistic regression analysis revealed that fracture type was an independent factor that affected the efficacy of a treatment (regression coefficient = − 1.24 < 0, P = 0.03), indicating that fracture severity was inversely proportional to the efficacy of a treatment for olecranon fracture. Furthermore, logistic regression analysis demonstrated that the treatment method was an independent factor that affected metalwork removal of olecranon fracture (regression coefficient 2.38 > 0, OR = 10.77, P < 0.01), indicating that the risk of metalwork removal in the TBW Group was 10.77 times that in the PF Group. Conclusion When initially discussing the surgical approach with patients, physicians should fully weigh the possibility that TBW may lead to a second surgery due to the higher risk of internal fixation removal and that TBW won’t yield better functional outcomes than PF .
Background Rheumatic arthritis (RA) is an autoimmune disease with bad effects. Recent researches have shown that circular RNAs (circRNAs) could affect the progress of RA, but the mechanism still indistinct. In this work, we explored the roles of circ_0025908 in RA. Methods The levels of circ_0025908, microRNA-137 (miR-137), and mRNA of homeodomain-interacting protein kinase 2 (HIPK2) were detected by quantitative real-time reverse transcription-polymerase chain reaction (qRT-PCR) in RA tissues. Meanwhile, the level of HIPK2 was quantified by Western blot analysis. Besides, the cell functions were examined by CCK8 assay, EdU assay, flow cytometry assay, ELISA, and Western blot. Furthermore, the interplay between miR-137 and circ_0025908 or HIPK2 was detected by dual-luciferase reporter assay. Results The levels of circ_0025908 and HIPK2 were upregulated, and the miR-137 level was decreased in RA tissues in contrast to that in normal tissues. For functional analysis, circ_0025908 deficiency inhibited cell vitality, cell mitotic cycle, cell proliferation, and immunoreaction in RA cells, whereas promoted cell apoptosis. Moreover, miR-137 was confirmed to repress the progression of RA cells by suppressing HIPK2. In mechanism, circ_0025908 acted as a miR-137 sponge to regulate the level of HIPK2. Conclusion Circ_0025908 facilitates the development of RA through increasing HIPK2 expression by regulating miR-137, which also offered an underlying targeted therapy for RA treatment.
Background Osteoarthritis (OA), a refractory disease, is one of the leading contributors for disability worldwide. Since chondrocyte is the only resident cell in cartilage, this study aims to explore the roles of miR-129-3p and CPEB1 in chondrocyte apoptosis in knee joint fracture-induced OA. Methods Cartilage was collected from 20 OA patients who underwent total knee replacement (OA group) and 20 patients with knee contusion (normal group). Then, miR-129-3p and CPEB1 levels in the cartilage were quantified by qRT-PCR. Primary rat chondrocytes in the knee were isolated and identified by toluidine blue staining and immunofluorescent staining of type II collagen. OA cellular models were induced by TNF-α treatment, in which miR-129-3p and CPEB1 expressions were assessed. Subsequently, cell viability, apoptosis, and the expression levels of apoptotic protein and caspase-3 were measured. Dual luciferase reporter assay identified the interaction between miR-129-3p and CPEB1. Results Patients in the OA group had decreased miR-129-3p expression and increased CPEB1 expression than those in the normal group. TNF-α treatment successfully induced the OA cellular model. Downregulated miR-129-3p and upregulated CPEB1 expressions were found in OA-treated chondrocytes. miR-129-3p overexpression or CPEB1 knockdown improved chondrocyte viability and attenuated apoptosis, and vice versa. miR-129-3p negatively regulated CPEB1, thus ameliorating apoptosis and enhancing cell viability. Conclusion miR-129-3p negatively targeted CPEB1 to facilitate chondrocyte viability and hamper apoptosis.
Objective: To explore the effect and mechanism of long noncoding RNA ERVK13-1 on osteosarcoma (OS) cell development by regulation of miR-873-5p/KLF5 axis. Methods: The expression of ERVK13-1 in the collected tissue was detected by RT-qPCR, and then the relationship between ERVK13-1 expression and clinical characteristics of OS patients was analyzed. After OS cell lines were transfected with miR-873-5p inhibitor, si-ERVK13-1, si-KLF5 or their negative controls, the expression of ERVK13-1, miR-873-5p, and KLF5 in OS cell lines were measured, followed by determination of their effects on cell proliferation, migration, and invasion abilities. Moreover, the binding relationships of ERVK13-1 and miR-873-5p, as well as miR-873-5p and KLF5, were verified by the dual-luciferase reporter gene assay. Results: Highly expressed ERVK13-1 was found in OS tissues, which was closely related to tumor size, tumor node metastasis, and distant metastasis. The overall survival of OS patients with high expression of ERVK13-1 was poorer than those with low expression of ERVK13-1. Elevated ERVK13-1 and KLF5 but suppressed miR-873-5p was observed in the OS cell lines U2OS and MG63. Transfection with miR-873-5p inhibitor enhanced the malignant potentials of OS cells, and transfection with si-ERVK13-1 or si-KLF5 reduced these abilities of OS cells. ERVK13-1 bound to miR-873-5p and KLF5 was a target gene of miR-873-5p. Conclusion: The ERVK13-1/miR-873-5p/KLF5 axis confers vital effect on the occurrence and progression of OS, thus providing possible guidance for the clinical treatment of OS.
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