Microspheres present comparable efficacy and safety profiles compared with polyvinyl alcohol for bronchial artery embolization treatment in hemoptysis patients.

BACKGROUND: The present study aimed to compare the efficacy and safety profiles of microspheres versus (vs.) polyvinyl alcohol (PVA) for bronchial artery embolization (BAE) treatment in patients with hemoptysis. METHODS: Totally, 152 patients with hemoptysis who were about to receive BAE treatment were consecutively enrolled and divided into microspheres group (N = 62) and PVA group (N = 90). Technical success and clinical success were assessed after BAE procedure, and the hemoptysis-recurrence status, survival status and adverse events were recorded during follow-up. RESULTS: Technical success rates were both 100% in microspheres group and PVA group; clinical success rate (96.8% vs. 100.0%, P = 0.165), 6-month (9.7% vs. 7.8%, P = 0.681) and 1-year (9.7% vs. 8.9%, P = 0.869) hemoptysis recurrence rate, 6-month (4.8% vs. 2.2%, P = 0.374) and 1-year (4.8% vs. 3.3%, P = 0.639) mortality were similar between microspheres group and PVA group. Furthermore, hemoptysis-free survival (P = 0.488) and overall survival (P = 0.321) were of no difference between two groups. In addition, all adverse events were mild, and there was no difference of adverse events between two groups (all P > 0.05). These data were validated by further multivariate regression analysis. CONCLUSIONS: Microspheres present comparable efficacy and safety profiles compared with PVA for the BAE treatment in patients with hemoptysis, providing evidence for embolic agent selection.

Downregulation of miR-221-3p by LncRNA TUG1 Promoting the Healing of Closed Tibial Fractures in Mice.

Objective: To probe into the effect of LncRNA TUG1 on the healing of closed tibial fracture in mice. Methods: The closed tibial fracture model of mice was established, selecting the mouse osteoblast line MC3T3-E1, with the cells separated into four groups. The expression levels of TUG1 and miR-221-3p were determined by RT-qPCR analysis, with the targeting relationship between TUG1 and miR-221-3p authenticated by dual luciferase reporter (DLR) assay, detection of cell migration (CM) ability based on Transwell cell migration (TCM) assay, and cell proliferation (CP) acquired by cell counting kit-8 (CCK-8). Results: Prediction results of the target gene by bioinformatics software showed that miR-221-3p had binding sites with the 3'-UTR of TUG1, and DLR assay authenticated the targeting relationship between LncRNA TUG1 and miR-221-3p. Downregulation of TUG1 inhibited osteoblast CP and CM and promoted osteoblast cell apoptosis (CA). Cell cycle analysis indicated that miR-221-3p provoked cell cycle arrest in G1 stage of MC3T3-E1 cells. The siLncRNA-NC group had higher anticyclin D1 and D3 levels than the siLncRNA TUG1 group, with a lower CA rate in the former, implying that miR-221-3p overexpression inhibited osteoblast CP and CM and LncRNA TUG1 inhibited CA. Downregulation of miR-221-3p partly reversed the retardation out of downregulating TUG1 on osteoblast CP and CM. Bcl-2 level was higher in the LncRNA TUG1 group compared to the siLncRNA TUG1 and miR-221-3p overexpression groups, with remarkably lower SDF-1 level in the miR-221-3p overexpression group than those in the control, miRNA-NC, and LncRNA TUG1 groups. Conclusion: The downregulation of miR-221-3p by LncRNA TUG1 can promote the healing of closed tibial fractures in mice.

STAT3 speeds up progression of osteoarthritis through NF-κB signaling pathway.

Osteoarthritis (OA) is the most common motor system disease in the elderly, with a high incidence and a huge social and economic burden. Therefore, it is urgent to study its potential pathogenesis to improve the therapeutic effect of the disease. In this study, we constructed a number of regulator-mediated OA dysfunction modules, and carried out in-depth analysis in order to examine the disease development process. Differential expression analysis, co-expression analysis and enrichment analysis were combined to screen genes related to disease progression. Subsequently, key regulatory factors in the process of OA were identified based on the pivotal regulators that may manipulate important parts of the module subnetwork. A total of 16 OA dysfunction modules were obtained, involving the aggregation of 3,239 module genes. Then, enrichment analysis showed that module genes were significantly involved in apoptosis, inflammation-related functions and signaling pathways. Finally, we revealed a series of regulators, including 842 ncRNA (miR-132-3p, miR-130a-3p and miR-590-3p), 59 transcription factors (NFKB1, RELA and STAT3). We consider that STAT3 is the core transcription factor and promotes the development of OA through the signal of NF-κB. Overall, our results provide biologists and pharmacists with a new way of thinking to reveal the disease process of OA, and provide a wider range of candidate targets for follow-up research.