Kun-Tsan Lee and Chin-Horng Su contributed equally to this work.

Backgrounds The aim of our study was to investigate failure rates of reconstruction plate and non-reconstruction plate, and find the best strategy for implant selection for different fracture types for midshaft clavicular fractures. Patients and methods Two hundred twenty-six consecutive patients with midshaft clavicular fractures who received open reduction and plate fixation during Jan 2012 to July 2017 were reviewed. The correlations between implant failure rates and risk factors including demographic data, fracture classifications, and implant types were analyzed. Results AO/OTA fracture classification and plate types are the most important factors affecting implant failure for midshaft clavicular fractures. Reconstruction plate had a significantly higher failure rate (53%) than that of non-reconstruction plates (3%) in comminuted midshaft clavicular (AO/OTA 15-2C) fractures ( P value < 0.01). However, the difference was not significant in AO/OTA 15-2A and 2B classifications. Conclusion Patients with comminuted midshaft clavicular (AO/OTA 15-2C) fractures treated with reconstruction plates had very high implant failure rates compared to non-reconstruction plates. We suggested that patients with comminuted midshaft clavicular (AO/OTA 15-2C) fractures treated with reconstruction plates need more protection and more frequent follow-up in the postoperative period.

The progression of osteoarthritis (OA) is mediated by adipokines, one of which is nesfatin-1, which is responsible for the production of inflammatory cytokines. However, how this molecule may affect the synthesis of the proinflammatory cytokine interleukin 1 beta (IL-1β) in OA is unclear. Our analyses of records from the Gene Expression Omnibus (GEO) dataset and clinical specimens of synovial tissue revealed higher levels of nesfatin-1 and IL-1β in OA samples compared with normal healthy tissue. We found that nesfatin-1 facilitates IL-1β synthesis in human OA synovial fibroblasts (OASFs) and suppresses the generation of micro-RNA (miR)-204-5p, as the miR-204-5p levels in OA patients were lower than those in healthy controls. Nesfatin-1-induced stimulation of IL-1β in human OASFs occurred via the suppression of miR-204-5p synthesis by the PI3K, Akt, AP-1 and NF-κB pathways. We suggest that nesfatin-1 is worth targeting in OA treatment.