Introduction Multiple rib fractures (≥ 3 displaced rib fractures and/or flail chest) are severe chest trauma with high morbidity and mortality. Rib fixation has become the first choice for multiple rib fracture treatment. However, the timing of surgical rib fixation is unclear. Materials and methods The present study explored whether early rib fracture fixation can improve the outcome of multiple rib fractures. The present research included patients who were hospitalized in three Jiangsu hospitals following diagnosis with multiple rib fractures. Patients received early rib fracture fixation (≤ 48 h) or delayed rib fracture fixation (> 48 h) utilizing computer-based random sequencing (in a 1:1 ratio). The primary outcome measures included hospital length of stay, intensive care unit (ICU) stay, mechanical ventilation, inflammatory cytokine levels, infection marker levels, infection, and mortality. Results A total of 403 individuals were classified into two groups, namely, the early group (n = 201) and the delayed group (n = 202). Patients belonging to the two groups had similar baseline clinical data, and there were no statistically significant differences between them. Early rib fracture fixation greatly decreased the length of stay in the ICU (4.63 days vs. 6.72 days, p < 0.001), overall hospital stay (10.15 days vs. 12.43 days, p < 0.001), ventilation days (3.67 days vs. 4.55 days, p < 0.001), and hospitalization cost (6900 USD vs. 7600 USD, p = 0.008). Early rib fracture fixation can decrease inflammatory cytokine levels and infection marker levels, prevent hyperinflammation and improve infection in patients with multiple rib fractures. The timing of rib fracture fixation does not influence the surgical procedure time, operative blood loss, 30-day all-cause mortality, or surgical site infection. Conclusion The findings from the present research indicated that early rib fracture fixation (≤ 48 h) is a safe, rational, effective and economical strategy and worth clinical promotion.

Circular RNA (circRNAs) Fibronectin Type III Domain Containing 3B (FNDC3B) (circFNDC3B) has been revealed to be involved in the progression of oesophageal squamous cell carcinoma (ESCC). Hence, the potential regulatory network of circFNDC3B in ESCC was further investigated. Levels of genes and proteins were examined by qRT-PCR and Western blot. In vitro assays were performed using colony formation assay, 5-Ethynyl-2 0 -deoxyuridine (EdU) assay, flow cytometry, wound healing assay, and transwell assay. The target relationship between miR-214-3p and circFNDC3B or cell division cycle 25 homologue A (CDC25A) was verified by dual-luciferase reporter and RIP assays. In vivo assay was carried out using the xenograft nude mice model. CircFNDC3B was highly expressed in ESCC, and high circFNDC3B expression was tightly associated with poor prognosis in ESCC patients. Functionally, circFNDC3B knockdown not only suppressed ESCC cell growth, migration and invasion in vitro, but hindered ESCC tumour growth in vivo. Mechanistically, circFNDC3B acted as a sponge for miR-214-3p to up-regulate the expression of its target CDC25A.Rescue experiments showed that miR-214-3p inhibitor reversed the anticancer effects of circFNDC3B knockdown. Moreover, forced expression of miR-214-3p suppressed the malignant phenotypes mentioned above, while this condition was abolished by CDC25A overexpression. CircFNDC3B silencing restrains the tumorigenesis of oesophageal squamous cell carcinoma through miR-214-3p/ CDC25A axis, which opens a new window to the development of novel therapeutic strategy for ESCC patients.