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Abstract Background Traumatic duodenal rupture is rare which accounts for only 2–10% of all Blunt abdominal trauma. The purpose of this study was to investigate the experience of diagnosis and treatment of traumatic duodenal rupture in children. Methods This was a retrospective case series study. Clinical data were collected from three children suffering from a traumatic duodenal rupture who received surgical treatment in our hospital from January 2013 to January 2023. Demographic characteristics, trauma mechanism, physical examination, auxiliary examination, operation timing and plan, postoperative management and follow-up of included patients were described. Summarize the importance of early diagnosis and treatment of this type of injury. Results Three children (1 male and 2 females) with duodenal rupture due to traumatic abdominal injury were included in the study, with average age of 8.2 years (range 2.75–13.25 years). Among them, One child was injured by heavy objects. The other two children had lumbar fracture and seat belt sign. All three patients underwent emergency operation within 24 h, and recovered well after surgery. No related complications seen during follow-up. Conclusions Duodenal rupture is a rare but fatal disease. Early identification and active abdominal exploration can reduce the incidence of related complications and mortality in children with blunt abdominal injury, especially those with seat belt sign. Simultaneously, the standardized postoperative management is significant for the cure of children.

Background Hepatic stellate cell (HSC) activation and hepatic fibrosis mediated biliary atresia (BA) development, but the underlying molecular mechanisms are poorly understood. This study aimed to investigate the roles of circRNA hsa_circ_0009096 in the regulation of HSC proliferation and hepatic fibrosis. Methods A cellular hepatic fibrosis model was established by treating LX-2 cells with transforming growth factor β (TGF-β1). RNaseR and actinomycin D assays were performed to detect hsa_circ_0009096 stability. Expression of hsa_circ_0009096, miR-370-3p, and target genes was detected using reverse transcription-qPCR. Direct binding of hsa_circ_0009096 to miR-370-3p was validated using dual luciferase reporter assay. Cell cycle progression and apoptosis of LX-2 cells were assessed using flow cytometry. The alpha-smooth muscle actin (α-SMA), collagen 1A1 (COL1A1), and TGF beta receptor 2 (TGFBR2) protein levels in LX-2 cells were analyzed using immunocytochemistry and western blotting. Results Hsa_circ_0009096 exhibited more resistance to RNase R and actinomycinD digestion than UTRN mRNA. Hsa_circ_0009096 expression increased significantly in LX-2 cells treated with TGF-β1, accompanied by elevated α-SMA and COL1A1 expression. Hsa_circ_0009096 siRNAs effectively promoted miR-370-3p and suppressed TGFBR2 expression in LX-2 cells, mediated by direct association of hsa_circ_0009096 with miR-370-3p. Hsa_circ_0009096 siRNA interfered with the cell cycle progression, promoted apoptosis, and reduced α-SMA and COL1A1 expression in LX-2 cells treated with TGF-β1. MiR-370-3p inhibitors mitigated the alterations in cell cycle progression, apoptosis, and α-SMA, COL1A1, and TGFBR2 expression in LX-2 cells caused by hsa_circ_0009096 siRNA. In conclusion, hsa_circ_0009096 promoted HSC proliferation and hepatic fibrosis during BA pathogenesis by accelerating TGFBR2 expression by sponging miR-370-3p.