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Background Hemobilia due to rupture of hepatic artery pseudoaneurysm and recurrent hemorrhage caused by hepatic artery collateral circulation are both rare complications after liver trauma. There have been a number of separate reports of both complications, but no cases have been reported in which the two events occurred in the same patient. Here we report a recurrent hemorrhage in the bile duct due to hepatic artery pseudoaneurysm secondary to collateral circulation formation after hepatic artery ligation in a patient with liver trauma. Case presentation A 52-year-old male patient was admitted to our hospital for liver trauma (Grade IV according to the American Association for the Surgery of Trauma (AAST) grading system) with active bleeding after a traffic accident. Hepatic artery ligation was performed for hemostasis. Three months after the surgery, the patient was readmitted for melena and subsequent hematemesis. Selective angiography examination revealed the formation of collateral circulation between the superior mesenteric artery and right hepatic artery. Moreover, a ruptured hepatic artery pseudoaneurysm was observed and transcatheter arterial embolization (TAE) was performed for hemostasis at the same time. After the treatment, the patient recovered very well and had an uneventful prognosis until the last follow-up. Conclusion For patients with hepatic trauma, the selection of the site of hepatic artery ligation and the diagnosis and treatment methods of postoperative biliary hemorrhage are crucial for the prognosis of the disease.

Polysaccharides from medicinal plants exert antitumor activity in many cancers. Our previous study demonstrated that polysaccharides extracted from the selenium-enriched Pyracantha fortuneana (Se-PFPs) showed antiproliferative effect in breast cancer cell line. This study aimed to investigate the antitumor effect of Se-PFPs in ovarian cancer cells in vitro and in vivo. Se-PFPs could decrease cell viability, induce apoptosis, and inhibit migratory and invasive potentials in HEY and SKOV3 cells. These findings are supported by reduced expression of cyclin D1, Bcl-2 and MMP-9, enhanced cleavage of PARP and caspase-3, elevated activity of caspase-3 and caspase-9, and EMT (epithelial to mesenchymal transition) inhibition (elevated expression of E-cadherin and cytokeratin 19, and reduced expression of N-cadherin, vimentin, ZEB1 and ZEB2). Moreover, Se-PFPs inhibited xenografted tumor growth through inhibiting cell proliferation and inducing cell apoptosis. More importantly, Se-PFPs significantly reduced cytoplasmic β-catenin particularly nuclear β-catenin expression but increased β-catenin phosphorylation in a GSK-3β-dependent mechanism. Furthermore, β-catenin knockdown exerted similar effects on cell proliferation and invasion as seen in Se-PFPs-treated cells, while β-catenin overexpression neutralized the inhibitory effects of Se-PFPs on cell proliferation and invasion. Take together,Se-PFPs exert antitumor activity through inhibiting cell proliferation, migration, invasion and EMT, and inducing cell apoptosis. These effects are achieved by the inhibition of β-catenin signaling. Thus Se-PFPs can be used as potential therapeutic agents in the prevention and treatment of ovarian cancer.