Objective To evaluate the effectiveness of enucleation for the treatment of huge hemangiomas. Methods From 1979 to 1998, enucleation was used for the treatment of hepatic cavernous hemangiomas in 126 patients, among them 18 with multiple tumors and 6 with centrally located lesions. For the tumors larger than 10 cm in diametre or located in theⅠ or Ⅷ segment of the liver, enucleation combined with intermittent inflow vascular occlusion was adopted. Results All cavernous hemangiomas in this group were enucleated successfully, there was no mortality. The median intraoperative blood loss was 1015?577*!ml(200*!ml～4*!500*!ml). Postoperative complications developed in 15 patients including pleural effusion in 10 and wound infection in 5. 54 patients were lost from follow up. None of the remaining 72 patients had recurrence at the follow up ranging from 6 months to 18 years and 4 months. Conclusion Enucleation of cavernous hemangioma of the liver is a safe and effective alternative to hepatectomy.

Pulmonary hypertension (PH) is an insidious pulmonary vasculopathy with high mortality and morbidity and its underlying pathogenesis is still poorly delineated. The hyperproliferation and apoptosis resistance of pulmonary artery smooth muscle cells (PASMCs) contributes to pulmonary vascular remodeling in pulmonary hypertension, which is closely linked to the downregulation of fork-head box transcriptional factor O1 (FoxO1) and apoptotic protein caspase 3 (Cas-3). Here, PA-targeted co-delivery of a FoxO1 stimulus (paclitaxel, PTX) and Cas-3 was exploited to alleviate monocrotaline-induced pulmonary hypertension. The co-delivery system is prepared by loading the active protein on paclitaxel-crystal nanoparticles, followed by a glucuronic acid coating to target the glucose transporter-1 on the PASMCs. The co-loaded system (170 nm) circulates in the blood over time, accumulates in the lung, effectively targets the PAs, and profoundly regresses the remodeling of pulmonary arteries and improves hemodynamics, leading to a decrease in pulmonary arterial pressure and Fulton's index. Our mechanistic studies suggest that the targeted co-delivery system alleviates experimental pulmonary hypertension primarily via the regression of PASMC proliferation by inhibiting cell cycle progression and promoting apoptosis. Taken together, this targeted co-delivery approach offers a promising avenue to target PAs and cure the intractable vasculopathy in pulmonary hypertension.