Treatment of Retroperitoneal Cavernous Lymphangioma: A Case Report

A 32-year-old man who complained of recurrent nauseat and vomiting was admitted to our hospital.The contrast-enhanced computed tomography revealed a cystic mass located behind the duodenum which was suggestive of lymphangioma.Laparoscopic resection of the retroperitoneal mass was successfully performed.The postoperatively pathological examination confirmed the diagnosis of cavernous lymphangioma.Ultrasound and enhanced CT can be used for making a preoperative diagnosis.Once symptoms of the disease develop,complete surgical resection should be performed.

Hepatocyte growth factor protects pulmonary endothelial barrier against oxidative stress and mitochondria-dependent apoptosis

Background:Pulmonary microvascular endothelial cells(PMVECs)were not complex,and the endothelial barrier was destroyed in the pathogenesis progress of acute lung injury(ALI)/acute respiratory distress syndrome(ARDS).Previous studies have demonstrated that hepatocyte growth factor(HGF),which was secreted by bone marrow mesenchymal stem cells,could decrease endothelial apoptosis.We investigated whether mTOR/STAT3 signaling acted in HGF protective effects against oxidative stress and mitochondria-dependent apoptosis in lipopolysaccharide(LPS)-induced endothelial barrier dysfunction and ALI mice.Methods:In our current study,we introduced LPS-induced PMEVCs with HGF treatment.To investigate the effects of mammalian target of rapamycin(mTOR)/signal transducer and activator of transcription 3(STAT3)pathway in endothelial oxidative stress and mitochondria-dependent apoptosis,mTOR inhibitor rapamycin and STAT3 inhibitor S3I-201 were,respectively,used to inhibit mTOR/STAT3 signaling.Moreover,lentivirus vector-mediatedmTORC1(Raptor)andmTORC2(Rictor)gene knockdown modifications were introduced to evaluatemTORC1 andmTORC1 pathways.Calcium measurement,reactive oxygen species(ROS)production,mitochondrial membrane potential and protein,cell proliferation,apoptosis,and endothelial junction protein were detected to evaluate HGF effects.Moreover,we used the ALI mouse model to observe the mitochondria pathological changes with an electron microscopein vivo.Results:Our study demonstrated that HGF protected the endothelium via the suppression of ROS production and intracellular calcium uptake,which lead to increased mitochondrial membrane potential(JC-1 and mitochondria tracker green detection)and specific proteins(complex I),raised anti-apoptosis Messenger Ribonucleic Acid level(B-cell lymphoma 2 and Bcl-xL),and increased endothelial junction proteins(VE-cadherin and occludin).Reversely,mTOR inhibitor rapamycin and STAT3 inhibitor S3I-201 could raise oxidative stress and mitochondria-dependent apoptosis even with HGF treatment in LPS-induced endothelial cells.Similarly,mTORC1 as well as mTORC2 have the same protective effects in mitochondria damage and apoptosis.Inin vivo experiments of ALI mouse,HGF also increased mitochondria structural integrity via the mTOR/STAT3 pathway.Conclusion:In all,these reveal that mTOR/STAT3 signaling mediates the HGF suppression effects to oxidative level,mitochondria-dependent apoptosis,and endothelial junction protein in ARDS,contributing to the pulmonary endothelial survival and barrier integrity.