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1.
Injury ; 48(2): 486-494, 2017 Feb.
Artigo em Inglês | MEDLINE | ID: mdl-27876350

RESUMO

PURPOSE: The present study aimed to evaluate the feasibility and clinical efficacy of bridging vein transplantation to deal with the vessel shortage during free vascularized fibular grafting for reconstructing infected bone defects of the femur. METHODS: Twelve patients (aged 15-58 years) with infected bone defects of the femur (between 6.0 and 18.0cm) were recruited in this study. Vacuum sealing drainage were applied after extensive debridement of the infected bone defects and irrigated with 0.9% sodium chloride solution for 1-2 weeks. After the drainage was clear and the focal infections were controlled, the free vascularized fibula was harvested for reconstructing the femoral bone defects. The vascularized fibula was grafted and fixated appropriately at the recipient site. The autogenous great saphenous vein was harvested, one end was anastomosed and bridged the vascular pedicles of the fibular grafts, and the other end anastomosed the artery and/or the vein in the recipient healthy site. RESULTS: Mean length of vein transplantation with vascularized fibular graft was 10.2 cm (range 7-15cm). All patients had good radiological healing without recorded nonunion or malunion. No patient developed deep infection or implant failure. Primary bone healing was achieved in 10 patients; however, 2 grafted fibular formed pseudarthrosis with the recipient femoral and then healed after a secondary surgery. One patient suffered from graft stress fracture after bone healing and healed after external fixation. After the mean follow-up of 30 months (9-72 months), according to the Enneking scoring system, clinical outcomes were excellent in 7 patients, good in 4 and fair in one. The functional recovery rate of the lesion limb was 89.4%. CONCLUSIONS: Free vascularized fibular graft with vein transplantation bridged vascular pedicle can effectively repair the infected bone, improve blood supply to the bone defect site, and help control infection. It is a feasible and effective treatment for infected bone defects of the femur with poor soft tissue conditions, or blood supply vessel shortage.


Assuntos
Fraturas do Fêmur/cirurgia , Fêmur/patologia , Fíbula/transplante , Fixação Interna de Fraturas/métodos , Osteomielite/cirurgia , Procedimentos de Cirurgia Plástica , Veias/transplante , Adolescente , Adulto , China , Desbridamento/métodos , Estudos de Viabilidade , Feminino , Fraturas do Fêmur/complicações , Fraturas do Fêmur/patologia , Fêmur/irrigação sanguínea , Fêmur/cirurgia , Fíbula/irrigação sanguínea , Consolidação da Fratura , Sobrevivência de Enxerto , Humanos , Masculino , Pessoa de Meia-Idade , Osteomielite/patologia , Estudos Retrospectivos , Resultado do Tratamento , Adulto Jovem
2.
Artigo em Chinês | WPRIM (Pacífico Ocidental) | ID: wpr-299867

RESUMO

<p><b>OBJECTIVE</b>To investigate the protective effect of extracts from Cichorium endivia (CEE) in H2O2-induced HepG2 cell oxidative stress injury, and explore the antioxidant mechanism of CEE in HepG2 cells.</p><p><b>METHOD</b>The viability of H2O2-induced HepG2 cells and the intracellular ROS level were measured by MTT assay and DCFH-DA fluorescence staining assay. The antioxidant-response element (ARE)-Luciferase activity was tested in HepG2 cells stably transected by ARE reporter gene. The fluorescence quantitative RT-PCR was adopted to determine the mRNA expressions of genes containing ARE sequence in HepG2 cells.</p><p><b>RESULT</b>The cell viability reduced, while the ROS level increased after HepG2 cells were treated by H2O2. Different concentrations of CEE could be added to significantly improve the above results. After HepG2 cells transected by ARE reporter gene were treated with different concentrations of CEE, the intracellular ARE activity could increase in a concentration-dependent manner. In addition, the mRNA expressions of regulatory genesGCLC, GCLM and HMOX-1 containing ARE sequence in HepG2 cells were up-regulated in a concentration-dependent manner by CEE.</p><p><b>CONCLUSION</b>CEE inhibited the H2O2-injured HepG2 cells by reducing the ROS level. CEE's antioxidant mechanism for HepG2 cells may be closely related to the antioxidant defense system associated with its effect of activating Nrf2-ARE pathway in HepG2 cells.</p>


Assuntos
Humanos , Antioxidantes , Farmacologia , Asteraceae , Química , Sobrevivência Celular , Medicamentos de Ervas Chinesas , Farmacologia , Células Hep G2 , Peróxido de Hidrogênio , Farmacologia , Espécies Reativas de Oxigênio , Metabolismo , Elementos de Resposta , Genética
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