BACKGROUND:Nano-hydroxyapatite helps to improve the mechanical properties of bone implants.
OBJECTIVE:To study the clinical effect of nano-hydroxyapatite artificial bone on col apsed fracture of the tibial plateau.
METHODS:Fourteen cases of col apsed fracture of the tibial plateau combined with bone defects from March 2010 to September 2012 were analyzed retrospectively. The bone defect range was from 1.5 cm×1.0 cm to 3.1 cm×4.5 cm. Al patients were treated with nano-hydroxyapatite artificial bone at an implant amount of 5-14 g. Clinical and X-ray observations were applied at 1 week, 1 month and 3 months postoperatively. Hospital for Special Surgery scores were employed for recovery of knee function.
RESULTS AND CONCLUSION:The patients were fol owed up for 12-27 months. Except for one case of a smal amount of wound exudates, no general side effects occurred in 13 cases. X-ray photo showed an integrity interface between nano-hydroxyapatite artificial bone and host bone at 3 months after treatment. Primary healing was obtained in al cases without any complications. Hospital for Special Surgery score was increased to (88.7±4.3) points at 1 year later. These findings indicate that the nano-hydroxyapatite artificial bone has a good biocompatibility and biomechanics, and it may be an ideal artificial bone for repairing col apsed fractures of the tibial plateau.

BACKGROUND:Human hypoxia-inducible factor-1 alpha can regulate the expression of osteogenic and angiogenic genes, and promote osteogenic activity. OBJECTIVE:To observe the expression of osteogenic genes in rat bone marrow mesenchymal stem cells carrying human hypoxia-inducible factor-1 alpha slow virus infection. METHODS:Hypoxia-inducible factor-1 alpha was obtained from Hela cells using RT-PCR. Lentivirus expression vector plasmid carrying hypoxia-inducible factor-1 alpha (Lenti-HIF-1α-eGFP) was constructed. 293Ta cells with LentiPac HIV mixed packaging plasmid was packaged, and then lentivirus was obtained. Rat bone marrow mesenchymal stem cells were isolated and cultured using direct whole bone marrow adherent method. Bone marrow mesenchymal stem cells were identified using flow cytometry. Bone marrow mesenchymal stem cells were infected with slow virus for 1, 4, 7 and 14 days. Bone morphogenetic protein-2, osteocalcin, osteopontin and alkaline phosphatase expression levels were detected in bone marrow mesenchymal stem cells using real-time fluorescent quantitative PCR. RESULTS AND CONCLUSION:Bone marrow mesenchymal stem cells were effectively infected with Lenti-HIF-1α-eGFP. Real-time fluorescent quantitative PCR results revealed that bone morphogenetic protein-2, osteocalcin, osteopontin and alkaline phosphatase began to obviously overexpress from 4 days after infection with Lenti-HIF-1α-eGFP until 14 days. Results suggested that hypoxia-inducible factor-1 alpha could elevate the osteogenic activity of bone marrow mesenchymal stem cells.

Objective To investigate the inhibitory effects and mechanisms of α-hederin,an active ingredient in Fruc-tus Akebiae,on hepatocellular carcinoma(HCC)cells.Methods HCC cells were divided into four groups and treated with α-hederin(0,10,20,and 30 μmol·L-1)for 24 h and 48 h,respectively.MTT assays were used to detect the cell proliferation rate,flow cytometry(FCM)was used to detect the apoptotic rate,transcriptomics was used to screen signaling pathways in α-hederin-treated HCC cells,RNA interference was exploited to verify the underlying signaling pathway,and real-time quantitative PCR(qRT-PCR)and Western blotting(WB)were used to detect expression changes of the mRNA and protein of TP53(p53),PMAIP1(Noxa),and apoptosis-associated proteins,Caspase9 and Caspase3.Results α-Hederin induced apoptosis by activa-ting apoptosis-associated proteins,PARP,Caspase9 and Caspase3.Transcriptomics,qRT-PCR,and WB results also showed that α-hederin increased the mRNA and protein expression of p53 and Noxa.Furthermore,α-hederin inhibited the protein degradation of p53 and Noxa,reversing the apoptosis decrease in p53/Noxa siRNA-knocked-down HCC cells.In vivo results showed that α-hederin inhibited the growth of HCC tumors.Conclusion α-hederin may induce the apoptosis of HCC cells by activating and stabilizing the p53/Noxa signaling pathway.