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.

BACKGROUND: Previous research demonstrated that a homozygous mutation of g.136372044G>A (S12N) in caspase recruitment domain family member 9 ( CARD9 ) is critical for producing Aspergillus fumigatus -induced ( Af -induced) T helper 2 (T H 2)-mediated responses in allergic bronchopulmonary aspergillosis (ABPA). However, it remains unclear whether the CARD9S12N mutation, especially the heterozygous occurrence, predisposes the host to ABPA. METHODS: A total of 61 ABPA patients and 264 controls (including 156 healthy controls and 108 asthma patients) were recruited for sequencing the CARD9 locus to clarify whether patients with this heterozygous single-nucleotide polymorphisms are predisposed to the development of ABPA. A series of in vivo and in vitro experiments, such as quantitative real-time polymerase chain reaction, flow cytometry, and RNA isolation and quantification, were used to illuminate the involved mechanism of the disease. RESULTS: The presence of the p.S12N mutation was associated with a significant risk of ABPA in ABPA patients when compared with healthy controls and asthma patients, regardless of Aspergillus sensitivity. Relative to healthy controls without relevant allergies, the mutation of p.S12N was associated with a significant risk of ABPA (OR: 2.69 and 4.17 for GA and AA genotypes, P = 0.003 and 0.029, respectively). Compared with patients with asthma, ABPA patients had a significantly higher heterozygous mutation (GA genotype), indicating that p.S12N might be a significant ABPA-susceptibility locus ( aspergillus sensitized asthma: OR: 3.02, P = 0.009; aspergillus unsensitized asthma: OR: 2.94, P = 0.005). The mutant allele was preferentially expressed in ABPA patients with heterozygous CARD9S12N , which contributes to its functional alterations to facilitate Af -induced T H 2-mediated ABPA development. In terms of mechanism, Card9 wild-type ( Card9WT ) expression levels decreased significantly due to Af -induced decay of its messenger RNA compared to the heterozygous Card9S12N . In addition, ABPA patients with heterozygous CARD9S12N had increased Af -induced interleukin-5 production. CONCLUSION Our study provides the genetic evidence showing that the heterozygous mutation of CARD9S12N , followed by allele expression imbalance of CARD9S12N , facilitates the development of ABPA.
Humans ; Aspergillosis, Allergic Bronchopulmonary/complications* ; Aspergillus fumigatus/genetics* ; Asthma/genetics* ; Aspergillus ; Mutation/genetics* ; CARD Signaling Adaptor Proteins/genetics*