[Soft tissue balancing in the total hip arthroplasty for severe developmental dysplasia of the hip in adults].

OBJECTIVE: To assess clinical result of soft tissue balancing in primary total hip arthroplasty for severe developmental dysplasia of the hip in adults. METHODS: From December 2000 to August 2006, 26 primary cementless total hip arthroplasties combined with soft tissue balancing were performed in 21 cases for the treatment of severe developmental dysplasia of the hip. Patients were classified as type III (20 hips) and type IV (6 hips) according to Crowe classification. All acetabular cups were placed in their original anatomic location by soft tissue releasing and subtrochanteric shortening osteotomy. Thereafter, postoperative clinical and radiological results were evaluated. RESULTS: The mean length of follow-up was 4.8 years (range, 13 months-7 years). Limp improved by at least one grade in 62% of the cases. Leg-length discrepancy was corrected significantly and osteotomy was undertaken in 13 hips with a mean decrease length of 0.9 cm by effective releasing. Harris scores improved significantly from a mean of 41.2 preoperatively to 89.6 postoperatively. No dislocations, infections and prosthesis loosening were found at the final follow-up evaluation. CONCLUSION: Soft tissue balancing in total hip arthroplasty can facilitate acetabular reconstruction to normalize the hip center in severe developmental dysplasia of the hip, as a result, satisfactory short-term result can be obtained by restoring normal function and anatomic structure.

Fungal spondylodiscitis in a patient recovered from H7N9 virus infection: a case study and a literature review of the differences between Candida and Aspergillus spondylodiscitis.

To report a rare case of fungal spondylodiscitis in a patient recovered from H7N9 virus infection and perform a literature review of the different characteristics of Candida and Aspergillus spondylodiscitis, we reviewed cases of spondylodiscitis caused by Candida and Aspergillus species. Data, including patients' information, pathogenic species, treatment strategy, outcomes, and relapses, were collected and summarized. The characteristics of Candida and Aspergillus spondylodiscitis were compared to see if any differences in clinical features, management, or consequences could be detected. The subject of the case study was first misdiagnosed as having a vertebral tumor, and then, following open biopsy, was diagnosed as having fungal spondylodiscitis. The patient made a good recovery following radical debridement. Seventy-seven additional cases of Candida spondylodiscitis and 94 cases of Aspergillus spondylodiscitis were identified in the literature. Patients with Candida spondylodiscitis tended to have a better outcome than patients with Aspergillus spondylodiscitis (cure rate 92.3% vs. 70.2%). Candida was found more frequently (47.8%) than Aspergillus (26.7%) in blood cultures, while neurological deficits were observed more often in patients with Aspergillus spondylodiscitis (43.6% vs. 25.6%). Candida spinal infections were more often treated by radical debridement (60.5% vs. 39.6%). Patients with Candida spondylodiscitis have better outcomes, which may be associated with prompt recognition, radical surgical debridement, and azoles therapy. A good outcome can be expected in fungal spondylodiscitis with appropriate operations and anti-fungal drugs.

miR-26b inhibits proliferation, migration, invasion and apoptosis induction via the downregulation of 6-phosphofructo-2-kinase/fructose-2,6-bisphosphatase-3 driven glycolysis in osteosarcoma cells.

MicroRNAs (miRNAs) are differentially expressed and play crucial roles in cancer development and progression. Elevated glycolysis provides survival advantage and metastatic phenotype. Emerging evidence indicates that glycolysis in cancers can be regulated by miRNAs. In the present study, the role of miR-26b in the proliferation, invasion and glycolytic phenotype of osteosarcoma (OS) cells was investigated. miR-26b was reported to be downregulated in OS tissues, however, the effect of miR-26b on OS has not been distinctly evaluated. The present study therefore investigated the miR-26b sensitivity mechanism in OS. To determine the role of miR-26, we reinstated its expression in the U2OS OS cell line through transfection with miR-26b mimics and examined the effects on cell proliferation, migration, invasion, cell cycle progression and glycolytic parameters. The computational prediction tool was employed to identify the molecular target of miR-26b and was confirmed experimentally. Restoration of miR-26b expression inhibited cell proliferation, migration and invasion, arrested cell cycle progression, and induced cell apoptosis accompanied by the downregulation of glycolytic phenotype. Moreover, the binding site for miR-26b was predicted in the 3'UTR of gene 6-phosphofructo-2-kinase/fructose­2,6-bisphosphatase-3 (PFKFB3), suggesting a role for miR-26b in metabolic alteration in OS cells. Further studies showed that overexpression of miR-26b repressed PFKFB3 mRNA and protein levels followed by modulation of the expression of glycolytic components (LDHA, GLUT-1) and markers of invasion and cell cycle such as MMP-9, MMP-2, cyclin D1 and p27. Collectively, the data suggested the tumor suppressive role of miR-26b which functions by targeting the glycolytic metabolism in OS cells, and providing a possible therapeutic strategy for OS patients by targeting miRNA expression.

Clinical significance of microRNA-130b in osteosarcoma and in cell growth and invasion.

OBJECTIVE: To investigate clinical significance of microRNA-130b (miR-130b) in osteosarcoma and its role in cell growth and invasion. METHODS: miR-130b expression was detected in 68 samples of surgically resected osteosarcoma and matched normal tumor-adjacent tissues by qRT-PCR. The expression of miR-130b was altered by corresponding vectors in osteosarcoma cells, and then Western blot was used to detect the expression of PPARγ. BrdU cell proliferation and Transwell assays were performed to determine cell proliferation and invasion. RESULTS: The expression of miR-130b in osteosarcoma tissues was significantly higher than that in normal tumor-adjacent tissues. Its expression in patients with metastasis was significantly higher than that in those without metastases. miR-130b expression in tumor tissues was significantly associated with tumor size, clinical stage and distant metastasis. And its expression was significantly correlated with overall survival and disease free survival. miR-130b overexpression obviously repressed the expression of PPARγ, and resulted in significant increase of Saos-2 cell proliferation and invasion. On the contrast, repressing miR-130b expression with its inhibitor significantly increased PPARγ expression, and inhibited MG-63 cell proliferation and invasion. CONCLUSIONS: The high-expression of miR-130b is correlated with the adverse clinicopathological features and poor prognosis in osteosarcoma. miR-130b may regulate proliferation and invasion of osteosarcoma cells by targeting PPARγ, suggesting miR-130b may play a key role in the progression of osteosarcoma.