Treatment of Supracondylar-Intercondylar Femoral Fractures with a Retrograde Intramedullary Nailing

PURPOSE: We analyzed the cases of supracondylar-intercondylar femoral fracture treated with retrograde intramedullary nail and report the clinical results and its usefulness. MATERIALS AND METHODS: We reviewed 17 cases of supracondylar-intercondylar femoral fracture that had been treated with retrograde intramedullary nail and each of patients had been followed up for a minimum one year. Post-operative functional assessment was performed using a scale developed by Sanders et al. The evaluation scale assesses range of motion, pain, walking ability, return to work, and alignment and shortening as measured on radiograph. RESULTS: According to functional assessment of Sanders et al, there were 6 excellent, 9 good, 1 fair, and 1 poor results, that is, 94% showed above excellent results. Bony union was obtained in average 5 months after operation. The post-operative complications were varus deformity in 1 case, wound infection in 1 case, stiffness of knee joint in 1 case, and metal failure in 1 case. CONCLUSION: The treatment of supracondylar-intercondylar femoral fracture with retrograde intramedullary nail is one of the good surgical options for clinically preferable results with the advantages in early joint motion and early ambulation.

Inhibition of BETA2/NeuroD by Id2

Id (Inhibitor of Differentiation) proteins belong to a family of transcriptional modulators that are characterized by a helix loop helix (HLH) region but lack the basic amino acid domain. Id proteins are known to interact with basic helix-loop-helix (bHLH) transcription factors and function as their negative regulators. The negative role of Id proteins has been well demonstrated in muscle development and some in neuronal cells. In this study, we investigated the effect of Id on the function of BETA2/NeuroD, a bHLH transcription factor responsible for neuron and endocrine cell specific gene expression. cDNAs of several Id isoforms were isolated by yeast two-hybrid system using the bHLH domain of E47, a ubiquitous bHLH partner as a bait. Id proteins expressed in COS M6 cells, were found in both cytosolic and nuclear fractions. Electrophoretic mobility shift assay showed that coexpression of Id2 proteins inhibited BETA2/ NeuroD binding to its target sequence, E-box. Id2 inhibited E-box mediated gene expression in a dose dependent manner in BETA2/NeuroD expressing HIT cells. Id coexpressed with BETA2/NeuroD in HeLa cells, inhibited the stimulatory activity of BETA2/NeuroD. These results suggest that Id proteins may negatively regulate tissue specific gene expression induced by BETA2/NeuroD in neuroendocrine cells and the inhibitory role of Id proteins during differentiation may be conserved in various tissues.