Objective: This study was performed to observe the effect of internal Balser plate fixation for treating unstable sternoclavicular joints (SCJ) and displaced medial clavicle fractures. Methods: From April 2009 to September 2016, 17 consecutive patients who underwent open reduction and internal Balser plate fixation for SCJ dislocations or medial clavicle fractures were retrospectively reviewed. There were 11 male and six female patients, with a mean age of 45.6 ± 15.5 years. Standardized treatment procedures consisted of reduction, creating a space posterior dorsal osteal face of the sternal manubrium, an inverted Balser plating, and postoperative immobilization. At follow-up, plain radiographs were assessed for fracture union, implant loosening, degenerative changes, and joint congruity. Clinical evaluation included: completion of the Disability of the Arm, Shoulder, and Hand (DASH) questionnaire; determination of the Constant and Murley score and visual analog scale (VAS) score; and assessment of intraoperative and postoperative complications. Results: All patients were followed up, at a mean follow-up of 20.1 ± 7.9 months, each fracture had a solid union, and each dislocation showed no sign of recurrent dislocation. The mean shoulder forward flexion was 162.9 ± 8.1. The mean DASH score was 5.2 ± 5.2 points. The mean Constant and Murley joint function score was 93.7 ± 7.9 points, with 15 excellent cases and two good cases. The mean VAS score was 1.1 ± 1.4 points, showing significant improvement compared with the VAS score preoperatively. Postoperative complications included one wound hematoma which was healed after a debridement and one recurrent instability due to hook migration, which underwent revision reconstruction. All patients were satisfied with their treatment outcome at the final follow-up. Conclusion: Sternoclavicular joints dislocation or medial clavicle fractures can be treated successfully with Balser plate fixation. This technique permits early functional exercise while preserving the SCJ.

These findings provide strong evidence of which IFN-gamma CA repeat and IRF-1 GT repeat polymorphisms influence the risk of asthma for children in Taiwan.

Progranulin (PGRN) is an autocrine growth factor that exerts crucial roles within cartilage tissue; however the molecular mechanisms underlying PGRN-mediated cartilage homeostasis remain elusive. In the present study, we investigated the role of PGRN in regulating chondrocyte homeostasis and its therapeutic potential for managing osteoarthritis (OA). We found that PGRN levels are significantly increased in human cartilage in mild OA and that its expression is decreased in the cartilage in severe OA. In vitro, treatment of primary rat chondrocytes with recombinant PGRN significantly enhanced the levels of collagen type II alpha 1 chain (COL2A1) and aggrecan, and attenuated TNF-α-induced up-regulation of matrix metallopeptidase 13 (MMP13) and ADAM metallopeptidase with thrombospondin type 1 motif 5 (ADAMTS5) in chondrocytes. These effects were abrogated in SIRT1-/- cells, indicating a causative role of SIRT1 in the effects of PGRN on protein expression in chondrocytes. Mechanistically, PGRN increased SIRT1 expression and activity, which reduced the acetylation levels of SRY-box transcription factor (SOX9) and transcription factor P65 (P65) and thereby promoted nuclear translocation of SOX9 and inhibited TNF-α-induced P65 nuclear accumulation to maintain chondrocyte homeostasis. In conclusion, our findings reveal a mechanism of action for PGRN that maintains cartilage homeostasis and support the notion that PGRN up-regulation may be a promising strategy for managing OA.