Objective To describe the surgical technique and outcomes of arthroscopic reconstruction anterior cruciate ligament (ACL) and posterior cruciate ligament (PCL) and repair of the injured posteromedial complex (PMC) or posterolateral complex (PLC) structures of the knee joint in treatment of multiple ligaments injuries of knee. Methods From March 2005 to May 2007, 43 patients with multiple ligaments injuries of knee underwent arthroscopic reconstruction. Twenty-four patients were treated with arthroscopic reconstruction of combined ACL and PCL with allograft tendons and augmentation of PMC. The other 19 patients were treated with repair the PLC in addition to reconstruction of ACL and PCL. The International Knee Documentation Committee (IKDC) and Lysholm knee score were used for function evaluation. Results All patients were followed up for 24 to 48 months with an average of 33.10±9.65 months. The stability recovered when stress was applied to the knee at 0° and 20° of flexion. According to IKDC there was a significant improvement from severely abnormal (graded D) in 43 cases before surgery to normal (graded A) in 29 cases (67%), nearly normal (graded B) 11 cases (26%) and abnormal (graded C) 3 cases (7%) at follow-up. The average Lysholm score of the all cases were 46.7±4.2 and 89.6±2.8 before operation and at final follow-up, respectively (t=8.563, P＜0.01). Conclusion Excellence clinical results and good stability were achieved with arthrescopic reconstruction of ACL and PCL combined with repair or augmentation of the PMC and PLC simultaneously.

Objective:To identify the differentially expressed snoRNAs in the carcinogenesis of cells induced by α-particles radiation and predict the targeted genes and RNA-co-expression networks.Methods:Full transcriptome expression microarray biochips were employed to screen the differentially expressed snoRNAs between human bronchial epithelial BEP2D cell line and its derivative malignantly transformed cell line BERP35T-4 established by α-particle irradiation. The expression changes of snoRNAs and their derived sdRNAs were confirmed by qRT-PCR. The functional domains, targets and co-expression networks of snoRNA were predicted by bioinformatics analysis.Results:Consistent with the result of microarray assay, the expression changes of the screened snoRNAs were confirmed by qRT-PCR. The expressions of sno116 family decreased in BERP35T-4, which was 0.105% ( t=26.60, P<0.01) of BEP2D, and they were generally down-regulated in radiation-induced carcinogenic BERP35T-4 cells and the human lung cancer cell lines A549 and H1299. It was also found that the expression level of the sdRNAs derived from sno116-14 was significantly different in the same cells. It was speculated that these less expressed sdRNAs of sno116-14 could be due to degradation as the consequence of interaction with their targets. The co-expression networks of sno116 family with other types of RNA were established, and the predicted targets of sno116-14 included ZNF280D, TFDP1, CCDC28B, RPS6KA3, CANX, RUNX1 and KALRN, which were related to the functions of cell proliferation and cytoskeletal structure. Conclusions:Some differentially expressed snoRNAs related to α-particle induced carcinogenesis have been identified. It is predicted that the target gene of sno116-14 is involved in the biological processes such as cell proliferation, cytoskeletal structure and the signaling pathways for function regulation, providing new information for the function model of C/D box snoRNAs and the mechanism of radiation carcinogenesis.

In growing children, growth plate cartilage has limited self-repair ability upon fracture injury always leading to limb growth arrest. Interestingly, one type of fracture injuries within the growth plate achieve amazing self-healing, however, the mechanism is unclear. Using this type of fracture mouse model, we discovered the activation of Hedgehog (Hh) signaling in the injured growth plate, which could activate chondrocytes in growth plate and promote cartilage repair. Primary cilia are the central transduction mediator of Hh signaling. Notably, ciliary Hh-Smo-Gli signaling pathways were enriched in the growth plate during development. Moreover, chondrocytes in resting and proliferating zone were dynamically ciliated during growth plate repair. Furthermore, conditional deletion of the ciliary core gene Ift140 in cartilage disrupted cilia-mediated Hh signaling in growth plate. More importantly, activating ciliary Hh signaling by Smoothened agonist (SAG) significantly accelerated growth plate repair after injury. In sum, primary cilia mediate Hh signaling induced the activation of stem/progenitor chondrocytes and growth plate repair after fracture injury.
Mice ; Animals ; Hedgehog Proteins/genetics* ; Receptors, G-Protein-Coupled/metabolism* ; Cilia/metabolism* ; Cartilage/metabolism* ; Regeneration