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Type C fractures of the distal humerus are difficult to treat and typically require open anatomical reduction and internal fixation. Here we describe our experience treating patients with type C distal humerus fractures using a trans-olecranon approach with bilateral plate fixation. Fifty-six patients (30 males, 26 females; mean age 49.8 years) were treated over a period of six years. Thirteen fractures were open and 43 closed; all were caused by falls or traffic accidents. All operations were performed successfully with no intraoperative complications. Mean duration of follow-up was 30 months (range 6-70). Mean duration of fracture healing was 2.8 months (range 2-4). Forty-seven out of 56 patients (84%) suffered no postoperative complications. One patient exhibited symptoms of ulnar nerve injury following surgery (nine exhibited symptoms before and after surgery). Two patients had mild cubitus varus deformities, four delayed olecranon osteotomy site healing, and two heterotopic ossifications. In summary, complications were minimal and outcomes satisfactory in patients with type C distal humerus fractures who underwent bilateral plate fixation via a trans-olecranon approach.

Background/Aims: Serine/threonine kinase 35 (STK35) may be associated with Parkinson disease and human colorectal cancer, but there have been no reports on the expression levels or roles of STK35 in osteosarcoma. Methods: STK35 mRNA expression was determined in osteosarcoma and bone cyst tissues by real-time PCR. Cell proliferation and apoptosis were assessed by Cell Counting Kit-8 (CCK-8) assay and flow cytometry analysis, respectively. Results: STK35 was up-regulated in osteosarcoma tissues as indicated by analyzing publicly available expression data (GEO dataset E-MEXP-3628) and real-time PCR analysis on our own cohort. We subsequently investigated the effects of STK35 knockdown on two osteosarcoma cell lines, MG63 and U2OS. STK35 knockdown inhibited the growth of osteosarcoma cells in vitro and in xenograft tumors. Meanwhile, STK35 knockdown enhanced apoptosis. Expression of the active forms and the activity of two major executioner caspases, caspase 3 and caspase 7, were also increased in osteosarcoma cells with STK35 silenced. Additionally, Gene Set Enrichment Analysis (GSEA) identified that the JAK/STAT signaling pathway was positively correlated with STK35 expression. The mRNA expression of STK35 was repressed by STAT3 small interfering RNA (siRNA), but not by siRNA of STAT4, STAT5A or STAT6. A luciferase reporter assay further demonstrated that STAT3 transcriptionally regulated STK35 expression. A chromatin immunoprecipitation (ChIP) assay confirmed the direct recruitment of STAT3 to the STK35 promoter. The promotion effects of STAT3 knockdown on cell apoptosis were partially abolished by STK35 overexpression. Furthermore, STK35 mRNA expression was positively correlated with STAT3 mRNA expression in osteosarcoma tissues by Pearson correlation analysis. Conclusions: These results collectively reveal that STAT3 regulates the transcription of STK35 in osteosarcoma. STK35 may exert an oncogenic role in osteosarcoma.