Sternal plate fixation for sternal wound reconstruction: initial experience (Retrospective study)

<p>Abstract</p> <p>Background</p> <p>Median sternotomy infection and bony nonunion are two commonly described complications which occur in 0.4 - 5.1% of cardiac procedures. Although relatively infrequent, these complications can lead to significant morbidity and mortality. The aim of this retrospective study is to evaluate the initial experience of a transverse plate fixation system following wound complications associated with sternal dehiscence with or without infection following cardiac surgery.</p> <p>Methods</p> <p>A retrospective chart review of 40 consecutive patients who required sternal wound reconstruction post sternotomy was performed. Soft tissue debridement with removal of all compromised tissue was performed. Sternal debridement was carried using ronguers to healthy bleeding bone. All patients underwent sternal fixation using three rib plates combined with a single manubrial plate (Titanium Sternal Fixation System^®, Synthes). Incisions were closed in a layered fashion with the pectoral muscles being advanced to the midline. Data were expressed as mean ± SD, Median (range) or number (%). Statistical analyses were made by using Excel 2003 for Windows (Microsoft, Redmond, WA, USA).</p> <p>Results</p> <p>There were 40 consecutive patients, 31 males and 9 females. Twenty two patients (55%) were diagnosed with sternal dehiscence alone and 18 patients (45%) with associated wound discharge. Thirty eight patients went on to heal their wounds. Two patients developed recurrent wound infection and required VAC therapy. Both were immunocompromised. Median post-op ICU stay was one day with the median hospital stay of 18 days after plating.</p> <p>Conclusion</p> <p>Sternal plating appears to be an effective option for the treatment of sternal wound dehiscence associated with sternal instability. Long-term follow-up and further larger studies are needed to address the indications, benefits and complications of sternal plating.</p

FOXO4 regulates metastasis by binding to and suppressing RUNX2 transactivation ability.

<p><b>A.</b> Promoter regions of <i>RUNX2, PIP, PGC, PLA2G16</i> and <i>CAMK2N1</i> showing potential FOXO (DBE) and RUNX2 (RBS) binding sites relative to first exons. <b>B.</b> Matrigel invasion assay of LNCaP cells expressing control, FOXO4 or FOXO4 plus RUNX2 shRNAs. Error bars, S.E. of triplicate experiments. **, P<0.02. <b>C.</b> Relative RUNX2 RNA levels, as assessed by qRT-PCR in control shRNA vs. shFOXO4 LNCaP cells, primary tumors or LN metastases. RNA levels in each control condition were set to 1. Error bars, S.E. of triplicate experiments. n.s., not significant. Lysates of HEK293T cells transfected with HA-RUNX2 and Myc-FOXO4 were either analyzed by IB for HA, Myc or GAPDH, or immunoprecipitated with anti-myc and blotted with anti-HA (<b>D</b>), or immunoprecipitated with anti-HA and blotted with anti-Myc (<b>E</b>). <b>F.</b> Chromatin from LNCaP[vector] (control) or LNCaP[shFOXO4] cells were immunoprecipitated with control IgG or RUNX2 Ab, and the precipitated DNA subjected to qPCR using PIP promoter primers (<a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0101411#pone.0101411.s007" target="_blank">Table S2</a>). Error bars, S.E. of triplicates. **, P<0.01. <b>G.</b> Chromatin from HEK293T cells transfected with expression plasmids for RUNX2, RUNX2+FOXO4 or empty vector were immunoprecipitated with control IgG or HA Ab, then analyzed for PIP DNA by qPCR as in <b>F</b>.</p