ObjectiveThe prefabrication of customized cranioplastic implants has been introduced to overcome the difficulties of intra-operative implant molding. The authors present a new technique, which consists of the prefabrication of implant molds using three-dimensional (3D) printers and polymethyl-methacrylate (PMMA) casting.MethodsA total of 16 patients with large skull defects (>100 cm2) underwent cranioplasty between November 2009 and April 2011. For unilateral cranial defects, 3D images of the skull were obtained from preoperative axial 1-mm spiral computed tomography (CT) scans. The image of the implant was generated by a digital subtraction mirror-imaging process using the normal side of the cranium as a model. For bilateral cranial defects, precraniectomy routine spiral CT scan data were merged with postcraniectomy 3D CT images following a smoothing process. Prefabrication of the mold was performed by the 3D printer. Intraoperatively, the PMMA implant was created with the prefabricated mold, and fit into the cranial defect.ResultsThe median operation time was 184.36±26.07 minutes. Postoperative CT scans showed excellent restoration of the symmetrical contours and curvature of the cranium in all cases. The median follow-up period was 23 months (range, 14-28 months). Postoperative infection was developed in one case (6.2%) who had an open wound defect previously.ConclusionCustomized cranioplasty PMMA implants using 3D printer may be a useful technique for the reconstruction of various cranial defects.

Abbreviations: cdc2, cell division cycle 2; cdk1, cycle dependent kinase 1; HIF-1α, hypoxia inducible factor-1α; Hsp, heat shock protein AbstractIn an oxygen-depleted environment, endothelial cells initiate an adaptive pattern of synthesis, which may enable them to survive hypoxic crises. Using high-resolution two-dimensional gel electrophoresis in conjunction with mass spectroscopy, we obtained a 24 differential display of proteins in the pancreatic endothelial cell line, MS-1, at four time points following induction of hypoxia. The induction of Wee1 under hypoxia was confirmed both at the mRNA and protein levels. The phosphorylation of cell division cycle 2, which is downstream of Wee1, was also increased after hypoxic exposure. In addition, pre-exposure to hypoxia attenuated a decrease in hydrogen peroxide-induced cell number. The induction of bax (a pro-apoptotic protein) and reduction of bcl (an anti-apoptotic protein) after hypoxia stimulus were also attenuated by hypoxic pre-exposure. Moreover, hydrogen peroxide-induced morphologic damage did not appear in the wild-type Wee1-expressing cells. Taken together, our results suggest that Wee1 may have important role in hypoxia-induced pathophysiological situations in endothelial cells.