The authors studied to demonstrate the efficacy of custom-made three-dimensional (3D)-printed titanium implants for reconstructing skull defects. From 2013 to 2015, 21 patients (8–62 years old, mean = 28.6-year old; 11 females and 10 males) with skull defects were treated. Total disease duration ranged from 6 to 168 months (mean = 33.6 months). The size of skull defects ranged from 84 × 104 to 154 × 193 mm. Custom-made implants were manufactured by Medyssey Co, Ltd (Jecheon, South Korea) using 3D computed tomography data, Mimics software, and an electron beam melting machine. The team reviewed several different designs and simulated surgery using a 3D skull model. During the operation, the implant was fit to the defect without dead space. Operation times ranged from 85 to 180 minutes (mean = 115.7 minutes). Operative sites healed without any complications except for 1 patient who had red swelling with exudation at the skin defect, which was a skin infection and defect at the center of the scalp flap reoccurring since the initial head injury. This patient underwent reoperation for skin defect revision and replacement of the implant. Twenty-one patients were followed for 6 to 24 months (mean = 14.1 months). The patients were satisfied and had no recurrent wound problems. Head computed tomography after operation showed good fixation of titanium implants and satisfactory skull-shape symmetry. For the reconstruction of skull defects, the use of autologous bone grafts has been the treatment of choice. However, bone use depends on availability, defect size, and donor morbidity. As 3D printing techniques are further advanced, it is becoming possible to manufacture custom-made 3D titanium implants for skull reconstruction.
Summary: Purpose:The purpose of this study is to determine the sensibility of each imaging tool in identifying focal cortical dysplasia (FCD) in children and adolescents with epilepsy and to define the prognostic factors of pediatric and adolescent epilepsy surgery.Methods:We identified 48 children with FCD who underwent resective surgery and analyzed their preoperative data. The results of various anatomic and functional neuroimaging studies were compared for accuracy in locating the lesion. We also investigated clinical factors that affected the outcome of surgical treatment.Key Findings:Brain magnetic resonance imaging (MRI) was able to localize FCD in 30 patients and fluorodeoxyglucose positron emission tomography (FDG‐PET) and/or subtraction ictal single photon emission computed tomography (SPECT) coregistered with MRI provided additional information that helped to define the lesion in 13 patients. When comparing the pathologic results between a mild malformation of cortical development (MCD) and FCD type I and II, we noted a strong tendency for patients with FCD to have MRI abnormalities (p = 0.005). In addition, severe pathologic features (Palmini’s classification, FCD type II) (p = 0.025) showed significant correlation with a better surgical outcome. To define the primary epileptogenic area, various interictal epileptiform discharges and the results of multimodal neuroimaging studies were helpful, and younger age at the time of operation could aid in more favorable surgical outcomes (p = 0.048).Significance:Our study showed a significant relationship between pathologic grade and the detectability of FCD by brain MRI. In addition, early surgery can be justified by showing that advanced neuroimaging studies in children with FCD and even with extensive epileptiform discharges have a higher rate of success.
Folic acid (FA) has traditionally been associated with prevention of neural tube defects; more recent work suggests that it may also be involved in in the prevention of adult onset diseases. As the role of FA in human health and disease expands, it also becomes more critical to understand the mechanisms behind FA action. In this work we examined the hypothesis that folate receptor alpha (FRα) acts as a transcription factor. FRα is a GPI-anchored protein and a component of the caveolae fraction. The work described here shows that FRα translocates to the nucleus, where it binds to cis-regulatory elements at promoter regions of Fgfr4 and Hes1, and regulates their expression. The FRα recognition domain mapped to AT rich regions on the promoters. Until this time FRα has only been considered as a folate transporter, these studies describe a novel role for FRα as a transcription factor.