ObjectiveIn the pediatric population the skull has not yet undergone ossification and it is assumed that the diagnostic rate of skull fractures by simple X-rays are lower than that of adults. It has been recently proposed that the diagnostic rates of skull fractures by 3-dimensional computer tomography (3D-CT) are higher than simple X-rays. The authors therefore attempted to compare the diagnostic rates of pediatric skull fractures by simple X-rays and 3D-CTs with respect to the type of fracture.MethodsOne-hundred patients aged less than 12 years who visited the Emergency Center for cranial injury were subject to simple X-rays and 3D-CTs. The type and location of the fractures were compared and Kappa statistical analysis and the t-test were conducted.ResultsAmong the 100 pediatric patients, 65 were male and 35 were female. The mean age was 50±45 months. 63 patients had simple skull fractures and 22 had complex fractures, and the types of fractures were linear fractures in 74, diastatic fractures 15, depressed fractures in 10, penetrating fracture in 1, and greenstick fractures in 3 patients. Statistical difference was observed for the predictive value of simple skull fractures' diagnostic rate depending on the method for diagnosis. A significant difference of the Kappa value was noted in the diagnosis of depressed skull fractures and diastatic skull fractures.ConclusionIn the majority of pediatric skull fractures, 3D-CT showed superior diagnosis rates compared to simple skull X-rays and therefore 3D-CT is recommended whenever skull fractures are suspected. This is especially true for depressed skull fractures and diastatic skull fractures.

Effective immunosuppression strategies and genetically modified animals have been used to prevent hyperacute and acute xenograft rejection; however, the underlying mechanisms remain unknown. In this study, we evaluated the expression of a comprehensive set of immune system-related genes (89 genes, including five housekeeping genes) in the blood of cynomolgus monkeys (~5 yr old) used as graft recipients, before and after the xenografting of the islets and heart from single and double α-1,3-galactosyltransferase (GalT) knockout (KO) pigs (<6 weeks old). The immunosuppressive regimen included administration of cobra venom factor, anti-thymocyte globulin, rituximab, and anti-CD154 monoclonal antibodies to recipients before and after grafting. Islets were xenografted into the portal vein in type 1 diabetic monkeys, and the heart was xenografted by heterotopic abdominal heart transplantation. Genes from recipient blood were analyzed using RT(2) profiler PCR arrays and the web-based RT(2) profiler PCR array software v.3.5. Recipients treated with immunosuppressive agents without grafting showed significant downregulation of CCL5, CCR4, CCR6, CD4, CD40LG, CXCR3, FASLG, CXCR3, FOXP3, GATA3, IGNG, L10, IL23A, TRAF6, MAPK8, MIF, STAT4, TBX21, TLR3, TLR7, and TYK2 and upregulation of IFNGR1; thus, genes involved in protection against viral and bacterial infection were downregulated, confirming the risk of infection. Notably, C3-level control resulted in xenograft failure within 2 days because of a 7- to 11-fold increase in all xenotransplanted models. Islet grafting using single GalT-KO pigs resulted in upregulation of CXCL10 and MX1, early inflammation, and acute rejection-associated signals at 2 days after xenografting. We observed at least 5-fold upregulation in recipients transplanted with islets grafts from single (MX1) or double (C3, CCR8, IL6, IL13, IRF6, CXCL10, and MX1) GalT-KO pigs after 77 days; single GalT-KO incurred early losses owing to immune attacks. Our results suggest that this novel, simple, non-invasive, and time-efficient procedure (requiring only 1.5 ml blood) for evaluating graft success, minimizing immune rejection, and blocking infection.

Metabolic regulation is critical for the maintenance of pluripotency and the survival of embryonic stem cells (ESCs). The transcription factor Tfcp2l1 has emerged as a key factor for the na€ ıve pluripotency of ESCs. Here, we report an unexpected role of Tfcp2l1 in metabolic regulation in ESCs-promoting the survival of ESCs through regulating fatty acid oxidation (FAO) under metabolic stress. Tfcp2l1 directly activates many metabolic genes in ESCs. Deletion of Tfcp2l1 leads to an FAO defect associated with upregulation of glucose uptake, the TCA cycle, and glutamine catabolism. Mechanistically, Tfcp2l1 activates FAO by inducing Cpt1a, a ratelimiting enzyme transporting free fatty acids into the mitochondria. ESCs with defective FAO are sensitive to cell death induced by glycolysis inhibition and glutamine deprivation. Moreover, the Tfcp2l1-Cpt1a-FAO axis promotes the survival of quiescent ESCs and diapause-like blastocysts induced by mTOR inhibition. Thus, our results reveal how ESCs orchestrate pluripotent and metabolic programs to ensure their survival in response to metabolic stress.