Background: The Ironman 70.3 race is also called a half Ironman, and consists of 1.9 km of swimming, 90.1 km of cycling, and 21.1 km of running. The authors provide practical insights that may be useful for medical support in future events by summarizing the process and results of on-scene medical care. Methods: The medical post was established at the transition area between the cycling and running courses, which was close to the finish line, and staffed with the headquarters team comprised of an emergency physician, an EMT, two nurses, and an ambulance with a driver. The other five ambulances were located throughout the course. The medical staff identified participants according to their numbers when providing medical support, and described complaints, treatment provided, and disposition. When treating non-participants, gender and age were recorded instead of numbers. The treatment records were analyzed after the race. Results: The medical team treated a total of 187 participants. One suffered cramps in the calf muscles during the swimming part of the course. Nineteen were treated for injuries suffered during the cycling race. A total of 159 were treated for injuries on the running course. Five casualties, all of which occurred during the cycling race, required transport to hospital. Conclusions: Medical directors preparing medical support during a triathlon event should expect severe injuries in the cycling course. In hot climates, staff may also suffer from heat injuries as well as runners, and proper attention should be paid to these risks.

ObjectivesMethyl-CpG binding protein 2 (MeCP2) is a ubiquitous epigenetic factor that represses gene expression by modifying chromatin. Mutations in the MeCP2 gene cause Rett syndrome, a progressive neurodevelopmental disorder. Recent studies also have shown that MeCP2 plays a role in carcinogenesis. Specifically, functional ablation of MeCP2 suppresses cell growth and leads to the proliferation of cancer cells. However, MeCP2's function in adult tissues remains poorly understood. We utilized a weight matrix-based comparison software to identify transcription factor binding site (TFBS) of MeCP2-regulated genes, which were recognized by cDNA microarray analysis.MethodsMeCP2 expression was silenced using annealed siRNA in HEK293 cells, and then a cDNA microarray analysis was performed. Functional analysis was carried out, and transcriptional levels in target genes regulated by MeCP2 were investigated. TFBS analysis was done within genes selected by the cDNA microarray analysis, using a weight matrix-based program and the TRANSFAC 6.0 database.ResultsAmong the differentially expressed genes with a change in expression greater than two-fold, 189 genes were up-regulated and 91 genes were down-regulated. Genes related to apoptosis and cell proliferation (JUN, FOSL2, CYR61, SKIL, ATF3, BMABI, BMPR2, RERE, and FALZ) were highly up-regulated. Genes with anti-apoptotic and anti-proliferative functions (HNRPA0, HIS1, and FOXC1) were down-regulated. Using TFBS analysis within putative promoters of novel candidate target genes of MeCP2, disease-related transcription factors were identified.ConclusionsThe present results provide insights into the new target genes regulated by MeCP2 under epigenetic control. This information will be valuable for further studies aimed at clarifying the pathogenesis of Rett syndrome and neoplastic diseases.