Data were collected at birth by maternal interview and from medical records. Follow-up data were obtained from 439 and 418 children at 3.5 and 7 years of age, respectively. Amnionitis was identified in 145 placentas (14.3%), with maternal reaction in 97.2% and fetal reaction in 48.3%. In multivariable analysis any amnionitis was find more significantly associated with a time from membrane rupture to delivery of 6 to 12 hours, but not with times beyond 12 hours, a duration of total labor exceeding 12 hours, ethnicity (incidences ranging from 8.8% in Indians to 23.5% in Chinese), male infant gender, and anaesthesia during

labor, and amnionitis was negatively associated with induction of labor. No associations were found with later allergic disease, atopy, or intelligence quotients. This high incidence of histologic amnionitis at term is similar to historical estimates, despite large reductions in time-related risk factors during labor. Significant ethnic variations contribute to the high incidence and are unexplained, but variation in genetic polymorphisms

for susceptibility factors is a possibility. “”Silent”" histologic amnionitis is a frequent cause of fetal immune activation with potential effects in later life.”
“Research in animal models implicates the retrotrapezoid nucleus (RTN) as a critical central chemoreceptor located in the brain stem. In rodents, RTN neurons co-express the tachykinin receptor NK1R INCB018424 cost and the transcription factor PHOX2B. In humans, PHOX2B mutations, which expand a polyalanine APR-246 in vivo tract in the protein, cause congenital central hypoventilation syndrome. Mice with analogous Phox2B mutations model this phenotype and lack PHOX2B

immunoreactivity in their RTNs. We evaluated PHOX2B immunoreactivity in sections of the caudal pons and medulla of 17 human fetuses and infants. The transcription factor was detected in brain stem nuclei that correspond to established sites of murine PHOX2B expression, including the RTN. The putative human RTN is located ventral to the facial nucleus and lateral to the superior olivary nucleus at the level of the pontomedullary junction.”
“Background and aims: Enteroendocrine cells sense gut luminal contents, and orchestrate digestive physiology whilst contributing to mucosal homeostasis and innate immunity. The terminal ileum is the key site of EEC expression but detailed assessment of their subtypes, lineage transcription factors and expression products has not been undertaken in terminal ileal Crohn’s disease. Recent Crohn’s disease gene wide association studies have linked the neuroendocrine transcription factor Phox2b; while autoantibodies to an enteroendocrine protein, ubiquitination protein 4a, have been identified as a disease behaviour biomarker.