Sleep architecture in children with common phenotype of obstructive sleep apnea

STUDY OBJECTIVES: In children, the effect of the common phenotype of obstructive sleep apnea (OSA) on sleep architecture is not adequately documented. The aim of this study was to evaluate sleep architecture in a pediatric population with the common phenotype of OSA. METHODS: The prospective cross-sectional study included 116 children in the age range of 3 to 8 years with suspected OSA and 51 healthy children. All children underwent standard overnight in-laboratory video polysomnography. Patients with obstructive apnea-hypopnea index ≥ 1, adenotonsillar hypertrophy, a long face, narrow palate or minor malocclusions, and no obesity were defined as a common phenotype. Polysomnographic parameters of sleep architecture and sleep clinical record were statistically analyzed according to OSA and its severity. RESULTS: In total, 94 pediatric patients (59.60% male) received the diagnosis of the common phenotype of OSA (mean age of 5.25 ± 1.39 years). A lower percentage of stage N3 sleep (27.70 ± 3.76% versus 31.02 ± 4.23%; P < .05), a greater percentage of stage N1 sleep (8.40 ± 3.98% versus 2.68 ± 3.02%, P < .01), reduced deep sleep efficiency (46.01 ± 4.98% versus 50.25 ± 3.72%; P < .05) and longer sleep latency (18.40 ± 8.48 minutes versus 9.90 ± 11.55 minutes, P < .01) were found in children with the common phenotype of OSA compared with healthy controls. No significant differences were found in total sleep time, sleep efficiency, and percentage of stage R sleep and stage N2 sleep between groups and in sleep stage distribution and cyclization. CONCLUSIONS: These findings suggest that the most common phenotype of pediatric OSA has a negative effect on the structure of sleep, but other clinical studies are needed to confirm this result

Modelling Duchenne muscular dystrophy in vitro with newly generated, blood cell-derived induced pluripotent stem cell line ORIONi003-A

Here, we present newly derived in vitro model for modeling Duchenne muscular dystrophy. Our new cell line was derived by reprogramming of peripheral blood mononuclear cells (isolated from blood from pediatric patient) with Sendai virus encoding Yamanaka factors. Derived iPS cells are capable to differentiate in vitro into three germ layers as verified by immunocytochemistry. When differentiated in special medium, our iPSc formed spontaneously beating cardiomyocytes. As cardiomyopathy is the main clinical complication in patients with Duchenne muscular dystrophy, the cell line bearing the dystrophin gene mutation might be of interest to the research community