Background: The conventional measure of sleep fragmentation is via polysomnographic evaluation of sleep architecture. Adults with OSA have disruption in their sleep cycles and spend less time in deep sleep stages. However, there is no available evidence to suggest that this is also true for children and published results have been inconclusive.
View Article and Find Full Text PDFStudy Objectives: The relationship between time-limited eating (TLE) and sleep quality is a topic of growing interest in the field of chronobiology. Data in adult cohorts shows that TLE may improve sleep quality, but this has not been evaluated in adolescents. The aim of this secondary analysis was to (1) examine the impact of 8-hour TLE on sleep parameters in youth with obesity and (2) explore if there was any association between sleep patterns and glycemic profiles.
View Article and Find Full Text PDFPurpose Of Review: This paper reviews how sleep is impacted in patients with Prader-Willi syndrome (PWS), focusing on sleep-related breathing disturbances and excessive daytime sleepiness (EDS).
Recent Findings: Hypothalamic dysfunction may underlie several aspects of the PWS phenotype. Central sleep apnea (CSA) can persist beyond infancy.
Study Objectives: Pulmonary hypertension (PH) is a rare yet serious complication of obstructive sleep apnea (OSA). Echocardiographic screening for PH is recommended in children with severe OSA, but the health care burden of universal screening is high. We sought to determine the prevalence of PH on echocardiogram among children with severe OSA and identify variables associated with a positive PH screen.
View Article and Find Full Text PDFObjectives: To assess sleep positions in children with both Down syndrome (DS) and obstructive sleep apnea (OSA) and determine if there is a preferred sleep position by severity of apnea.
Methods: A single-center retrospective review of patients with both DS and OSA was performed. Caregivers reported sleep position utilized greater than 50% of observed sleep time.
Prader-Willi syndrome (PWS) is an imprinted genetic disorder conferred by loss of paternal gene expression from chromosome 15q11.2-q13. Individuals with PWS have impairments in ventilatory control and are predisposed toward sleep disordered breathing due to a combination of characteristic craniofacial features, obesity, hypotonia, and hypothalamic dysfunction.
View Article and Find Full Text PDFAccurate chromosome segregation depends on precise regulation of mitosis by the spindle checkpoint. This checkpoint monitors the status of kinetochore-microtubule attachment and delays the metaphase to anaphase transition until all kinetochores have formed stable bipolar connections to the mitotic spindle. Components of the spindle checkpoint include the mitotic arrest defective (MAD) genes MAD1-3, and the budding uninhibited by benzimidazole (BUB) genes BUB1 and BUB3.
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