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Masa, Juan F.; Duran-Cantolla, Joaquin; Capote, Francisco; Cabello, Marta; Abad, Jorge; Garcia-Rio, Francisco; Ferrer, Antoni; Fortuna, Ana M.; Gonzalez-Mangado, Nicolas; de la Peña, Monica; Aizpuru, Felipe; Barbe, Ferran; Montserrat, Jose M.; , ; Larrateguy, Luis D.;
Spilsbury, James C.; Storfer-Isser, Amy; Rosen, Carol L.; Redline, Susan
doi: 10.5665/sleep.4318pmid: 25325456
AbstractStudy Objective:To study the incidence, remission, and prediction of obstructive sleep apnea (OSA) from middle childhood to late adolescence.Design:Longitudinal analysis.Setting:The Cleveland Children's Sleep and Health Study, an ethnically mixed, urban, community-based cohort, followed 8 y.Participants:There were 490 participants with overnight polysomnography data available at ages 8–11 and 16–19 y.Measurements and Results:Baseline participant characteristics and health history were ascertained from parent report and US census data. OSA was defined as an obstructive apnea- hypopnea index ≥ 5 or an obstructive apnea index ≥ 1. OSA prevalence was approximately 4% at each examination, but OSA largely did not persist from middle childhood to late adolescence. Habitual snoring and obesity predicted OSA in cross-sectional analyses at each time point. Residence in a disadvantaged neighborhood, African-American race, and premature birth also predicted OSA in middle childhood, whereas male sex, high body mass index, and history of tonsillectomy or adenoidectomy were risk factors among adolescents. Obesity, but not habitual snoring, in middle childhood predicted adolescent OSA.Conclusions:Because OSA in middle childhood usually remitted by adolescence and most adolescent cases were incident cases, criteria other than concern alone over OSA persistence or incidence should be used when making treatment decisions for pediatric OSA. Moreover, OSA's distinct risk factors at each time point underscore the need for alternative risk-factor assessments across pediatric ages. The greater importance of middle childhood obesity compared to snoring in predicting adolescent OSA provides support for screening, preventing, and treating obesity in childhood.
Hakim, Fahed; Wang, Yang; Carreras, Alba; Hirotsu, Camila; Zhang, Jing; Peris, Eduard; Gozal, David
doi: 10.5665/sleep.4320pmid: 25325461
AbstractBackground:Sleep fragmentation (SF) is highly prevalent and may constitute an important contributing factor to excessive weight gain and the metabolic syndrome. Increased endoplasmic reticulum (ER) stress and activation of the unfolded protein response (UPR) leading to the attenuation of leptin receptor signaling in the hypothalamus leads to obesity and metabolic dysfunction.Methods:Mice were exposed to SF and sleep control (SC) for varying periods of time during which ingestive behaviors were monitored. UPR pathways and leptin receptor signaling were assessed in hypothalami. To further examine the mechanistic role of ER stress, changes in leptin receptor (ObR) signaling were also examined in wild-type mice treated with the ER chaperone tauroursodeoxycholic acid (TUDCA), as well as in CHOP −/+ transgenic mice.Results:Fragmented sleep in male mice induced increased food intake starting day 3 and thereafter, which was preceded by increases in ER stress and activation of all three UPR pathways in the hypothalamus. Although ObR expression was unchanged, signal transducer and activator of transcription 3 (STAT3) phosphorylation was decreased, suggesting reduced ObR signaling. Unchanged suppressor of cytokine signaling-3 (SOCS3) expression and increases in protein-tyrosine phosphatase 1B (PTP1B) expression and activity emerged with SF, along with reduced p-STAT3 responses to exogenous leptin. SF-induced effects were reversed following TUDCA treatment and were absent in CHOP −/+ mice.Conclusions:Sleep fragmentation (SF) induces hyperphagic behaviors and reduced leptin signaling in hypothalamus that are mediated by activation of endoplasmic reticulum (ER) stress, and ultimately lead to increased PTP1B activity. ER stress pathways are therefore potentially implicated in SF-induced weight gain and metabolic dysfunction, and may represent a viable therapeutic target.
doi: 10.5665/sleep.4322pmid: 25325457
AbstractStudy Objectives:D. melanogaster is an excellent animal model to study how the circadian (≅ 24-h) timing system and sleep regulate daily wake-sleep cycles. Splicing of a temperature-sensitive 3'-terminal intron (termed dmpi8) from the circadian clock gene period (per) regulates the distribution of daily activity in Drosophila. The role of dmpi8 splicing on daily behavior was further evaluated by analyzing sleep.Design:Transgenic flies of the same genetic background but expressing either a wild-type recombinant per gene or one where the efficiency of dmpi8 splicing was increased were exposed to different temperatures in daily light-dark cycles and sleep parameters measured. In addition, transgenic flies were briefly exposed to a variety of sensory-mediated stimuli to measure arousal responses.Results:Surprisingly, we show that the effect of dmpi8 splicing on daytime activity levels does not involve a circadian role for per but is linked to adjustments in sensory-dependent arousal and sleep behavior. Genetically altered flies with high dmpi8 splicing efficiency remain aroused longer following short treatments with light and non-photic cues such as mechanical stimulation.Conclusions:We propose that the thermal regulation of dmpi8 splicing acts as a temperature-calibrated rheostat in a novel arousal mechanism, so that on warm days the inefficient splicing of the dmpi8 intron triggers an increase in quiescence by decreasing sensory-mediated arousal, thus ensuring flies minimize being active during the hot midday sun despite the presence of light in the environment, which is usually a strong arousal cue for diurnal animals.
Jordan, Amy S.; Cori, Jennifer M.; Dawson, Andrew; Nicholas, Christian L.; O'Donoghue, Fergal J.; Catcheside, Peter G.; Eckert, Danny J.; McEvoy, R. Doug; Trinder, John
doi: 10.5665/sleep.4324pmid: 25325511
Churchill, Shervin S.; Kieckhefer, Gail M.; Bjornson, Kristie F.; Herting, Jerald R.
doi: 10.5665/sleep.4326pmid: 25325444
AbstractObjectives:The goal of this study was to describe sleep patterns and accomplishment of daily life habits in children with Down syndrome (DS) and to investigate the relationship between subjective indicators of sleep disturbance with functional outcomes in daily life.Design:Cross-sectional study with an Internet sampleSetting:Online survey filled out at homeParticipants:110 parents of children with DS and 29 parents of children with typical development (TD), age 5 to 18 years.Interventions:N/A.Measurements and Results:Children's Sleep Habits Questionnaire was employed to collect information about sleep disturbances in 8 domains (subscales) and a total score. The Life Habits questionnaire (Life-H) sampled information about daily life habits in 11 domains. Multivariable regression modeling was used to assess the associations between sleep disturbances and the accomplishment of daily life habits. Sleep disordered breathing (SDB) was a significant explanatory factor in 10 of 11 daily life habits and the total Life-H score. Sleep anxiety and parasomnias significantly influenced the accomplishment of life habits in children with DS as compared to children with typical development. When evaluated in multivariable models in conjunction with the other 7 domains of sleep disturbances, SDB was the most dominant explanatory factor for accomplishment of life habits.Conclusions:Sleep disturbances are negatively related to accomplishment of daily life functions. Prevention and treatment of sleep problems, particularly sleep disordered breathing, in children with Down syndrome may lead to enhanced accomplishment of daily life habits and activities.
Garrity, Abigail G.; Botta, Simhadri; Lazar, Stephanie B.; Swor, Erin; Vanini, Giancarlo; Baghdoyan, Helen A.; Lydic, Ralph
doi: 10.5665/sleep.4328pmid: 25325438
AbstractStudy Objectives:Dexmedetomidine is used clinically to induce states of sedation that have been described as homologous to nonrapid eye movement (NREM) sleep. A better understanding of the similarities and differences between NREM sleep and dexmedetomidine-induced sedation is essential for efforts to clarify the relationship between these two states. This study tested the hypothesis that dexmedetomidine-induced sedation is homologous to sleep.Design:This study used between-groups and within-groups designs.Setting:University of Michigan.Participants:Adult male Sprague Dawley rats (n = 40).Interventions:Independent variables were administration of dexmedetomidine and saline or Ringer's solution (control). Dependent variables included time spent in states of wakefulness, sleep, and sedation, electroencephalographic (EEG) power, adenosine levels in the substantia innominata (SI), and activation of pCREB and c-Fos in sleep related forebrain regions.Measurements and Results:Dexmedetomidine significantly decreased time spent in wakefulness (-49%), increased duration of sedation (1995%), increased EEG delta power (546%), and eliminated the rapid eye movement (REM) phase of sleep for 16 h. Sedation was followed by a rebound increase in NREM and REM sleep. Systemically administered dexmedetomidine significantly decreased (-39%) SI adenosine levels. Dialysis delivery of dexmedetomidine into SI did not decrease adenosine levels. Systemic delivery of dexmedetomidine did not alter c-Fos or pCREB expression in the horizontal diagonal band, or ventrolateral, median, and medial preoptic areas of the hypothalamus.Conclusions:Dexmedetomidine significantly altered normal sleep phenotypes, and the dexmedetomidine-induced state did not compensate for sleep need. Thus, in the Sprague Dawley rat, dexmedetomidine-induced sedation is characterized by behavioral, electrographic, and immunohistochemical phenotypes that are distinctly different from similar measures obtained during sleep.
Showing 1 to 10 of 20 Articles
doi: 10.5665/sleep.4316pmid: 25325508
AbstractIntroduction:Unlike other prevalent diseases, obstructive sleep apnea (OSA) has no simple tool for diagnosis and therapeutic decision-making in primary healthcare. Home single-channel nasal pressure (HNP) may be an alternative to polysomnography for diagnosis but its use in therapeutic decisions has yet to be explored.Objectives:To ascertain whether an automatically scored HNP apnea-hypopnea index (AHI), used alone to recommend continuous positive airway pressure (CPAP) treatment, agrees with decisions made by a specialist using polysomnography and several clinical variables.Methods:Patients referred by primary care physicians for OSA suspicion underwent randomized polysomnography and HNP. We analyzed the total sample and both more and less symptomatic subgroups for Bland and Altman plots to explore AHI agreement; receiver operating characteristic curves to establish area under the curve (AUC) measurements for CPAP recommendation; and therapeutic decision efficacy for several HNP AHI cutoff points.Results:Of the 787 randomized patients, 35 (4%) were lost, 378 (48%) formed the more symptomatic and 374 (48%) the less symptomatic subgroups. AHI bias and agreement limits were 5.8 ± 39.6 for the total sample, 5.3 ± 38.7 for the more symptomatic, and 6 ± 40.2 for the less symptomatic subgroups. The AUC were 0.826 for the total sample, 0.903 for the more symptomatic, and 0.772 for the less symptomatic subgroups. In the more symptomatic subgroup, 70% of patients could be correctly treated with CPAP.Conclusion:Automatic home single-channel nasal pressure scoring can correctly recommend CPAP treatment in most of more symptomatic patients with OSA suspicion. Our results suggest that this device may be an interesting tool in initial OSA management for primary care physicians, although future studies in a primary care setting are necessary.Clinical Trials Information:Clinicaltrial.gov identifier: NCT01347398.
AbstractStudy Objectives:To compare changes in end-tidal CO2, genioglossus muscle activity and upper airway resistance following tone-induced arousal and the return to sleep in healthy individuals with small and large ventilatory responses to arousal.Design:Observational study.Setting:Two sleep physiology laboratories.Patients or Participants:35 men and 25 women with no medical or sleep disorders.Interventions:Auditory tones to induce 3-s to 15-s cortical arousals from sleep.Measurements and Results:During arousal from sleep, subjects with large ventilatory responses to arousal had higher ventilation (by analytical design) and tidal volume, and more marked reductions in the partial pressure of end-tidal CO2 compared to subjects with small ventilatory responses to arousal. However, following the return to sleep, ventilation, genioglossus muscle activity, and upper airway resistance did not differ between high and low ventilatory response groups (Breath 1 on return to sleep: ventilation 6.7 ± 0.4 and 5.5 ± 0.3 L/min, peak genioglossus activity 3.4% ± 1.0% and 4.8% ± 1.0% maximum, upper airway resistance 4.7 ± 0.7 and 5.5 ± 1.0 cm H2O/L/s, respectively). Furthermore, dilator muscle activity did not fall below the pre-arousal sleeping level and upper airway resistance did not rise above the pre-arousal sleeping level in either group for 10 breaths following the return to sleep.Conclusions:Regardless of the magnitude of the ventilatory response to arousal from sleep and subsequent reduction in PETCO2, healthy individuals did not develop reduced dilator muscle activity nor increased upper airway resistance, indicative of partial airway collapse, on the return to sleep. These findings challenge the commonly stated notion that arousals predispose to upper airway obstruction.