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Sökning: L773:0161 8105 OR L773:1550 9109

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  • Akerstedt, Torbjörn, et al. (författare)
  • Sleep homeostasis during repeated sleep restriction and recovery : support from EEG dynamics.
  • 2009
  • Ingår i: Sleep. - 0161-8105 .- 1550-9109. ; 32:2, s. 217-22
  • Tidskriftsartikel (refereegranskat)abstract
    • STUDY OBJECTIVES: Sleep reduction normally causes a homeostatic response during subsequent recovery sleep, but this does not seem to be true for repeated partial sleep loss. The aim of the present study was to test the response to repeated partial sleep loss through detailed focus on spectral data and parts of sleep. DESIGN: The experiment involved 4 h of sleep across 5 days in the laboratory (partial sleep deprivation [PSD]), followed by 3 days of recovery sleep. PSD was achieved through a delayed bedtime. Nine individuals participated. To avoid "laboratory monotony," subjects were permitted to leave the lab for a few hours each day. MEASUREMENTS AND RESULTS: All sleep stages and the latencies to sleep and slow wave sleep (SWS) showed a significant reduction during PSD. However, SWS and TST (total sleep time) during the first half of sleep increased gradually across days with PSD. During the first recovery sleep, SWS was significantly increased, while stage 1 and latency to stage 3 were reduced. All were back to baseline on the second night of recovery sleep. Summed spectral power during the first 3.8 h of sleep showed a gradual and robust increase (50% above baseline) in the range 1.25-7.25 Hz across days with PSD up to first recovery sleep and then returned to baseline. CONCLUSIONS: SWS and summed power density in a broad low-frequency band respond to repeated partial sleep deprivation in a dose-response fashion during the first 4 h sleep, apparently reflecting a robust and stable homeostatic response to sleep loss.
  • Araghi, Marzieh Hosseini, et al. (författare)
  • Effectiveness of Lifestyle Interventions on Obstructive Sleep Apnea (OSA) : Systematic Review and Meta-Analysis
  • 2013
  • Ingår i: Sleep. - : Oxford University Press. - 0161-8105 .- 1550-9109. ; 36:10, s. 1553-1562
  • Forskningsöversikt (refereegranskat)abstract
    • Background: Obstructive sleep apnea (OSA) is a common sleep disorder associated with several adverse health outcomes. Given the close association between OSA and obesity, lifestyle and dietary interventions are commonly recommended to patients, but the evidence for their impact on OSA has not been systematically examined. Objectives: To conduct a systematic review and meta-analysis to assess the impact of weight loss through diet and physical activity on measures of OSA: apnea-hypopnea index (AHI) and oxygen desaturation index of 4% (ODI4). Methods: A systematic search was performed to identify publications using Medline (1948-2011 week 40), EMBASE (from 1988-2011 week 40), and CINAHL (from 1982-2011 week 40). The inverse variance method was used to weight studies and the random effects model was used to analyze data. Results: Seven randomized controlled trials (519 participants) showed that weight reduction programs were associated with a decrease in AHI (-6.04 events/h [95% confidence interval -11.18, -0.90]) with substantial heterogeneity between studies (I-2 = 86%). Nine uncontrolled before-after studies (250 participants) showed a significant decrease in AHI (-12.26 events/h [95% confidence interval -18.51, -6.02]). Four uncontrolled before-after studies (97 participants) with ODI4 as outcome also showed a significant decrease in ODI4 (-18.91 episodes/h [95% confidence interval -23.40, -14.43]). Conclusions: Published evidence suggests that weight loss through lifestyle and dietary interventions results in improvements in obstructive sleep apnea parameters, but is insufficient to normalize them. The changes in obstructive sleep apnea parameters could, however, be clinically relevant in some patients by reducing obstructive sleep apnea severity. These promising preliminary results need confirmation through larger randomized studies including more intensive weight loss approaches.
  • Axelsson, John, et al. (författare)
  • Sleepiness as motivation : a potential mechanism for how sleep deprivation affects behavior
  • 2020
  • Ingår i: Sleep. - 0161-8105 .- 1550-9109. ; 43:6
  • Tidskriftsartikel (refereegranskat)abstract
    • STUDY OBJECTIVES: To determine how sleepiness and sleep deprivation drive the motivation to engage in different behaviors.METHODS: We studied the sleepiness of 123 participants who had been randomized to sleep deprivation or normal sleep, and their willingness to engage in a range of everyday behaviors.RESULTS: Self-reported sleepiness was a strong predictor of the motivation to engage in sleep-preparatory behaviors such as shutting one's eyes (OR=2.78, 95%CI: 2.19-3.52 for each step up on the Karolinska Sleepiness Scale) and resting (OR=3.20, CI: 2.46-4.16). Sleepiness was also related to the desire to be cared for by a loved one (OR=1.49, CI: 1.22-1.82), and preparedness to utilize monetary and energy resources to get to sleep. Conversely, increased sleepiness was associated with a decreased motivation for social and physical activities (e.g., be with friends OR=0.71, CI: 0.61-0.82; exercise OR=0.65, CI: 0.56-0.76). Sleep deprivation had similar effects as sleepiness on these behaviors. Neither sleepiness nor sleep deprivation had strong associations with hunger, thirst, or food preferences.CONCLUSIONS: Our findings indicate that sleepiness is a dynamic motivational drive that promotes sleep-preparatory behaviors and competes with other drives and desired outcomes. Consequently, sleepiness may be a central mechanism by which impaired alertness, e.g., due to insufficient sleep, contributes to poor quality of life and adverse health. We propose that sleepiness helps organize behaviors toward the specific goal of assuring sufficient sleep, in competition with other needs and incentives. A theoretical framework on sleepiness and its behavioral consequences are likely to improve our understanding of several disease mechanisms.
  • Baldanzi, Gabriel, et al. (författare)
  • Evening chronotype is associated with elevated biomarkers of cardiometabolic risk in the EpiHealth cohort: a cross-sectional study
  • 2021
  • Ingår i: Sleep. - 0161-8105 .- 1550-9109.
  • Tidskriftsartikel (refereegranskat)abstract
    • Study objectives: Individuals with evening chronotype have a higher risk of cardiovascular and metabolic disorders, although the underlying mechanisms are not well understood. In a population- based cohort, we aimed to investigate the association between chronotype and 242 circulating proteins from three panels of established or candidate biomarkers of cardiometabolic processes. Methods: In 2,471 participants (49.7% men, mean age 61.2±8.4 SD years) from the EpiHealth cohort, circulating proteins were analyzed with a multiplex proximity extension technique. Participants self- reported their chronotype on a five-level scale from extreme morning to extreme evening chronotype. With the intermediate chronotype set as the reference, each protein was added as the dependent variable in a series of linear regression models adjusted for confounders. Next, the chronotype coefficients were jointly tested and the resulting p-values adjusted for multiple testing using false discovery rate (5%). For the associations identified, we then analyzed the marginal effect of each chronotype category. Results: We identified 17 proteins associated with chronotype. Evening chronotype was positively associated with proteins previously linked to insulin resistance and cardiovascular risk, namely retinoic acid receptor protein 2, fatty acid-binding protein adipocyte, tissue-type plasminogen activator, and plasminogen activator inhibitor 1 (PAI-1). Additionally, PAI-1 was inversely associated with the extreme morning chronotype. Conclusions: In this population-based study, proteins previously related with cardiometabolic risk were elevated in the evening chronotypes. These results may guide future research in the relation between chronotype and cardiometabolic disorders. 
  • Benedict, Christian, et al. (författare)
  • Acute sleep deprivation increases serum levels of neuron-specific enolase (NSE) and S100 calcium binding protein B (S-100B) in healthy young men.
  • 2014
  • Ingår i: Sleep. - 1550-9109 .- 0161-8105. ; 37:1, s. 195-8
  • Tidskriftsartikel (refereegranskat)abstract
    • To investigate whether total sleep deprivation (TSD) affects circulating concentrations of neuron-specific enolase (NSE) and S100 calcium binding protein B (S-100B) in humans. These factors are usually found in the cytoplasm of neurons and glia cells. Increasing concentrations of these factors in blood may be therefore indicative for either neuronal damage, impaired blood brain barrier function, or both. In addition, amyloid β (Aβ) peptides 1-42 and 1-40 were measured in plasma to calculate their ratio. A reduced plasma ratio of Aβ peptides 1-42 to 1-40 is considered an indirect measure of increased deposition of Aβ 1-42 peptide in the brain.
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