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Journal articles on the topic 'Sleep markers'

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Author: Grafiati
Published: 10 December 2022
Last updated: 28 January 2023

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1

Rector, David M., Jennifer L. Schei, Hans P. A. Van Dongen, Gregory Belenky, and James M. Krueger. "Physiological markers of local sleep." European Journal of Neuroscience 29, no. 9 (May 2009): 1771–78. http://dx.doi.org/10.1111/j.1460-9568.2009.06717.x.

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2

Martínez-Rodríguez, Jose E., and Joan Santamaria. "CSF markers in sleep neurobiology." Clinica Chimica Acta 362, no. 1-2 (December 2005): 12–25. http://dx.doi.org/10.1016/j.cccn.2005.05.014.

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3

Orr, William C., Joe A. Othman, and O. H. Rundell. "Genetic Markers in Familial Narcolepsy." Sleep 14, no. 3 (May 1991): 270–71. http://dx.doi.org/10.1093/sleep/14.3.270.

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4

Dennis, Jeff A., Ahmad Alazzeh, Ann Marie Kumfer, Rebecca McDonald-Thomas, and Alan N. Peiris. "The Association of Unreported Sleep Disturbances and Systemic Inflammation: Findings from the 2005-2008 NHANES." Sleep Disorders 2018 (October 9, 2018): 1–8. http://dx.doi.org/10.1155/2018/5987064.

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Background/Objective. Sleep apnea is associated with elevated inflammatory markers. A subgroup of patients never report sleep disturbances to their physician. The inflammatory status of this subgroup is not known. The present study aims to evaluate two inflammatory markers, C-reactive protein (CRP) and red cell distribution width (RDW), in those with unreported sleep disturbances and compares these findings to those with and without reported sleep disorders. We also investigate the utility of RDW as an inflammatory marker in sleep disorders. Methods. Sample includes 9,901 noninstitutionalized, civilian, nonpregnant adults from the 2005-2008 National Health and Nutrition Examination Survey, a nationally representative, cross-sectional U.S. study. Sleep questionnaire and laboratory data were used to compare inflammatory markers (CRP and RDW) in five subgroups of individuals: reporting physician-diagnosed sleep apnea, reporting another physician-diagnosed sleep disorder, reported sleep disturbance to physician with no resulting diagnosis, unreported sleep disturbance (poor sleep quality not reported to physician), and no diagnosed sleep disorder or sleep disturbance. Results. Individuals with unreported sleep disturbance had significantly higher odds of elevated RDW (>13.6%) when compared to those without a sleep disturbance in adjusted models (OR=1.33). Those with unreported sleep disturbance had significantly higher odds of elevated CRP levels (>1 mg/L) than those without sleep disturbances (OR 1.34), although the association was not significant when adjusted for obesity and other controls. Conclusion. Self-identified unreported sleep disturbances are associated with significantly higher odds of elevated RDW than those without sleep disturbances. RDW may serve as a valuable indicator in identifying individuals at higher risk for sleep apnea and other sleep disorders.
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Hirsch, Sophie, Jane Gaultney, and Patricia Crane. "018 The Role of Inflammatory Markers in Sleep in Individuals Post-Myocardial Infarction." Sleep 44, Supplement_2 (May 1, 2021): A9. http://dx.doi.org/10.1093/sleep/zsab072.017.

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Abstract Introduction Despite positive secondary prevention strategies post myocardial infarction (MI), including statin use and lifestyle changes, 32% of the annual MIs are recurrent (MIR). As coronary heart disease is related to atherosclerosis, a chronic inflammatory process, and sleep is associated with cardiovascular disease and innate immunity, understanding the role of sleep and inflammation and MIR is important in developing interventions to improve sleep, reduce inflammation, and delay or prevent MIR. This study aimed to explore the role of sleep quality and inflammatory markers on MIRs. Methods We conducted a secondary analysis of cross-sectional data of individuals (N=156) having at least one or more MIs within the last 3 to 7 years. Using the hypothalamus-pituitary-adrenal axis model (Irwin, 2019), we tested sleep quality (Pittsburgh Sleep Quality Index [PSQI]) predicting MIR, using inflammatory markers (hs C-Reactor Protein [CRP], Interleukin-1ß [IL-1ß] and Tumor Necrosis Factor alpha [TNFα]) as the simultaneous indirect paths. Race, sex and body mass index (BMI) were also examined using moderated mediation. Results The sample ranged in age from 34 to 92 (M = 65.37, SD = 12.13), BMI averaged 31.11 (SD = 7.34), and was comprised of mostly male (57.1%) and White adults (67.9%). PSQI predicted only IL-1ß (ß= .02; p < .01). IL-1ß predicted MIR (ß = .80, p = .05). The direct effect of PSQI to MIR was not significant (p =.12), the indirect path via IL-1ß was. This relationship was not moderated by race, sex, nor BMI. Conclusion IL-1ß is an inflammatory marker elevated after acute MI which does not reflect our selected sample. Inflammation may be an important marker of risk for MIR in those with poor sleep quality. Future studies should examine other markers of inflammation and sleep in those with MIR. Support (if any):
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6

Mendlewicz, Julien, I. Schweitzer, N. Biddle, G. Szmukler, and B. M. Davies. "SLEEP DEPRIVATION, DIETING, AND DEPRESSION MARKERS." Lancet 329, no. 8524 (January 1987): 105–6. http://dx.doi.org/10.1016/s0140-6736(87)91945-3.

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Mullen, PaulE, and ChristopherR Linsell. "SLEEP DEPRIVATION, DIETING, AND DEPRESSION MARKERS." Lancet 329, no. 8528 (February 1987): 323. http://dx.doi.org/10.1016/s0140-6736(87)92043-5.

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8

Goel, Namni. "Genetic Markers of Sleep and Sleepiness." Sleep Medicine Clinics 12, no. 3 (September 2017): 289–99. http://dx.doi.org/10.1016/j.jsmc.2017.03.005.

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9

Wang, Lei, Paul Y. Kim, David E. McCarty, Clifton Frilot, Andrew L. Chesson, Simona Carrubba, and Andrew A. Marino. "EEG recurrence markers and sleep quality." Journal of the Neurological Sciences 331, no. 1-2 (August 2013): 26–30. http://dx.doi.org/10.1016/j.jns.2013.04.019.

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10

Kaufmann, Christopher, and Katie Stone. "INTERACTIONS BETWEEN SLEEP AND BIOLOGICAL MARKERS OF AGING." Innovation in Aging 6, Supplement_1 (November 1, 2022): 363. http://dx.doi.org/10.1093/geroni/igac059.1435.

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Abstract There is well documented evidence that sleep architecture and circadian patterns change as people age in part due to accumulation of comorbidities, polypharmacy, and other factors inherent to the aging process. While a number of studies have examined sleep in the context of these factors, recent advances in the assessment of biological aging (including epigenetic age, metabolomics, and measurement of inflammatory biomarkers) have made it possible to identify potential mechanisms by which sleep impacts the aging course. In this symposium, we will highlight research that investigates the link between sleep disturbances and biological factors in order to identify whether sleep could be a modifiable risk factor for accelerated aging. Our first presentation will examine the association between insomnia symptoms and short sleep duration with epigenetic age acceleration using data from the Health and Retirement Study. Second, we will describe whether objectively measured sleep characteristics are associated with a number of metabolomic markers of aging. The third presentation will center around the extent to which social disparities in presence of inflammatory biomarkers may be mediated by sleep quality. Finally, we will examine how daytime sleepiness may be associated with longitudinal BMI trajectories. These presentations will, as a whole, highlight the importance of sleep as a contributor to healthy aging and longevity, and inform the development of interventional approaches targeting biological mechanisms to promote successful aging more broadly.
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Chiem, Emily, Kathleen O'Hora, Vardui Grigoryan, Carolyn Amir, Michael Irwin, Jessica Chiang, and Carrie Bearden. "0495 Sleep Disturbance Features Differentially Influence Inflammatory Markers in Adolescents." Sleep 45, Supplement_1 (May 25, 2022): A219—A220. http://dx.doi.org/10.1093/sleep/zsac079.492.

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Abstract Introduction Sleep disruption has profound effects on immune function. Many adolescents do not get adequate amounts of sleep each night, and chronic sleep disturbance has been associated with increased risk of several inflammatory diseases. However, the relationship between sleep disturbances and inflammation during adolescence is not well understood. In this study, we examined the relationship between specific features of sleep disruption and cytokine levels in adolescents. Methods A total of 88 adolescents (18.36 ± 0.51 years, 56.8% female) completed the Pittsburgh Sleep Quality Index (PSQI), a self-reported questionnaire used to assess subjective sleep quality over a 1-month time period. Blood plasma samples were obtained for each participant at the same timepoint to measure levels of pro-inflammatory cytokines (Interleukin (IL)-6, IL-8, tumor-necrosis factor (TNF)-alpha, and interferon (IFN)-gamma), anti-inflammatory cytokine (IL-10), and C-reactive protein (CRP). Samples were assayed using a Meso Scale Discovery multiplex immunoassay. Linear regression models were used to test the effect of PSQI sleep latency, duration, efficiency, quality, disturbance, and total score on each cytokine level, while covarying for sex and body mass index. We corrected for multiple comparisons using a False Discovery Rate (FDR) correction. Results Overall, disruption in sleep was associated with distinct cytokine differences. Worse sleep, reflected by the PSQI total score and greater sleep disturbance, was associated with lower IL-6 levels (p=0.013, p=0.015, respectively), however theses associations were attenuated to a trend after FDR correction (q=0.083, q=0.092, respectively). Longer sleep latency was also associated with lower IL-6 (p=0.028), and IFN (p=0.016) levels, however these effects were also attenuated after FDR correction (q=0.138, q=0.094, respectively). Reduced sleep efficiency was associated with higher TNF (q=0.046) and CRP (q=0.021) levels. Conclusion Our findings show that different components of sleep disruption have varying effects on cytokine release, resulting in an overall blunted immune response. This underscores the significant impact of sleep disturbances on perturbing immune function during this critical developmental period. Support (If Any)
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12

Janackova, Sona, and Emilia Sforza. "Neurobiology of Sleep Fragmentation: Cortical and Autonomic Markers of Sleep Disorders." Current Pharmaceutical Design 14, no. 32 (November 1, 2008): 3474–80. http://dx.doi.org/10.2174/138161208786549335.

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13

Mendlewicz, J. "Sleep-related chronobiological markers of affective illness." International Journal of Psychophysiology 10, no. 3 (January 1991): 245–52. http://dx.doi.org/10.1016/0167-8760(91)90035-v.

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14

Lévy, Patrick, and Jean-Louis Pépin. "Sleep fragmentation: clinical usefulness of autonomic markers." Sleep Medicine 4, no. 6 (November 2003): 489–91. http://dx.doi.org/10.1016/j.sleep.2003.07.003.

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15

Reddy, A., and L. Li. "0040 Relationship Between Inflammatory Markers and Sleep in Healthy Adolescents." Sleep 43, Supplement_1 (April 2020): A16. http://dx.doi.org/10.1093/sleep/zsaa056.039.

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Abstract Introduction Multiple studies in different countries show a trend of adolescents having insufficient sleep. Review of literature strongly suggests role of cytokines in sleep regulation. Different inflammatory markers like tumor necrosis factor (TNF)α, C-reactive protein (CRP) and interleukins (IL) are sleep regulatory substances. Most of the studies showing relation between cytokines and sleep are seen in adults. In our study, we were interested in finding the relationship between sleep quality and inflammatory markers in healthy adolescents. Methods Twenty eight female and male, African American and White, healthy adolescents aged 15–18 completed the study. Sleep quality was measured using the Pediatric Sleep Questionnaires (PSQ), including snoring, daytime sleepiness and hyperactive behavior. Blood sample was collected from each participant for measuring the inflammatory factors. Results Partial Pearson correlation analysis showed that global PSQ score and hyperactive behavior were significantly correlated with TNF α (r=0.37 for both). Snoring was significantly correlated with leptin, CRP and IL-6 in healthy adolescents. No other correlations were observed. Conclusion Consistent with findings in adults, we have observed an association between inflammatory markers and poor sleep in healthy adolescents. Our findings suggest the importance to improve sleep quality in adolescents for better health outcomes. Support None of the authors have any conflict of interest. This research was supported by awards, P30DK056336 and P30DK079626, from the National Institute of Diabetes And Digestive And Kidney Diseases to Nutrition Obesity Research Center and Diabetes Research Center, respectively, at the University of Alabama at Birmingham.
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Hita-Yañez, Eva, Mercedes Atienza, and Jose L. Cantero. "Polysomnographic and Subjective Sleep Markers of Mild Cognitive Impairment." Sleep 36, no. 9 (September 1, 2013): 1327–34. http://dx.doi.org/10.5665/sleep.2956.

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Herttrich, Theresa, Johann Daxer, Andreas Hiemisch, Jens Kluge, Andreas Merkenschlager, Jürgen Kratzsch, Kathrin Scheuermann, et al. "Association of sleep characteristics with adiposity markers in children." Journal of Pediatric Endocrinology and Metabolism 33, no. 7 (July 28, 2020): 845–52. http://dx.doi.org/10.1515/jpem-2019-0517.

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AbstractBackgroundAccumulating evidence suggests a relationship between sleep alterations and overweight/obesity in children. Our aim was to investigate the association of sleep measures other than obstructive sleep apnea or sleep duration with overweight/obesity and metabolic function in children.MethodsWe conducted a prospective cohort study in school- aged children (aged 5 to 8 years, prepubertal, and 12 to 15 years, pubertal) with overweight/obesity and normal-weight children. All children underwent a standardized in-laboratory polysomnography followed by a fasting blood assessment for glucose and metabolic testing. Subjective sleep measures were investigated by a 7-day sleep diary and questionnaire. We analyzed prepubertal and pubertal groups separately using logistic regression and partial correlation analyses.ResultsA total of 151 participants were analyzed. Overweight/obese children had significantly higher odds for arousal index (prepubertal children: 1.28, Confidence interval (CI): 1.06, 1.67; pubertal children: 1.65, CI: 1.19, 2.29) than normal-weight children, independent of age and gender. In prepubertal children, arousal-index was positively associated with C-peptide (r=0.30, p=0.01), whereas Minimum O2 saturation was negatively associated with triglycerides (r=−0.34, p=0.005), adjusting for age and sex. However, associations were attenuated by further adjustment for body mass index standard deviation scores (BMI-SDS). In pubertal children, higher level of apnea-hypopnea-index and pCO2 predicted increased lipoprotein (a) levels (r=0.35, p=0.03 and r=0.40, p=0.01, respectively), independent of age, sex, and BMI-SDS. A negative association was found between pCO2 and high-density lipoprotein (HDL)-cholesterol (r=−0.40, p=0.01).ConclusionsOverall, we report that sleep quality as measured by arousal index may be compromised by overweight and obesity in children and warrants attention in future intervention programs.
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Henriques-Filho, Paulo Sérgio A., and Riccardo Pratesi. "Sleep apnea and REM sleep behavior disorder in patients with Chiari malformations." Arquivos de Neuro-Psiquiatria 66, no. 2b (June 2008): 344–49. http://dx.doi.org/10.1590/s0004-282x2008000300012.

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BACKGROUND: Chiari malformations (CM) may result in the appearance of REM sleep behavior disorder (RBD) and sleep apnea syndrome (SAS) that can be considered markers of brain stem dysfunction. PURPOSE: To evaluate the frequency of RBD and SAS in patients with CM type I and II. METHOD: Were evaluated 103 patients with CM by means of full night polysomnography. Were scoring different sleep stages, frequency of abnormal movements (through video monitoring) and abnormal respiratory events. RESULTS: Of the 103 patients, 36 showed CM type I and 67 CM type II. Episodes of RBD were observed in 23 patients. Abnormal apnea-hypopnea index (AHI) was observed in 65 patients. CONCLUSION: The high rate of RBD suggests that this parassomnia and the increased frequency of central sleep apnea episodes, may be considered as a marker of progressive brain stem dysfunction.
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Roehrs, T., G. Koshorek, D. Withrow, and T. Roth. "0374 Markers for Hypnotic Abuse Liability: Cortisol in Insomnia?" Sleep 41, suppl_1 (April 2018): A143. http://dx.doi.org/10.1093/sleep/zsy061.373.

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20

Streckenbach, Bettina, Martin Osswald, Stefan Malesevic, Renato Zenobi, and Malcolm Kohler. "Validating Discriminative Signatures for Obstructive Sleep Apnea in Exhaled Breath." Cells 11, no. 19 (September 24, 2022): 2982. http://dx.doi.org/10.3390/cells11192982.

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Rapid and reliable tools for the diagnosis and monitoring of obstructive sleep apnea (OSA) are currently lacking. Prior studies using a chemical analysis of exhaled breath have suggested the existence of an OSA-specific metabolic signature. Here, we validated this diagnostic approach and the proposed marker compounds, as well as their potential to reliably diagnose OSA. In this cross-sectional observational study, exhaled breath was analyzed using secondary electrospray ionization high-resolution mass spectrometry. The study cohort included untreated OSA patients, OSA patients treated with continuous positive airway pressure and healthy subjects. The robustness of previously reported OSA markers was validated based on detectability, significant differences between groups (Mann–Whitney U test) and classification performance. The breath analysis of 118 participants resulted in 42 previously reported markers that could be confirmed in this independent validation cohort. Nine markers were significantly increased in untreated OSA compared to treated OSA, with a subset of them being consistent with a previous validation study. An OSA prediction based on the confirmed OSA signature performed with an AUC of 0.80 (accuracy 77%, sensitivity 73% and specificity 80%). As several breath markers were clearly found to be repeatable and robust in this independent validation study, these results underscore the clinical potential of breath analysis for OSA diagnostics and monitoring.
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Landolt, Hans-Peter, Julia V. Rétey, Karin Tönz, Julie M. Gottselig, Ramin Khatami, Isabelle Buckelmüller, and Peter Achermann. "Caffeine Attenuates Waking and Sleep Electroencephalographic Markers of Sleep Homeostasis in Humans." Neuropsychopharmacology 29, no. 10 (July 14, 2004): 1933–39. http://dx.doi.org/10.1038/sj.npp.1300526.

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22

Stanek, Agata, Klaudia Brożyna-Tkaczyk, and Wojciech Myśliński. "Oxidative Stress Markers among Obstructive Sleep Apnea Patients." Oxidative Medicine and Cellular Longevity 2021 (July 19, 2021): 1–8. http://dx.doi.org/10.1155/2021/9681595.

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Obstructive sleep apnea (OSA) is a chronic respiratory disorder, which can be present in up to 50% of the population, depending on the country. OSA is characterized by recurrent episodes of partial or complete obstruction of the upper airways with consistent movement of the respiratory musculature during sleep. Apneas and hypopneas can lead to a decrease in oxygen saturation, an increase in carbon dioxide in the blood, and subsequent arousals and sleep fragmentation caused by repetitive activation of the central nervous system. As a consequence, intermittent hypoxemia and consequent reoxygenation result in the production of reactive oxygen species, leading to systematic oxidative stress, which is postulated to be a key mechanism of endothelial dysfunction and increased risk for cardiovascular disorders in patients with OSA. In this review, various biomarkers of oxidative stress, including high-sensitivity C-reactive protein, pregnancy-associated plasma protein-A, superoxide dismutase, cell-free DNA, 8-hydroxy-2-deoxyguanosine, advanced oxidation protein products, lipid peroxidation products, receptor for advanced glycation end-products, and thioredoxin are discussed. Biomarkers of oxidative stress have the potential to be used to assess disease severity and treatment response. Continuous positive airway pressure (CPAP) is one of the most common noninvasive treatments for OSA; it keeps the upper airways open during sleep. This reduces episodes of intermittent hypoxia, reoxygenation, and arousal at night. CPAP has been shown to have anti-inflammatory properties and decrease oxidative stress. The administration of certain compounds, like vitamins A, C, and E as well as N-acetylcysteine and allopurinol, can decrease oxidative stress markers. However, their role in the treatment of OSA remains unclear.
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23

de Natale, Edoardo Rosario, Heather Wilson, and Marios Politis. "Predictors of RBD progression and conversion to synucleinopathies." Current Neurology and Neuroscience Reports 22, no. 2 (February 2022): 93–104. http://dx.doi.org/10.1007/s11910-022-01171-0.

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Abstract Purpose of review Rapid eye movement (REM) sleep behaviour disorder (RBD) is considered the expression of the initial neurodegenerative process underlying synucleinopathies and constitutes the most important marker of their prodromal phase. This article reviews recent research from longitudinal research studies in isolated RBD (iRBD) aiming to describe the most promising progression biomarkers of iRBD and to delineate the current knowledge on the level of prediction of future outcome in iRBD patients at diagnosis. Recent findings Longitudinal studies revealed the potential value of a variety of biomarkers, including clinical markers of motor, autonomic, cognitive, and olfactory symptoms, neurophysiological markers such as REM sleep without atonia and electroencephalography, genetic and epigenetic markers, cerebrospinal fluid and serum markers, and neuroimaging markers to track the progression and predict phenoconversion. To-date the most promising neuroimaging biomarker in iRBD to aid the prediction of phenoconversion is striatal presynaptic striatal dopaminergic dysfunction. Summary There is a variety of potential biomarkers for monitoring disease progression and predicting iRBD conversion into synucleinopathies. A combined multimodal biomarker model could offer a more sensitive and specific tool. Further longitudinal studies are warranted to iRBD as a high-risk population for early neuroprotective interventions and disease-modifying therapies.
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Allen, S., G. Elder, R. Sharman, Z. M. Gotts, and J. G. Ellis. "0326 Identification of Objective and Subjective Markers of Sleep Health." Sleep 41, suppl_1 (April 2018): A125. http://dx.doi.org/10.1093/sleep/zsy061.325.

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Laxminarayan, Srinivas, Sridhar Ramakrishnan, Chao Wang, Anne Germain, and Jaques Reifman. "0883 EEG Connectivity Markers In Combat-exposed Veterans With PTSD." Sleep 42, Supplement_1 (April 2019): A355. http://dx.doi.org/10.1093/sleep/zsz067.881.

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Squyres, Emily, Danica Slavish, and Jennifer Graham-Engeland. "380 The role of self-esteem and sleep on inflammatory markers in young adults." Sleep 44, Supplement_2 (May 1, 2021): A151. http://dx.doi.org/10.1093/sleep/zsab072.379.

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Abstract Introduction Disturbed sleep is common among young adults and is associated with poorer health and developmental outcomes. A large percentage of young adults also struggle with low self-esteem. Together, disturbed sleep and low self-esteem may deplete coping resources, heighten to reactivity to stress, and increase disease risk. Yet no studies to our knowledge have examined interactions between self-esteem and sleep on biomarkers of health among young adults. Methods To address this gap, we investigated associations between sleep quality, self-esteem, and two inflammatory markers, C-reactive protein (CRP) and interleukin-6 (IL-6), in a sample of 60 young adults (mean age 25.3 ± 4.0 years old, 53% female, 83% White). Participants completed a baseline survey to assess self-esteem (Rosenberg Self-Esteem Questionnaire) and sleep quality (Pittsburgh Sleep Quality Index [PSQI] sleep quality item), followed by 14 days of self-reported sleep disturbances each morning (PROMISTM sleep disturbances short-form; averaged across the 14 days). A plasma blood draw was then collected to assess CRP and IL-6 approximately one week after the end of the daily portion. Results Lower self-esteem (b = -0.04, 95%CI [-0.06,-0.01], p = 0.015) and lower sleep quality were each associated with higher CRP (b = -0.34, 95%CI [-0.62, -0.07], p = 0.015), but not IL-6. Greater daily sleep disturbances were marginally associated with higher CRP (b = 0.37, 95%CI [-0.06,-0.79], p = 0.088]. Interactions between self-esteem and either sleep quality or sleep disturbances did not predict CRP or IL-6. Conclusion Our results suggest low self-esteem and poorer sleep are each associated with higher levels of inflammation but may not interact to exacerbate risk. It is possible low self-esteem and poor sleep each lead to negative emotions or engagement in risky behaviors (e.g., substance use, sedentary behavior) that impact levels of inflammatory markers. Overall, our results highlight the importance of assessing both sleep and personality traits in relation to biomarkers of health among young adults. Support (if any) American Psychological Association Dissertation Research Award
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Kalinkin, A. L., and A. S. Sorokin. "Sleep disorders — risk factors and hypertension markers in young people with normal body weight." Russian Journal of Cardiology 26, no. 4 (May 22, 2021): 4290. http://dx.doi.org/10.15829/1560-4071-2021-4290.

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Aim. To assess the relationship between different types of sleep disorders, sleep-related symptoms and hypertension (HTN).Material and methods. This cross-sectional study based on the online survey of persons aged 18-39 years with a body mass index of 18-25 kg/m2.Results. According to the results, the HTN risk in persons aged 18-39 years with normal body mass index increases 2 or more times in the presence of various types of sleep disorders and related symptoms. The prevalence of HTGN depends on the patient's phenotype, i.e. from a combination of different types of sleep disorders and sleep-related symptoms.Conclusion. Given the widespread prevalence of various sleep disorders, as well as the relationship between sleep disorders and hypertension in young people, it is necessary to develop preventive measures aimed at reducing the HTN risk by restoring healthy sleep. We also suggest that various sleep disorders may be the primary link in the development of essential HTN.
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Weljie, Aalim M., Peter Meerlo, Namni Goel, Arjun Sengupta, Matthew S. Kayser, Ted Abel, Morris J. Birnbaum, David F. Dinges, and Amita Sehgal. "Oxalic acid and diacylglycerol 36:3 are cross-species markers of sleep debt." Proceedings of the National Academy of Sciences 112, no. 8 (February 9, 2015): 2569–74. http://dx.doi.org/10.1073/pnas.1417432112.

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Sleep is an essential biological process that is thought to have a critical role in metabolic regulation. In humans, reduced sleep duration has been associated with risk for metabolic disorders, including weight gain, diabetes, obesity, and cardiovascular disease. However, our understanding of the molecular mechanisms underlying effects of sleep loss is only in its nascent stages. In this study we used rat and human models to simulate modern-day conditions of restricted sleep and addressed cross-species consequences via comprehensive metabolite profiling. Serum from sleep-restricted rats was analyzed using polar and nonpolar methods in two independent datasets (n= 10 per study, 3,380 measured features, 407 identified). A total of 38 features were changed across independent experiments, with the majority classified as lipids (18 from 28 identified). In a parallel human study, 92 metabolites were identified as potentially significant, with the majority also classified as lipids (32 of 37 identified). Intriguingly, two metabolites, oxalic acid and diacylglycerol 36:3, were robustly and quantitatively reduced in both species following sleep restriction, and recovered to near baseline levels after sleep restriction (P< 0.05, false-discovery rate < 0.2). Elevated phospholipids were also noted after sleep restriction in both species, as well as metabolites associated with an oxidizing environment. In addition, polar metabolites reflective of neurotransmitters, vitamin B3, and gut metabolism were elevated in sleep-restricted humans. These results are consistent with induction of peroxisome proliferator-activated receptors and disruptions of the circadian clock. The findings provide a potential link between known pathologies of reduced sleep duration and metabolic dysfunction, and potential biomarkers for sleep loss.
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Johann, Anna F., Elisabeth Hertenstein, Simon D. Kyle, Chiara Baglioni, Bernd Feige, Christoph Nissen, Dieter Riemann, and Kai Spiegelhalder. "Perfectionism and Polysomnography-Determined Markers of Poor Sleep." Journal of Clinical Sleep Medicine 13, no. 11 (November 15, 2017): 1319–26. http://dx.doi.org/10.5664/jcsm.6806.

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Chokroverty, Sudhansu, Sushanth Bhat, and Mitchell Rubinstein. "Periorbital integrated potentials: useful phasic REM sleep markers." Sleep Medicine 37 (September 2017): 74–76. http://dx.doi.org/10.1016/j.sleep.2017.06.016.

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dos Santos, Altair B., Kristi A. Kohlmeier, and George E. Barreto. "Are Sleep Disturbances Preclinical Markers of Parkinson’s Disease?" Neurochemical Research 40, no. 3 (November 30, 2014): 421–27. http://dx.doi.org/10.1007/s11064-014-1488-7.

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32

Kawada, Tomoyuki. "Inflammatory markers in patients with obstructive sleep apnea." Sleep and Breathing 20, no. 2 (January 11, 2016): 889–90. http://dx.doi.org/10.1007/s11325-015-1302-z.

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Sarkisian, K., L. J. Mason, E. C. McCanlies, M. E. Andrew, C. M. Burchfiel, and J. M. Violanti. "Levels of Inflammatory Markers and Quality of Sleep." Annals of Epidemiology 23, no. 9 (September 2013): 587. http://dx.doi.org/10.1016/j.annepidem.2013.06.038.

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Wilder-Smith, A., F. B. Mustafa, A. Earnest, L. Gen, and P. A. MacAry. "Impact of partial sleep deprivation on immune markers." Sleep Medicine 14, no. 10 (October 2013): 1031–34. http://dx.doi.org/10.1016/j.sleep.2013.07.001.

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Motivala, Sarosh J., Avishay Sarfatti, Luis Olmos, and Michael R. Irwin. "Inflammatory Markers and Sleep Disturbance in Major Depression." Psychosomatic Medicine 67, no. 2 (March 2005): 187–94. http://dx.doi.org/10.1097/01.psy.0000149259.72488.09.

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Krysta, Krzysztof, Marek Krzystanek, Agnieszka Bratek, and Irena Krupka-Matuszczyk. "Sleep and inflammatory markers in different psychiatric disorders." Journal of Neural Transmission 124, S1 (December 9, 2015): 179–86. http://dx.doi.org/10.1007/s00702-015-1492-3.

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Alshaarawy, Omayma, Srinivas Teppala, and Anoop Shankar. "Markers of Sleep-Disordered Breathing and Prediabetes in US Adults." International Journal of Endocrinology 2012 (2012): 1–8. http://dx.doi.org/10.1155/2012/902324.

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Background. Prediabetes is a preclinical stage in the hyperglycemia continuum where subjects are at increased risk of developing diabetes. Several studies reported a positive association between markers of sleep-disordered breathing (SDB) and diabetes. However, few studies investigated the relationship between SDB markers and prediabetes.Methods. We examined 5,685 participants ≥20 years from the National Health and Nutrition Examination Survey (NHANES) 2005–2008. The exposure of interest was SDB markers including sleep duration, snoring, snorting, and daytime sleepiness. The outcome was prediabetes (n=2058), among subjects free of diabetes.Results. SDB markers were associated with prediabetes. Compared to those without any sleep disturbance, the multivariable odds ratio (OR) (95% confidence interval (CI)) of prediabetes among those with three or more SDB markers was 1.69 (1.28–2.22). In subgroup analyses, the association between SDB markers and prediabetes was stronger among women (OR (95% CI) = 2.09 (1.36–3.23) when compared to men (1.52 (1.00–2.35)) and was present among non-Hispanic whites (2.66 (1.92–3.69)) and Mexican Americans (1.99 (1.13–3.48)), but not among non-Hispanic blacks (1.10 (0.70–1.73)).Conclusion. SDB markers were associated with prediabetes. This association was stronger in women and was present mainly in non-Hispanic whites and Mexican Americans.
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Xiao, Qian, Joshua Sampson, Aladdin Shadyab, Andrea LaCroix, Kristine Yaffe, and Katie Stone. "ASSOCIATIONS BETWEEN SLEEP AND REST: ACTIVITY CHARACTERISTICS AND METABOLOMIC PROFILES IN OLDER MEN." Innovation in Aging 6, Supplement_1 (November 1, 2022): 363–64. http://dx.doi.org/10.1093/geroni/igac059.1437.

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Abstract The association of sleep and rest-activity rhythms (RAR) with metabolic health is not fully understood. Previous studies have identified multiple metabolite markers in amino acid and lipid pathways associated with various characteristics of sleep. However, most of the studies used self-reported sleep, and limited studies have examined 24-hour RAR profiles, a more complete picture of activity. We studied 950 older men and measured metabolomics from fasting blood samples. We identified numerous metabolomic markers that were cross-sectionally associated with actigraphy-based measures of sleep (total sleep time, sleep efficiency, sleep timing) and RAR (amplitude, acrophase, mesor and overall rhythmicity). The majority of the associated metabolites were amino acids and lipids from a wide range of pathways, including metabolism pathways of branched chain amino acid metabolism, fatty acids, and gamma-glutamyl amino acids. Our preliminary findings suggest that sleep and RAR are widely involved in human metabolism.
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Lisse, J., C. Fiebelman, L. Wang, N. Ercal, V. Samaranayake, G. Olbricht, and M. Thimgan. "0037 Molecular Markers Of Biological Aging In Predicted Short-lived Flies." Sleep 41, suppl_1 (April 2018): A15. http://dx.doi.org/10.1093/sleep/zsy061.036.

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Smail, Emily, Brion Maher, Ann Moore, Pei-Lun Kuo, Mark Wu, Dominique Low, Katie Stone, and Adam Spira. "Links of Sleep Duration with Biomarkers of Accelerated Aging: the Baltimore Longitudinal Study of Aging." Innovation in Aging 5, Supplement_1 (December 1, 2021): 665–66. http://dx.doi.org/10.1093/geroni/igab046.2512.

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Abstract Sleep disorders and sleep deprivation have been linked to markers of biological aging, including methylation change and increases in white blood cell and neutrophil counts. However, little is known regarding the association of sleep duration with biological markers of aging. We investigated links of self-reported sleep duration with biological aging markers in 615 participants in the Baltimore Longitudinal Study of Aging (BLSA) aged ≥50 years (mean = 71.0 ± 11.2, 49.6% women, 68.8% white) with data on self-reported sleep duration in hours (i.e., ≤6 (n=131), &gt;6 to 7 (n=234), &gt;7 (n=250)), demographics, and genetic and methylation data (mDNA). Our aging biomarker outcomes were four epigenetic clocks (Horvath, Hannum, PhenoAge, and GrimAge), mDNA-estimated PAI1, and estimated granulocyte count. After adjustment for age, sex, and race, compared to those sleeping ≤6 hours, those reporting &gt;7 hours of sleep had faster biological aging according to Hannum age-acceleration, PhenoAge, GrimAge, mDNA-estimated PAI1, and granulocyte count. In addition, sleep duration interacted with age, such that compared to individuals reporting ≤6 hours of sleep, individuals reporting &gt;6 to 7 hours showed lower GrimAge with increasing age, and with sex, such that males with longer sleep duration (&gt;6 to 7 and &gt;7 hours) showed a lower granulocyte count compared to females. Findings suggest that both short and long sleep duration are associated with and may contribute to accelerated aging. Prospective studies in larger samples are needed to examine whether changes in sleep duration precede changes in aging biomarkers.
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Simon, Stacey, Haseeb Rahat, Anne-Marie Carreau, Yesenia Garcia-Reyes, Ann Halbower, Laura Pyle, Kristen J. Nadeau, and Melanie Cree-Green. "Poor Sleep Is Related to Metabolic Syndrome Severity in Adolescents With PCOS and Obesity." Journal of Clinical Endocrinology & Metabolism 105, no. 4 (January 4, 2020): e1827-e1834. http://dx.doi.org/10.1210/clinem/dgz285.

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Abstract Context Polycystic ovary syndrome (PCOS) is a common endocrine disorder and is associated with metabolic syndrome (MS). Development of MS in PCOS is likely multifactorial and may relate to poor sleep. Objective The objective of this research is to investigate differences in objective markers of sleep in adolescents with obesity and PCOS with and without MS. We also aimed to examine the relationships between markers of sleep with MS markers. Design A cross-sectional study was conducted. Participants Participants included adolescents with PCOS and obesity with MS (N = 30) or without MS (N = 36). Outcome Measures Hormone and metabolic measurements, abdominal magnetic resonance imaging for hepatic fat fraction, actigraphy to estimate sleep, and overnight polysomnography (PSG). Results Adolescents with obesity and PCOS who also had MS had significantly worse sleep-disordered breathing including higher apnea-hypopnea index (AHI, P = .02) and arousal index (P = .01) compared to those without MS. Actigraphy showed no differences in habitual patterns of sleep behaviors including duration, timing, or efficiency between groups. However, a greater number of poor sleep health behaviors was associated with greater number of MS components (P = .04). Higher AHI correlated with higher triglycerides (TG) (r = 0.49, P = .02), and poorer sleep efficiency correlated with higher percentage of liver fat (r = –0.40, P = .01), waist circumference (r = –0.46, P &lt; .01) and higher TG (r = –0.34, P = .04). Conclusions Among girls with PCOS and obesity, sleep-disordered breathing was more prevalent in those with MS, and poor sleep behaviors were associated with metabolic dysfunction and more MS symptoms. Sleep health should be included in the assessment of adolescents with PCOS and obesity.
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Ye, Lichuan, Andrew Miller, Deborah Bruner, Sudeshna Paul, Jennifer Felger, Evanthia Wommack, Kristin Higgins, Dong Shin, Nabil Saba, and Canhua Xiao. "0577 Sleep Quality and Its Association with Inflammation Over Time in Patients Undergoing Radiation Therapy for Head and Neck Cancer." Sleep 45, Supplement_1 (May 25, 2022): A254. http://dx.doi.org/10.1093/sleep/zsac079.574.

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Abstract Introduction Sleep disturbance is a prominent concern in patients with cancer with detrimental effect on health outcomes. Although inflammation has been proposed as a potential mechanism of sleep disturbance, there is a dearth of longitudinal data supporting the relationship between cancer-related sleep disturbance and inflammatory markers. The goal of this prospective longitudinal study was to examine the change in sleep quality and its association with inflammatory markers in patients undergoing radiation therapy for head and neck cancer. Methods A total of 176 patients who had head and neck cancer without distant metastases were assessed before, immediately after, and at 3 and 12 months after radiotherapy. Sleep quality was assessed by the Pittsburgh Sleep Quality Index (PSQI). Peripheral blood inflammatory markers were measured using standard techniques at the same four assessment times. Generalized estimating equations with exchangeable within-subject correlation matrix were used to analyze repeated measures. Results The participants were mostly middle-aged White (79.5%) men (74.0%) who were married or living with significant others (70.0%) and received concurrent chemoradiotherapy (80.1%). Using the PSQI of 5 as the cut-off, 66.3% of the participants were poor sleepers at baseline, and this rate increased to 82.8% immediately after, then dropped to 56.8% at 3 months and 46.2% 12 months after therapy. Being single (p=0.007), taking antidepressants (p=0.020), and with feeding tube (p=0.01) were identified to be significantly associated with poor sleep quality over time. Controlling for relevant demographic and clinical factors, changes in sleep quality were associated with changes of circulating levels of two inflammatory markers, C-reactive protein (CRP) and interlukin-1 receptor antagonist (IL-1ra). Increased CRP and IL-1ra levels were associated with higher PSQI global scores (beta=0.826, p=0.007 for CRP; beta=1.412, p=0.050 for IL-1ra), indicating worse sleep quality. Conclusion Patients with head and neck cancer experienced poor sleep quality, especially immediately after treatment completion and in those who were single, depressed, or with feeding tube. Inflammation is associated with cancer-related sleep disturbance and both sleep and inflammation may be potential targets to promote health outcomes in patients with cancer. Support (If Any) The study was supported by NIH/NINR K99/R00NR014587, NIH/NINR R01NR015783, NIH/NCI P30CA138292.
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Wang, Chao, Sridhar Ramakrishnan, Srinivas Laxminarayan, Andrey Dovzhenok, Anne Germain, and Jaques Reifman. "0074 Can We Identify Reproducible Brain-activity Markers Of PTSD During Sleep?" Sleep 42, Supplement_1 (April 2019): A31. http://dx.doi.org/10.1093/sleep/zsz067.073.

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44

Song, Sunmi, Natasha N. DeMeo, David M. Almeida, Marzieh Majd, Christopher G. Engeland, and Jennifer E. Graham-Engeland. "The longitudinal connection between depressive symptoms and inflammation: Mediation by sleep quality." PLOS ONE 17, no. 5 (May 26, 2022): e0269033. http://dx.doi.org/10.1371/journal.pone.0269033.

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Although there is a strong association between depressive symptoms and markers of inflammation, it remains unclear whether depressive symptoms at one point in life may predict inflammation later in life. Moreover, despite extant literature linking sleep with both depressive symptoms and inflammation, there is little research investigating poor sleep as a mechanism linking depressive symptoms with later inflammation. The links between depression and physical health can also vary by gender. In longitudinal analyses with data from the Midlife in the United States (MIDUS) study, we examined whether depressive symptoms were associated with inflammatory markers 11 years later and whether these associations were mediated by sleep disturbances or moderated by gender. Participants reported depressive symptoms and demographic information at baseline. At 11-year follow-up, the same participants (n = 968) reported depressive symptoms, sleep quality and duration using validated scale items, and provided a blood sample from which inflammatory markers interleukin-6 (IL-6) and C-reactive protein (CRP) were quantified. Actigraphy assessment of sleep was obtained in a subsample (n = 276). After adjusting for concurrent depressive symptoms and other relevant covariates, baseline depressive symptoms were associated with CRP 11 years later in the full sample, and with IL-6 among women. Subjective sleep quality mediated the association between depressive symptoms and CRP. Results suggest that depressive symptoms may be longitudinally associated with inflammation; however, directionality issues cannot be determined from the present work, particularly as inflammation markers (which might have been associated with baseline depressive symptoms) were not available at baseline. Findings further suggest that longitudinal associations between depressive symptoms and inflammation may potentially be explained by sleep and may reflect gender specific patterns.
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45

Swanson, Christine M., Steven A. Shea, Wendy M. Kohrt, Kenneth P. Wright, Sean W. Cain, Mirjam Munch, Nina Vujović, Charles A. Czeisler, Eric S. Orwoll, and Orfeu M. Buxton. "Sleep Restriction With Circadian Disruption Negatively Alter Bone Turnover Markers in Women." Journal of Clinical Endocrinology & Metabolism 105, no. 7 (May 4, 2020): 2456–63. http://dx.doi.org/10.1210/clinem/dgaa232.

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Abstract Purpose The purpose of this work is to determine whether an uncoupling of bone turnover markers (BTMs) occurs in women exposed to the combination of sleep restriction with circadian disruption (SRCD), as previously reported in men. Methods Four bone biomarkers (N-terminal propeptide of type I procollagen [P1NP] and osteocalcin = bone formation; C-telopeptide [CTX] = bone resorption; sclerostin = bone formation inhibitor) were measured in bihourly samples over 24 hours at baseline and after approximately 3 weeks of sleep restriction (~5.6 hours of sleep/24 hours) with concurrent circadian disruption (SRCD, recurring 28-hour “day” in dim light). Maximum likelihood estimation in a repeated-measures model was used to assess the effects of SRCD and age on bone biomarkers. Results Five women were young (22 ± 2.8 years) and four were older (58 ± 1.8 years). Baseline bone biomarker levels did not differ by age (all P ≥ .07). Bone formation markers were lower after SRCD (estimate ± SEE, ΔP1NP = –9.5 ± 2.8 μg/L, P = .01; Δosteocalcin = –2.3 ± 0.9 ng/mL, P = .04). The P1NP decline was greater in young women (ΔP1NP = –12.9 ± 3.7 μg/L, P = .01). After SRCD, CTX was significantly higher in young women (0.182 ± 0.069 ng/mL, P = .04) but did not change in older women. Conclusions These pilot data are similar to previous findings in men and suggest that SRCD negatively altered bone metabolism in women by decreasing markers of bone formation and, in young women, increasing a marker of bone resorption. If sustained, this pattern of BTM uncoupling may lead to bone loss and lower bone mineral density.
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Yakovlev, A. V., S. D. Mayanskaya, A. N. Vergazova, L. P. Plutalova, P. B. Mazina, N. N. Mayanskaya, and N. F. Yakovleva. "Adipose tissue dysfunction markers in obese patients with obstructive sleep apnea syndrome." Kazan medical journal 96, no. 2 (April 15, 2015): 134–37. http://dx.doi.org/10.17750/kmj2015-134.

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Aim. To examine the relationship between obstructive sleep apnea syndrome and metabolic dysfunction in obese patients.Methods. The study included 66 male patients aged 53±5.11 years with previously diagnosed obstructive sleep apnea syndrome and obesity (body mass index ≥30 kg/m2). Cardiorespiratory monitoring, 24-hour blood pressure monitoring was performed in all patients; low density lipoprotein, triglycerides, high density lipoprotein, total cholesterol and glucose blood levels, as well as adiponectin and leptin blood concentrations were measured in all patients.Results. Blood pressure level and leptin blood concentration were significantly higher in patients with severe form of obstructive sleep apnea syndrome. There was no statistically significant relationship found between the lipid profile parameters and other adipokines and the severity of obstructive sleep apnea syndrome. The data analysis also revealed association between the elevated levels of leptin and the classic cardiovascular risk factors - arterial hypertension and low density lipoprotein level.Conclusion. The revealed associations may indicate the additional role of leptin as the biochemical marker of early development of obstructive breathing sleep disorders in patients with abdominal obesity, as well as the early manifestation of other components of metabolic syndrome - arterial hypertension and dyslipidemia with concomitant significant increase in cardiovascular risk.
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Barateau, Lucie, Régis Lopez, Sofiene Chenini, Anna-Laura Rassu, Sabine Scholz, Manuela Lotierzo, Jean-Paul Cristol, Isabelle Jaussent, and Yves Dauvilliers. "Association of CSF orexin-A levels and nocturnal sleep stability in patients with hypersomnolence." Neurology 95, no. 21 (September 1, 2020): e2900-e2911. http://dx.doi.org/10.1212/wnl.0000000000010743.

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ObjectiveTo evaluate the associations between CSF orexin-A (ORX) levels and markers of nocturnal sleep stability, assessed by polysomnography.MethodsNocturnal polysomnography data and ORX levels of 300 drug-free participants (55% men, 29.9±15.5 years, ORX level 155.1±153.7 pg/mL) with hypersomnolence were collected. Several markers of nocturnal sleep stability were analyzed: sleep and wake bouts and sleep/wake transitions. Groups were categorized according to ORX levels, in 2 categories (deficient ≤110; >110), in tertiles (≤26, 26–254, >254), and compared using logistic regression models. Results were adjusted for age, sex, and body mass index.ResultsWe found higher number of wake bouts (43 vs 25, p < 0.0001), sleep bouts (43 vs 25.5, p < 0.0001), and index of sleep bouts/hour of sleep time, but lower index of wake bouts/hour of wake time (41.4 vs 50.6, p < 0.0001), in patients with ORX deficiency. The percentage of wake bouts <30 seconds was lower (51.3% vs 60.8%, p < 0.001) and of wake bouts ≥1 minutes 30 seconds higher (7.7% vs 6.7%, p = 0.02) when ORX deficient. The percentage of sleep bouts ≤14 minutes was higher (2–5 minutes: 23.7% vs 16.1%, p < 0.0001), and of long sleep bouts lower (>32 minutes 30 seconds: 7.3% vs 18.3%, p < 0.0001), when ORX deficient. These findings were confirmed when groups were categorized according to ORX tertiles, with a dose–response effect of ORX levels in post hoc comparisons, and in adjusted models.InterpretationThis study shows an association between ORX levels and nocturnal sleep stabilization in patients with hypersomnolence. Sleep and wake bouts are reliable markers of nighttime sleep stability that correlate with CSF ORX levels in a dose-dependent manner.
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Nielsen, Mette S., Jonas S. Quist, Jean-Philippe Chaput, Stine-Mathilde Dalskov, Camilla T. Damsgaard, Christian Ritz, Arne Astrup, Kim F. Michaelsen, Anders Sjödin, and Mads F. Hjorth. "Physical Activity, Sedentary Time, and Sleep and the Association With Inflammatory Markers and Adiponectin in 8- to 11-Year-Old Danish Children." Journal of Physical Activity and Health 13, no. 7 (July 2016): 733–39. http://dx.doi.org/10.1123/jpah.2015-0123.

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Background:Inflammatory markers, adiponectin, and movement/nonmovement behaviors have all been linked to risk factors for cardiovascular disease; however, the association between childhood movement/nonmovement behaviors and inflammatory markers and adiponectin is unknown.Methods:We explored the association between accelerometer determined moderate-to-vigorous physical activity (MVPA), sedentary time, and sleep (7 days/8 nights) and fasting C-reactive protein (CRP), interleukin-6 (IL-6), and adiponectin in 806 school children. A sleep variability score was calculated.Results:MVPA was negatively associated with adiponectin in boys and girls (P < .001) and with CRP and IL-6 in girls (P < .05) independent of sleep duration, sedentary time, age, fat mass index (FMI), and pubertal status. Sedentary time was positively associated with adiponectin in boys and girls (both P < .001), and sleep duration with adiponectin in boys independent of age, FMI, and pubertal status (P < .001); however, these associations disappeared after mutual adjustments for movement behavior. Sleep duration variability was positively associated with CRP in girls independent of all covariates (P < .01).Conclusion:MVPA remained negatively associated with inflammatory markers and adiponectin, and sleep duration variability positively associated with CRP after adjustment for FMI, pubertal status, and other movement behavior. The inverse association between MVPA and adiponectin conflicts with the anti-inflammatory properties of adiponectin.
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49

Barateau, L., R. Lopez, S. Chenini, A. Rassu, S. Scholz, M. Lotierzo, J. Cristol, I. Jaussent, and Y. Dauvilliers. "0750 Nocturnal Sleep Stability and Cerebrospinal Fluid Orexin-A Levels: Sleep and Wake Bouts." Sleep 43, Supplement_1 (April 2020): A285. http://dx.doi.org/10.1093/sleep/zsaa056.746.

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Abstract Introduction The orexin (ORX)/hypocretin system stabilizes sleep-wake regulation by sustaining long periods of wakefulness in humans and animals. We aimed to evaluate the relationships between cerebrospinal fluid (CSF) ORX levels and markers of nocturnal sleep stability assessed by polysomnography (PSG) in humans. Methods Nocturnal PSG data and CSF ORX levels of 300 drug-free subjects (55% men, 29.9±15.5 years old, mean ORX levels 155.1±153.7 pg/mL) with a complaint of hypersomnolence were collected in the National Reference Center for Narcolepsy, France. Several markers of nocturnal sleep stability were analyzed: wake (WB), sleep bouts (SB), and sleep/wake transitions. Groups were categorized according to ORX levels: two categories (≤110, &gt;110 pg/mL, the current established threshold of ORX-deficiency), and tertiles (≤26,]26;254], &gt;254 pg/mL); and were compared using logistic regression models. Results were adjusted for age, gender and body mass index. Results ORX-deficient subjects had more WB, SB, and sleep-wake transitions than the others. The WB duration was longer and the SB duration shorter in ORX-deficient category. The proportion of the shortest WB (30 sec) was lower in the ORX-deficient category whereas the proportion of WB above 1 min 30 sec was higher. The proportion of SB ≤ 14min was higher among ORX-deficient patients, with opposite results for longer SB. Subsequent analyses performed in the population categorized according to tertiles of CSF ORX-A confirmed all these findings, with a strong dose-response effect of ORX levels in post-hoc comparisons. All results remained highly significant in adjusted statistical models. Conclusion This study provides a strong evidence of the direct effect of ORX on nocturnal sleep stabilization in humans. WB and SB are reliable markers of nighttime sleep stability, strongly correlated to CSF ORX-A levels in a dose dependent way. These PSG biomarkers are promising to be applied in clinical and research settings. Support none
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Ibáñez-del Valle, Vanessa, Rut Navarro-Martínez, Maria Luisa Ballestar-Tarín, and Omar Cauli. "Salivary Inflammatory Molecules as Biomarkers of Sleep Alterations: A Scoping Review." Diagnostics 11, no. 2 (February 10, 2021): 278. http://dx.doi.org/10.3390/diagnostics11020278.

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Poor sleep quality and sleep disorders are the most common problems in people, affecting health-related quality of life. Various studies show an association between sleep disorders and altered levels of stress hormones and inflammatory cytokines measured in saliva. The main objective of this article is to provide an analysis of the current evidence related to changes in inflammatory markers in the saliva and their associations with sleep quality measurement (both objective and subjective methods) in healthy subjects and in sleep-related disorders. To that end, a scoping review was carried out, following the PRISMA criteria in the bibliographic search in several databases: PubMed, EBSCO, and SCOPUS. Eleven of the articles are from the adult population and two from the child-youth population. They mainly measure the relationship between sleep and interleukin-1β (IL-1β), interleukin-6 (IL-6), and tumor necrosis factor alpha (TNFα) alpha, as well as other inflammatory markers such as myeloperoxidase (MPO) and prostaglandin-endoperoxide synthase 2. An analysis shows the relationship between these salivary biomarkers and sleep quality, especially in the case of IL-6 in both healthy subjects and several pathologies associated with sleep-disorders. The results for TNFα and IL-1β measurements are still inconclusive and the difference with IL-6 was assessed. Two studies reported interventions that result in sleep improvement and are accompanied by the normalization of inflammatory changes detected in the saliva. As it is an easy-to-apply and non-invasive method, the measurement of salivary cytokines can be very useful in chronobiology studies. Further studies are required to determine the sensitivity of salivary inflammatory markers in monitoring biological rhythms and acting as biomarkers in the detection of sleep disorders and sleep interventions.
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