Pathological Sleep and Wakefulness in the ICU and Weaning Failure: A Causal Relationship?
Ontology highlight
ABSTRACT:
SUBMITTER: Schwarz EI
PROVIDER: S-EPMC6727162 | biostudies-literature |
REPOSITORIES: biostudies-literature
Similar Datasets
Project description: Not available
| S-EPMC6727165 | biostudies-literature
Project description:BackgroundSleep had never been assessed immediately after extubation in patients still in the ICU. However, sleep deprivation may alter respiratory function and may promote respiratory failure. We hypothesized that sleep alterations after extubation could be associated with an increased risk of post-extubation respiratory failure and reintubation. We conducted a prospective observational cohort study performed at the medical ICU of the university hospital of Poitiers in France. Patients at high-risk of extubation failure (> 65 years, with any underlying cardiac or lung disease, or intubated > 7 days) were included. Patients intubated less than 24 h, with central nervous or psychiatric disorders, continuous sedation, neuroleptic medication, or uncooperative were excluded. Sleep was assessed by complete polysomnography just following extubation including the night. The main objective was to compare sleep between patients who developed post-extubation respiratory failure or required reintubation and the others.ResultsOver a 3-year period, 52 patients had complete polysomnography among whom 12 (23%) developed post-extubation respiratory failure and 8 (15%) required reintubation. Among them, 10 (19%) had atypical sleep, 15 (29%) had no deep sleep, and 33 (63%) had no rapid eye movement (REM) sleep. Total sleep time was 3.2 h in median [interquartile range, 2.0-4.4] in patients who developed post-extubation respiratory failure vs. 2.0 [1.1-3.8] in those who were successfully extubated (p = 0.34). Total sleep time, and durations of deep and REM sleep stages did not differ between patients who required reintubation and the others. Reintubation rates were 21% (7/33) in patients with no REM sleep and 5% (1/19) in patients with REM sleep (difference, - 16% [95% CI - 33% to 6%]; p = 0.23).ConclusionsSleep assessment by polysomnography after extubation showed a dramatically low total, deep and REM sleep time. Sleep did not differ between patients who were successfully extubated and those who developed post-extubation respiratory failure or required reintubation.
| S-EPMC8105690 | biostudies-literature
Project description:In the modern era, sleep deprivation (SD) is one of the most common health problems that has a profound influence on an individual's quality of life and overall health. Studies have identified the possibility that lack of sleep can stimulate inflammatory responses. NLRP3 inflammasome, a key component of the innate immune responses, initiates inflammatory responses by enhancing proinflammatory cytokine release and caspase-1-mediated pyroptosis. In this study, NLRP3 modification, its proinflammatory role, and potential targeted therapies were reviewed with regard to SD-induced outcomes. A growing body of evidence has showed the importance of the mechanistic connections between NLRP3 and the detrimental consequences of SD, but there is a need for more clinically relevant data. In animal research, (i) some animals show differential vulnerability to the effects of SD compared to humans. (ii) Additionally, the effects of sleep differ depending on the SD technique employed and the length of SD. Moreover, paying attention to the crosstalk of all the driving factors of NLRP3 inflammasome activation such as inflammatory responses, autonomic control, oxidative stress, and endothelial function is highly recommended. In conclusion, targeting NLRP3 inflammasome or its downstream pathways for therapy could be complicated due to the reciprocal and complex relationship of SD with NLRP3 inflammasome activation. However, additional research is required to support such a causal claim.
| S-EPMC9815451 | biostudies-literature
Project description:Interest in time-resolved connectivity in fMRI has grown rapidly in recent years. The most widely used technique for studying connectivity changes over time utilizes a sliding windows approach. There has been some debate about the utility of shorter versus longer windows, the use of fixed versus adaptive windows, as well as whether observed resting state dynamics during wakefulness may be predominantly due to changes in sleep state and subject head motion. In this work we use an independent component analysis (ICA)-based pipeline applied to concurrent EEG/fMRI data collected during wakefulness and various sleep stages and show: 1) connectivity states obtained from clustering sliding windowed correlations of resting state functional network time courses well classify the sleep states obtained from EEG data, 2) using shorter sliding windows instead of longer non-overlapping windows improves the ability to capture transition dynamics even at windows as short as 30 s, 3) motion appears to be mostly associated with one of the states rather than spread across all of them 4) a fixed tapered sliding window approach outperforms an adaptive dynamic conditional correlation approach, and 5) consistent with prior EEG/fMRI work, we identify evidence of multiple states within the wakeful condition which are able to be classified with high accuracy. Classification of wakeful only states suggest the presence of time-varying changes in connectivity in fMRI data beyond sleep state or motion. Results also inform about advantageous technical choices, and the identification of different clusters within wakefulness that are separable suggest further studies in this direction.
| S-EPMC7753906 | biostudies-literature
Project description:Adequate sleep quantity and quality is required to maintain vigilance, cognitive and learning processes. A decrease of sleep quantity preflight and on the International Space Station (ISS) has been reported. Recent counter-measures have been implemented to better regulate sleep opportunities on ISS. In our study, astronauts were allocated enough time for sleep the night before the recordings. However, for proper sleep recovery, the quality of sleep is also critical. Unfortunately, data on sleep quality have yet to be acquired from the ISS. Here, we investigate sleep pressure markers during wakefulness in five astronauts throughout their 6-month space mission by the mean of electroencephalographic recordings. We show a global increase of theta oscillations (5-7 Hz) on the ISS compared to on Earth before the mission. We also show that local sleep-like events, another marker of sleep pressure, are more global in space (p < 0.001). By analysing the performances of the astronauts during a docking simulation, we found that local sleep-like events are more global when reaction times are slower (R 2 = 0.03, p = 0.006) and there is an increase of reaction times above 244 ms after 2 months in space (p = 0.012). Our analyses provide first evidence for increased sleep pressure in space and raise awareness on possible impacts on visuomotor performances in space.
| S-EPMC6497715 | biostudies-literature
Project description:Poor sleep health is associated with a wide array of increased risk for cardiovascular, metabolic and mental health problems as well as all-cause mortality in observational studies, suggesting potential links between sleep health and lifespan. However, it has yet to be determined whether sleep health is genetically or/and causally associated with lifespan. In this study, we firstly studied the genome-wide genetic association between four sleep behaviors (short sleep duration, long sleep duration, insomnia, and sleep chronotype) and lifespan using GWAS summary statistics, and both sleep duration time and insomnia were negatively correlated with lifespan. Then, two-sample Mendelian randomization (MR) and multivariable MR analyses were applied to explore the causal effects between sleep behaviors and lifespan. We found that genetically predicted short sleep duration was causally and negatively associated with lifespan in univariable and multivariable MR analyses, and this effect was partially mediated by coronary artery disease (CAD), type 2 diabetes (T2D) and depression. In contrast, we found that insomnia had no causal effects on lifespan. Our results further confirmed the negative effects of short sleep duration on lifespan and suggested that extension of sleep may benefit the physical health of individuals with sleep loss. Further attention should be given to such public health issues.
| S-EPMC10883970 | biostudies-literature
Project description:Study objectivesSleep is a prominent behavioral and biochemical state observed in all animals studied, including platyhelminth flatworms. Investigations into the biochemical mechanisms associated with sleep-and wakefulness-are important for understanding how these states are regulated and how that regulation changed with the evolution of new types of animals. Unfortunately, beyond a handful of vertebrates, such studies on invertebrates are rare.MethodsWe investigated the effect of seven neurotransmitters, and one pharmacological compound, that modulate either sleep or wakefulness in mammals, on flatworms (Girardia tigrina). Flatworms were exposed via ingestion and diffusion to four neurotransmitters that promote wakefulness in vertebrates (acetylcholine, dopamine, glutamate, histamine), and three that induce sleep (adenosine, GABA, serotonin) along with the H1 histamine receptor antagonist pyrilamine. Compounds were administered over concentrations spanning three to five orders of magnitude. Flatworms were then transferred to fresh water and video recorded for analysis.ResultsDopamine and histamine decreased the time spent inactive and increased distance traveled, consistent with their wake-promoting effect in vertebrates and fruit flies; pyrilamine increased restfulness and GABA showed a nonsignificant trend towards promoting restfulness in a dose-dependent manner, in agreement with their sleep-inducing effect in vertebrates, fruit flies, and Hydra. Similar to Hydra, acetylcholine, glutamate, and serotonin, but also adenosine, had no apparent effect on flatworm behavior.ConclusionsThese data demonstrate the potential of neurotransmitters to regulate sleep and wakefulness in flatworms and highlight the conserved action of some neurotransmitters across species.
| S-EPMC9216492 | biostudies-literature
Project description:Slow waves (0.5-4 Hz) predominate in the cortical electroencephalogram during non-rapid eye movement (NREM) sleep in mammals. They reflect the synchronization of large neuronal ensembles alternating between active (UP) and quiescent (Down) states and propagating along the neocortex. The thalamic contribution to cortical UP states and sleep modulation remains unclear. Here we show that spontaneous firing of centromedial thalamus (CMT) neurons in mice is phase-advanced to global cortical UP states and NREM-wake transitions. Tonic optogenetic activation of CMT neurons induces NREM-wake transitions, whereas burst activation mimics UP states in the cingulate cortex and enhances brain-wide synchrony of cortical slow waves during sleep, through a relay in the anterodorsal thalamus. Finally, we demonstrate that CMT and anterodorsal thalamus relay neurons promote sleep recovery. These findings suggest that the tonic and/or burst firing pattern of CMT neurons can modulate brain-wide cortical activity during sleep and provides dual control of sleep-wake states.
| S-EPMC6438460 | biostudies-literature
Project description:Postextubation distress after a successful spontaneous breathing trial (SBT) is associated with increased morbidity and mortality. Lung ultrasound determination of changes in lung aeration predicts weaning failure. It remains unknown whether this derecruitment is related to alveolar epithelial dysfunction or not.To verify whether lung alveolar type I epithelial cell injury marker sRAGE (soluble form of the receptor for advanced glycation end-products) is predictive of postextubation distress and weaning failure or not, and to verify whether plasma sRAGE levels can be related to lung derecruitment during the process of weaning from mechanical ventilation or not. INTERVENTIONS MEASUREMENTS: 88 patients from 2 intensive care units were included in this observational prospective study. Plasma sRAGE levels were measured in duplicate by ELISA before, at the end of a 60-minute SBT, and 4 hours after extubation. To quantify lung aeration, a lung ultrasound score was calculated.34% of extubated patients experienced postextubation distress. Patients with or without postextubation distress had comparable sRAGE levels before SBT, after SBT, and 4 hours after extubation. In patients with postextubation distress, sRAGE levels were not predictive of the need for mechanical ventilation. sRAGE levels were not associated with lung aeration as assessed by echography. Patients who succeeded SBT (86%) and those who failed (14%) had no differences in sRAGE levels, before (median 1111 vs 1021 pg/mL, p?=?0,87) and at the end of SBT (1165 vs 1038 pg/mL, p?=?0.74).Plasma levels of sRAGE do not predict postextubation distress or SBT failure/success in patients weaning from mechanical ventilation. Lung aeration loss during a successful weaning trial predicts postextubation distress, but may not be evaluable by plasma levels of sRAGE, a marker of alveolar type I epithelial cell injury.ClinicalTrials.gov NCT01098773.
| S-EPMC3664630 | biostudies-literature
Project description:BackgroundPathological scars, including keloids and hypertrophic scars, represent a significant dermatological challenge, and emerging evidence suggests a potential role for the gut microbiota in this process.MethodsUtilizing a two-sample Mendelian randomization (MR) methodology, this study meticulously analyzed data from genome-wide association studies (GWASs) relevant to the gut microbiota, keloids, and hypertrophic scars. The integrity and reliability of the results were rigorously evaluated through sensitivity, heterogeneity, pleiotropy, and directionality analyses.ResultsBy employing inverse variance weighted (IVW) method, our findings revealed a causal influence of five bacterial taxa on keloid formation: class Melainabacteria, class Negativicutes, order Selenomonadales, family XIII, and genus Coprococcus2. Seven gut microbiota have been identified as having causal relationships with hypertrophic scars: class Alphaproteobacteria, family Clostridiaceae1, family Desulfovibrionaceae, genus Eubacterium coprostanoligenes group, genus Eubacterium fissicatena group, genus Erysipelotrichaceae UCG003 and genus Subdoligranulum. Additional sensitivity analyses further validated the robustness of the associations above.ConclusionOverall, our MR analysis supports the hypothesis that gut microbiota is causally linked to pathological scar formation, providing pivotal insights for future mechanistic and clinical research in this domain.
| S-EPMC11250559 | biostudies-literature