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[This corrects the article DOI: 10.1162/netn_a_00272.].

Sleep inertia is the brief period of impaired alertness and performance experienced immediately after waking. Little is known about the neural mechanisms underlying this phenomenon. A better understanding of the neural processes during sleep inertia may offer insight into the awakening process. We observed brain activity every 15 min for 1 hr following abrupt awakening from slow wave sleep during the biological night. Using 32-channel electroencephalography, a network science approach, and a within-subject design, we evaluated power, clustering coefficient, and path length across frequency bands under both a control and a polychromatic short-wavelength-enriched light intervention condition. We found that under control conditions, the awakening brain is typified by an immediate reduction in global theta, alpha, and beta power. Simultaneously, we observed a decrease in the clustering coefficient and an increase in path length within the delta band. Exposure to light immediately after awakening ameliorated changes in clustering. Our results suggest that long-range network communication within the brain is crucial to the awakening process and that the brain may prioritize these long-range connections during this transitional state. Our study highlights a novel neurophysiological signature of the awakening brain and provides a potential mechanism by which light improves performance after waking. Using a graphical framework approach, our findings suggest that following awakening from slow wave sleep: (a) a prioritization scheme may underlie recovery rates for different behaviors; (b) long-range neural connections orchestrating local-global operations are uniquely disrupted; and (c) light is able to minimize disruption to long-range connections, revealing the potential mechanism through which light acts as a countermeasure. This research (a) advances the knowledge of neural processes during the transition from sleep to wakefulness; (b) demonstrates a mechanism underlying a brain-behavior relationship that may serve as a target for future countermeasure research; and (c) applies a novel methodological approach to sleep-wake brain states. Further research is needed to apply this analytical method to alternative interventions and sleep-wake transition scenarios.

PurposeThe composition of the subchondral bone marrow and cartilage endplate (CEP) could affect intervertebral disc health by influencing vertebral perfusion and nutrient diffusion. However, the relative contributions of these factors to disc degeneration in patients with chronic low back pain (cLBP) have not been quantified. The goal of this study was to use compositional biomarkers derived from quantitative MRI to establish how CEP composition (surrogate for permeability) and vertebral bone marrow fat fraction (BMFF, surrogate for perfusion) relate to disc degeneration.MethodsMRI data from 60 patients with cLBP were included in this prospective observational study (28 female, 32 male; age = 40.0 ± 11.9 years, 19–65 [mean ± SD, min–max]). Ultra-short echo-time MRI was used to calculate CEP T2* relaxation times (reflecting biochemical composition), water-fat MRI was used to calculate vertebral BMFF, and T1ρ MRI was used to calculate T1ρ relaxation times in the nucleus pulposus (NP T1ρ, reflecting proteoglycan content and degenerative grade). Univariate linear regression was used to assess the independent effects of CEP T2* and vertebral BMFF on NP T1ρ. Mixed effects multivariable linear regression accounting for age, sex, and BMI was used to assess the combined relationship between variables.ResultsCEP T2* and vertebral BMFF were independently associated with NP T1ρ (p = 0.003 and 0.0001, respectively). After adjusting for age, sex, and BMI, NP T1ρ remained significantly associated with CEP T2* (p = 0.0001) but not vertebral BMFF (p = 0.43).ConclusionPoor CEP composition plays a significant role in disc degeneration severity and can affect disc health both with and without deficits in vertebral perfusion.

Purpose: Increased sugar consumption is associated with metabolic conditions that can result in poor health outcomes. To investigate the impact of sugars such as glucose and fructose in the body, this study aims to determine the timing of effects and assess the impact of these effects. This study aims to demonstrate acute effects in metabolism as a result of sugar metabolism.Methods: Six male participants were imaged on a 3T MRI scanner at a fasted state then subsequently every hour for up to eight measurements. Between scanning sessions, they consume a 13C labeled glucose or fructose shake, have breath collected, and have blood drawn; this is repeated on a separate day to satisfy the other experimental condition. The MRI exam consists of Proton Density Fat Fraction (PDFF), proton Magnetic Resonance Spectroscopy (1H MRS), and 13C MRS. The images are processed to analyze liver volume and the spectra from the MR Spectroscopy are normalized and the peaks are quantified.Results: Liver volume is significantly different from baseline measurements at 2-, 3-, and 4-hours post-feeding with p=0.032, p=0.003, and p=0.009 respectively. Fat content is significantly different from baseline measurements at 3- and 4-hours post-feeding with p=0.026 and p=0.048 respectively. Different MR measures of fat fraction in the body produce a significant positive correlation (p=0.003). The median change of lipids (CH2) positively correlates with the median change in glycerol (p=0.011). Fat fraction does not significantly correlate with the blood measures taken, but when high choline and low choline groups are separated, new formed lipids in the blood and long-term storage of fat differ significantly, p=0.021 and p=0.03 respectively.Conclusions: Choline classification of participants resulted in a difference in new lipids in the blood and long-term storage in the liver. Low choline individuals tended to export less lipids in the blood and store more in the liver. High choline individuals exported more lipids and retained less in the liver. MR exams of the liver evaluate the health of the liver and burden to abdominal organs, whereas blood collection provided a glimpse into cardiovascular burden.

Sleep inertia is the brief period of impaired alertness and performance experienced immediately after waking. While the neurobehavioral symptoms of sleep inertia are well-described, less is known about the neural mechanisms underlying this phenomenon. A better understanding of the neural processes during sleep inertia may offer insight into the cognitive impairments observed and the awakening process generally. We observed brain activity following abrupt awakening from slow wave sleep during the biological night. Using electroencephalography (EEG) and a network science approach, we evaluated power, clustering coefficient, and path length across frequency bands under both a control condition and a blue-enriched light intervention condition in a within-subject design. We found that under control conditions, the awakening brain is typified by an immediate reduction in global theta, alpha, and beta power. Simultaneously, we observed a decrease in the clustering coefficient and an increase in path length within the delta band. Exposure to blue-enriched light immediately after awakening ameliorated these changes, but only for clustering. Our results suggest that long-range network communication within the brain is crucial to the waking process and that the brain may prioritize these long-range connections during this transitional state. Our study highlights a novel neurophysiological signature of the awakening brain and provides a potential mechanistic explanation for the effect of light in improving performance after waking. Competing Interest Statement The authors have declared no competing interest.