bluuebunny/crossref_metadata_2025_split huggingface dataset:
0085 Dream Bizarreness Is Related to Specific Aspects of Metacognition That Are Influenced by Personality
Authors: Price Michael , Haque Zehra , Garza Lydia , Westerberg Carmen 
Published: April 2024

Abstract

Introduction
According to the continuity hypothesis, dreams reflect waking life experiences. Metacognition, the awareness of one’s thought processes, is minimal during typical dreaming but is assumed to be greater during lucid dreams, when the dreamer is aware they are dreaming and can sometimes control dream content. Therefore, one hypothesis is that lucid dreams may be more continuous with waking life than non-lucid dreams and thus contain less bizarre content than non-lucid dreams. However, support for this hypothesis is mixed and it may be incomplete, as metacognition typically includes multiple components, including the awareness of thinking and the regulation of processes involved in thinking. Additionally, these various metacognitive aspects may be differentially influenced by personality.

Methods
To further examine how dream bizarreness relates to metacognition, 416 participants completed a survey including measures of dreaming frequency, sleep quality, multiple aspects of metacognition, and the Big 5 personality traits. Participants also reported their most recent lucid and non-lucid dreams which were scored for bizarreness. Relationships between dream bizarreness, metacognition, and personality were subsequently assessed.

Results
Seventy-eight participants were able to report both a lucid and non-lucid dream and contributed to analyses. In contrast to the continuity hypothesis, lucid dreams were more bizarre than non-lucid dreams, and regression analyses revealed that non-lucid dream bizarreness positively predicted awareness of dream dissociation, whereas higher lucid dream bizarreness was associated with fewer negative beliefs about uncontrollability and danger. Finally, higher neuroticism and lower conscientiousness were associated with higher negative beliefs about uncontrollability and danger. No relationships between personality and dream dissociation were present.

Conclusion
The hypothesis that, due to greater metacognitive awareness, lucid dreams are less bizarre than non-lucid dreams, was not supported. Instead, bizarre non-lucid dreams may emerge with increased self-disconnection and bizarre lucid dreams may occur when worry about losing control and associated dangers therein is low. Additionally, due to the observed relationships between personality and metacognition, low neuroticism and high conscientiousness may also increase the bizarreness of lucid dreams. Collectively, these results suggest that dream bizarreness may reflect specific aspects of metacognition rather than a general awareness that one is dreaming.

Support (if any)
0091 Influence of Evening Alcohol Intake on Nocturnal Heart Rate
Authors: Bender Stephen , Bigalke Jennifer , Bigalke Jeremy , Carter Jason 
Published: April 2024

Abstract

Introduction
Binge alcohol consumption has detrimental effects on cardiovascular health and sleep. The simultaneous influence on sleep and cardiovascular measures may lead to an adverse nocturnal cardiac profile. The aim of the present study was to examine the impact of evening alcohol consumption on nocturnal heart rate (HR) patterns. We hypothesized that alcohol intake would result in a sustained increase in HR throughout the night and reduced HR dipping relative to pre-sleep wakefulness.

Methods
In a randomized crossover design, ten participants (5 male, 5 female; 26±2 yrs; 28±1 kg/m2) underwent a night of binge alcohol consumption and a fluid control separated by one month. Sleep and nocturnal HR were measured using continuous overnight polysomnography and electrocardiogram. HR was averaged across 15-minute intervals over the 8-hour sleep period.

Results
Consistent with our initial hypothesis, a condition effect was observed whereby average raw HR was increased following alcohol consumption (Fluid Control: 60±3 vs. Alcohol: 66±3 beats/min, p=0.003). This condition effect was absent when examining average change in HR relative to a 15-minute wakefulness period (Fluid Control: ∆-2.3±0.6 vs. Alcohol: ∆-2.7±1.1 beats/min change, p=0.75). A condition x time effect was present in both average raw HR (p=0.003) and relative HR change from wakefulness (p=0.01). Contrary to our hypothesis, post hoc analyses revealed that the alcohol condition demonstrated augmented relative HR dipping 15 (Fluid Control: ∆-3.2±0.6 vs. Alcohol: ∆-4.8±0.8 beats/min) and 30 minutes (Fluid Control: ∆-3.1±1.1 vs. Alcohol: ∆-6.0±1.0 beats/min) after lights out. However, a substantial increase in relative HR was observed in the alcohol condition when compared to the control 210 (Fluid Control: ∆-3.1±0.8 vs. Alcohol: ∆1.1±1.0 beats/min) and 225 minutes (Fluid Control: ∆-3.6±0.6 vs. Alcohol: ∆1.6±1.5 beats/min) after lights out.

Conclusion
Evening binge alcohol consumption increased HR throughout the sleep period. The overnight profile demonstrated that alcohol elicited a steeper decline in nocturnal HR immediately after lights out, but a significant augmentation of HR during the later portion of the night. The observed elevation in overall HR and further relative increase in the second half of the night may contribute to cardiovascular risk following alcohol intake.

Support (if any)
NIH (AA-024892; U54GM115371; P20GM103474).
0092 Influence of Evening Alcohol Consumption on Nocturnal Cardiac Reactivity During NREM vs REM Sleep
Authors: Beisert Jenna-Marie , Talukdar Ankita , Solis-Montenegro Tatiana , Bigalke Jennifer , Bigalke Jeremy , Carter Jason 
Published: April 2024

Abstract

Introduction
Chronic alcohol consumption disrupts sleep, especially rapid eye movement (REM). However, the impact of alcohol on nocturnal cardiovascular responses to cortical arousal during non-REM (NREM) and REM sleep remains unknown. This present study investigated the impact of evening binge alcohol on heart rate (HR) reactivity following nocturnal cortical arousals in NREM vs. REM sleep. We hypothesized that alcohol intake would lead to increased HR responsiveness following cortical arousals in both sleep stages.

Methods
Fifteen healthy adults (6 male, 9 female; 27±2 yrs.; 28±1 kg/m2) underwent two testing conditions (i.e., alcohol vs fluid control) separated by one month in a randomized cross-over design. In the alcohol condition, a dosage of 4-5 drinks, two hours before bed was given based off the NIAAA definition of binge drinking (i.e., 1g/kg men, 0.85 g/kg women). In the control condition, a volume matched fluid-control was used. Overnight polysomnography with continuous electrocardiogram was used to quantify sleep, arousals, and nocturnal HR following each condition. HR responses were characterized for 20 cardiac cycles following spontaneous cortical arousals.

Results
Absolute HR was elevated following binge alcohol consumption in both REM (Placebo: 65±2 vs. Alcohol: 73±3 beats/min, p&lt; 0.001) and NREM (Placebo: 64±2 vs. Alcohol: 71±3 beats/min, p&lt; 0.001) sleep. In NREM there was a significant condition x time effect in HR reactivity (p&lt; 0.001). NREM early phase HR arousal responsiveness was blunted in cardiac cycles 2,3, and 4 (all p&lt; 0.05) following alcohol consumption, but HR remained elevated in the latter half at cardiac cycle 15 (Placebo: Δ-0.9±1.0 vs. Alcohol: Δ0.9±0.7 beats/min, P=0.038). There was no condition (P=0.916) or condition x time interaction effect (P=0.999) on HR reactivity during REM sleep.

Conclusion
The present study observed an increase in absolute HR in both REM and NREM sleep following evening alcohol intake. However, alcohol has differential effects on HR reactivity to arousal during REM and NREM sleep, whereby the initial HR response to cortical arousals is blunted, but the recovery response is augmented during NREM sleep. These findings point to a stage-specific effect of evening binge alcohol consumption on nocturnal cardiac reactivity to naturally occurring arousals.

Support (if any)
NIH (AA-024892; U54GM115371; P20GM103474).
0093 Acute Effects of Diaphragmatic Breathing on Circulatory Dynamics and Autonomic Function During Sleep in Young Men
Authors: Kobayashi Ryota , Negoro Hideyuki 
Published: April 2024

Abstract

Introduction
Increased arterial stiffness during rest and blood pressure (BP) during sleep are independent risk factors for cardiovascular disease (Boutouyrie et al.2021, Kario et al.2019). Slow, deep breathing is a useful nonpharmacological intervention to control hypertension (Chang et al.2013). However, the acute effects of diaphragmatic breathing before sleep on arterial stiffness during rest and BP during sleep are unknown. In this study, we investigated the acute effects of diaphragmatic breathing before sleep on arterial stiffness, BP, and cardiac autonomic function in young men.

Methods
Fifteen healthy young men (age: 20.0 ± 0 years, Height: 170 ± 5 cm, Weight: 56 ± 3 kg) participated in this study and underwent two separate sessions in a randomized controlled crossover design: 4-4-8 breathing (BT) protocol (12 consecutive breaths of 4 seconds of inhalation, 4 seconds of pause, and 8 seconds of exhalation through the nose) and control (CON) without 4-4-8 breathing. Brachial-ankle pulse wave velocity (PWV) reflected systemic arterial stiffness and carotid-femoral PWV reflecting central (aortic) arterial stiffness measured using an automated pulse wave testing device. BP was measured simultaneously using an automated oscillometric device. Autonomic function was measured from high-frequency (HF) and low-frequency (LF) components by HR variability spectral analysis. Arterial stiffness, BP, HF, and LF were measured before (baseline) and 30 and 60 min and 24 hours after the 4-4-8 breathing technique. BP, HF, and LF were measured while sleeping.

Results
There was a significant decrease in the baPWV and LF at 30 min after the BT trial compared to baseline values (P&lt; 0.05). cfPWV on both trials was unchanged. There was a significant increase in the HF at 30 min after the BT trial compared to baseline values (P&lt; 0.05). BP and LF during sleep were lower in the BT trial than in the CON trial (P&lt; 0.05). HF during sleep was higher in the BT trial than in the CON trial (P&lt; 0.05).

Conclusion
A novel finding of this study is that practicing slow, diaphragmatic breathing with relatively long exhalation times may reduce arterial stiffness during rest and BP during sleep through activation of the parasympathetic nervous system.

Support (if any)
0094 Habitual Sleep and Autonomic Function in Humans
Authors: Solis-Montenegro Tatiana , Bigalke Jeremy , Bigalke Jennifer , Carter Jason 
Published: April 2024

Abstract

Introduction
Insufficient habitual sleep duration and efficiency are commonly experienced in modern society and are associated with cardiovascular disease development. A potential mediator of this relationship may be impairment in cardiovascular regulation via the autonomic nervous system. The purpose of the present study was to assess the relationships between habitual total sleep time (TST), sleep efficiency (SE), muscle sympathetic nerve activity (MSNA), and heart rate variability (HRV) in a robust sample of healthy adults. We hypothesized that shorter TST would be associated with increased sympathetic and decreased parasympathetic activity.

Methods
A minimum 7 days of at-home, objective actigraphy sleep monitoring was collected in 75 healthy young adults (39 males, 36 females; 24±1 years; 25±1 kg/m2). In each participant, three seated sphygmomanometer recordings were used to determine resting mean arterial blood pressure (MAP). Prior to laboratory testing, participants were asked to refrain from caffeine and exercise for 12 hours, and alcohol for 24 hours. All participants underwent an autonomic function test that simultaneously assessed heart rate (HR, electrocardiogram), beat-to-beat blood pressure (finger plethysmography) and MSNA (microneurography) during 10 minutes of quiet rest. R-R intervals were used to quantify both time (i.e., RMSSD and pNN50) and frequency (high-frequency heart rate variability; HF-HRV) domain HRV parameters. RMSSD and HF-HRV were log-transformed due to non-normal distributions.

Results
Contrary to our hypothesis, habitual TST was not associated with resting MAP (R=0.173, P=0.137), HR (R=-0.137, P=0.241), MSNA (R=-0.186, P = 0.110), RMSSDlog10 (R=0.085, P=0.468), pNN50 (R=0.043, P=0.711), or HF-HRVlog10 (R=0.019, P=0.869). Similarly, SE was not associated with resting MAP (R=0.112, P=0.339), HR (R=-.037, P=0.751), MSNA (R=-0.033, P = 0.778), RMSSDlog10 (R=-0.006, P=0.956), pNN50 (R= -0.003, P=0.983), or HF-HRV (R=-0.028, P=0.810).

Conclusion
Our findings do not support a relationship between habitual TST or SE and measures of autonomic nervous system activity in healthy adults. However, a more pronounced effect may be observed in populations with established sleep disorders such as insomnia and obstructive sleep apnea. Further research is necessary to establish the independent effect of objective sleep quantity and quality on autonomic control in these populations.

Support (if any)
NIH AA-024892
0096 Simulated Night Shift Schedule Alters Endogenous Temporal Regulation of Glucose and Insulin
Authors: Lundholm Kirsie , Skene Debra , McDermott Jason , Liu Peter , Gaddameedhi Shobhan , Van Dongen Hans , Satterfield Brieann 
Published: April 2024

Abstract

Introduction
Shift workers experience misalignment between internally-driven circadian rhythms and externally-driven behavioral schedules. Mounting evidence from hormone-, cytokine-, exosome-, proteome-, and metabolome-based biomarker analyses of blood samples predicts disruption of glucose and insulin regulatory pathways during night shift schedules. Here, we quantified circulating glucose and insulin concentrations in a constant routine (CR) protocol to assess functional metabolic outcomes of prior simulated shift work.

Methods
Healthy adults (N=14; aged 22–34; 4 females) completed a 7-day/6-night in-laboratory study, with randomization to either a 3-day simulated day shift (DS) schedule (n=7) with nighttime sleep (22:00–06:00) and 3 daytime meals (07:30, 13:00, 19:30), or a 3-day simulated night shift (NS) schedule (n=7) with daytime sleep (10:00–18:00) and 3 nighttime meals (19:30, 01:00, 07:30). A 24h CR protocol followed, during which participants stayed awake under constant behavioral and environmental conditions, including hourly isocaloric snacks. Serum collected via intravenous catheter every 6h during the CR was assayed using glucose colorimetric detection and human insulin ELISA. Glucose and insulin concentrations were analyzed with mixed-effects ANOVAs with fixed effects of prior simulated shift condition (day, night) and sampling time (01:30, 07:30, 13:30, 19:30) and their interaction, with a random effect over participants on the intercept. Mixed-effects cosinor regression analyses were conducted to compare endogenous circadian rhythms between conditions.

Results
For glucose, there was a significant condition*time interaction (F[3,30]=4.99, P=0.006), with a 9.34±2.42h delay (mean±SE) of the endogenous circadian glucose rhythm after simulated NS compared to DS (t[12]=3.85, P=0.002). For insulin, there were significant effects of condition (F[1,30]=5.93, P=0.021) and time (F[3,30]=3.01, P=0.046), with no significant endogenous rhythmicity after simulated DS, but the appearance of a circadian rhythm with reduced insulin concentrations after simulated NS (t[12]=-3.32, P=0.006).

Conclusion
Under constant routine, we found altered endogenous temporal patterns of glucose and insulin after just 3 days of simulated NS compared to DS. Our results indicate that biomarker and omics-based predictions of disrupted glucose and insulin regulatory pathways have functional significance evident in circulating glucose and insulin concentrations. This may explain the insulin resistance and increased risk of metabolic disorders observed in shift workers.

Support (if any)
Andy Hill CARE Fund FY22-POP-02 and WSU CPPS start-up funds
0097 Cardiovascular Effects of Long-Term Sleep Fragmentation in Mice
Authors: Badran Mohammad , Puech Clementine , Khalyfa Abdelnaby , Gozal David 
Published: April 2024

Abstract

Introduction
Sleep Fragmentation (SF) is a prevalent phenomenon and also a pathognomonic feature of obstructive sleep apnea (OSA). SF is associated with OSA-related morbidities. However, it remains unclear whether prolonged SF exposures contribute to the development of specific cardiovascular morbidities in OSA. In this study, we postulate that chronic SF may induce structural and functional changes in the cardiac and vascular systems.

Methods
Male C57Bl/6J mice (n=8) were housed in custom-designed cages with a near-silent motorized mechanical sweeper crossing the cage in 2-min intervals or sleep control (SC, sweeper inactive) for 12 hours during the light period for 12 weeks. Mean arterial blood pressure (MBP) was assessed using tail-cuff method, while aortic peak velocity (indicator of systolic function), E/A ratio (indicator of diastolic function), coronary flow velocity reserve (CFVR), and pulse wave velocity (PWV) were assessed using Doppler Flow Velocity System. Then, left anterior descending coronary arteries and thoracic aorta were excised, mounted on wire myographs, and used to obtain endothelium-dependent relaxation dose-response curves to acetylcholine (ACh)

Results
MBP was significantly elevated in SF mice (107 ± 7 mmHg) after 12 weeks when compared to SC (89 ± 5 mmHg, p &lt; 0.0001). Systolic and diastolic function, and CFVR were not affected by the 12 weeks of SF exposure. However, SF mice had higher PWV (4.3 ± 0.6 mm/msec) when compared to SC mice (3.1 ± 0.2 mm/msec). Coronary maximal ACh-induced vasodilation was impaired in SF mice (67 ± 9%) when compared to SC (86 ± 5%, p &lt; 0.001). Aortic maximal ACh-induced vasodilation was not affected by 12 weeks of SF.

Conclusion
long-term SF, a hallmark characteristic of OSA, promotes cardiovascular perturbations including coronary artery dysfunction and arterial stiffness, thereby supporting a role for sleep fragmentation in the cardiovascular morbidity of OSA.

Support (if any)
Supported by NIH grant R01-HL166617
0098 Chronic Sleep Restriction Results in Abnormal Bone Development in Adolescent Rats
Authors: Everson Carol , Toth Jeffrey , Wang Mei 
Published: April 2024

Abstract

Introduction
Adolescence is often plagued by years of inadequate sleep at a time when nearly half of the adult skeletal mass is accrued and peak bone mass is attained. Previously we reported that chronic sleep restriction (SR) in adult male rats causes strikingly abnormal bone health. The purpose of this study was to test our hypothesis that SR results in abnormal bone development.

Methods
Chronic SR in juvenile rats from 42–60 d of age was produced by a validated modification of the Bergmann-Rechtschaffen paradigm with ambulation controls (AC). For five-day periods, sleep time was protected for 4 hours/day to model late bedtimes and early awakenings on schooldays, with a 35% sleep reduction for the rest of the time. Between five-day SR periods, sleep was undisturbed for 48 hours to model weekend catch-up sleep. Harvested femurs were studied for bone integrity by biomechanical testing (males and females, SR vs AC, N=3-4/sex/grp) and bone quality by micro-CT (male SR vs AC, N=4/grp). To investigate recovery, other male rats were studied at 90 and 120 d of age (N=5-6/grp) after chronic SR during 42–60 d of age.

Results
Chronic SR resulted in weak femurs, indicated by a 21% decrease in work to failure by three-point bending [N=7-8/grp pooled sexes, SR: 57 (SD 14); AC: 72 (SD 13) mJ, P&lt; 0.02)]. By sex, there was a 23% decreased work to failure in male SR juveniles (P&lt; 0.03) and a nonsignificant 17% decrease in female SR juveniles vs AC, but no differences in fat or lean body mass, leg muscle masses or femoral length. Trabeculae were decreased in number [SR vs AC, 1.9 (SD 0.4) and 2.4 (SD 0.4) /mm, P&lt; 0.05] with increased spacing [SR vs AC, 552 (SD 122) and 419 (SD 66) µm, P=0.05]. In post-SR rats aged to 90 and 120 d, femoral work to failure was decreased by &gt;44% (P&lt; 0.004, P&lt; 0.03 respectively).

Conclusion
Chronic SR during adolescence results in abnormal bone development with deficits that persist into adulthood. Failure to achieve peak bone mass or maintain bone in adolescence is known to significantly affect the progression to osteopenia/osteoporosis in later life.

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0099 Impact of Sleep and Timing of Vaccination on Neutralizing Antibody Responses to the COVID-19 Vaccine
Authors: Prather Aric , Dutcher Ethan , Mason Ashley , Robinson James , Drury Stacy , Hecht Frederick , Epel Elissa 
Published: April 2024

Abstract

Introduction
Vaccines remain the primary mitigating strategy to reduce the burden of disease caused by COVID-19. As such, there is a pressing need to identify factors that promote more robust and durable immune responses to vaccination. Sleep and circadian processes, such as the timing of vaccine administration, have been hypothesized to play a meaningful role in predicting durability of antibody responses; however, empirical data supporting links between sleep and timing on COVID-19 vaccine response is limited.

Methods
We recruited 428 adults (aged 18-88 years old) naive to the COVID-19 vaccination series and SARS-CoV-2 infection who received the mRNA COVID-19 vaccine series (% Pfizer; % Moderna) and underwent blood draws to quantify neutralizing antibody responses (nAB) 1 and 6 months post vaccination series. They completed sleep questionnaires (Pittsburgh Sleep Quality Index) and a week of sleep diaries at three time points. In addition, 198 participants wore a wearable device (Oura Ring) for 2 months to capture behavioral sleep metrics. Time of day of vaccine was obtained by self-report as part of the daily diaries.

Results
Analyses revealed that independent of age, sex, BMI, smoking status, and vaccine type, poorer global sleep quality was associated with lower nABs 6-months post vaccination (F(1, 424.3)=5.30, p=0.02). We also did detected a trend-level 3-way interaction between vaccine type, time point, and OURA based sleep duration indicating that shorter sleep duration was associated with lower 6-month nAB in those who received the Pfizer vaccine (b=0.17, SE=0.07, p=0.009). In analyses examining the impact of time of day of vaccine administration on nABs, we failed to find any evidence that timing of vaccine administration was associated with nABs at 1 or 6 months post vaccination (Dose 1: F(1, 330.1)=0.01, p=0.91; Dose 2: F(1, 344.5)=0.46, p=0.50).

Conclusion
Findings suggest that better global sleep quality is associated with greater nAB durability to the COVID-19 vaccine, and among those who received the Pfizer vaccine, longer average sleep duration promoted higher nAB 6-months post-vaccination. However, there was no clear evidence indicating that timing of vaccination administration was relevant to nAB responses. Further research is warranted including investigations into whether sleep interventions can enhance vaccine efficacy.

Support (if any)
R24AG048024