11 research outputs found

    Sleep Deprivation Does Not Influence Photic Resetting of Circadian Activity Rhythms in Drosophila

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    Previous investigations in humans and rodent animal models have assessed the interplay of sleep in the circadian system’s phase responses to nighttime light exposure. The resulting data have been mixed, but generally support a modulatory role for sleep in circadian photic resetting (not an absolute requirement). Drosophila have been historically used to provide important insights in the sleep and circadian sciences. However, no experiments to date have evaluated how immediate sleep need or recent sleep history affects their pacemaker’s phase readjustments to light. We did so in the current study by (1) forcing separate groups of animals to stay awake for 1 or 4 h after they were shown a broadspectrum pulse (15 min during the first half of the night, 950 lux), or (2) placing them on a restricted sleep schedule for a week before light presentation without any subsequent sleep disruption. Forced sleep restriction, whether acute or chronic, did not alter the size of light-induced phase shifts. These data are consistent with observations made in other diurnal animals and raise the possibility, more broadly, that phototherapies applied during sleep—such as may be necessary during the winter months—may still be efficacious in individuals experiencing sleep-continuity problems such as insomnia

    Overexpression screen of chromosome 21 genes reveals modulators of Sonic hedgehog signaling relevant to Down syndrome

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    Trisomy 21 and mutations in the Sonic hedgehog (SHH) signaling pathway cause overlapping and pleiotropic phenotypes including cerebellar hypoplasia, craniofacial abnormalities, congenital heart defects and Hirschsprung disease. Trisomic cells derived from individuals with Down syndrome possess deficits in SHH signaling, suggesting that overexpression of human chromosome 21 genes may contribute to SHH-associated phenotypes by disrupting normal SHH signaling during development. However, chromosome 21 does not encode any known components of the canonical SHH pathway. Here, we sought to identify chromosome 21 genes that modulate SHH signaling by overexpressing 163 chromosome 21 cDNAs in a series of SHH-responsive mouse cell lines. We confirmed overexpression of trisomic candidate genes using RNA sequencing in the cerebella of Ts65Dn and TcMAC21 mice, model systems for Down syndrome. Our findings indicate that some human chromosome 21 genes, including DYRK1A, upregulate SHH signaling, whereas others, such as HMGN1, inhibit SHH signaling. Individual overexpression of four genes (B3GALT5, ETS2, HMGN1 and MIS18A) inhibits the SHH-dependent proliferation of primary granule cell precursors. Our study prioritizes dosage-sensitive chromosome 21 genes for future mechanistic studies. Identification of the genes that modulate SHH signaling may suggest new therapeutic avenues for ameliorating Down syndrome phenotypes. © 2023. Published by The Company of Biologists Ltd.Immediate accessThis item from the UA Faculty Publications collection is made available by the University of Arizona with support from the University of Arizona Libraries. If you have questions, please contact us at [email protected]

    Associations between Insomnia Symptoms and Anxiety Symptoms in Adults in a Community Sample of Southeastern Pennsylvania, USA

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    Although insomnia is reliably associated with anxiety symptoms, aspects of insomnia may differentially relate to one anxiety symptom versus another. Therefore, treatment for insomnia comorbidity with anxiety might be individually tailored to optimize treatment response. Working from this hypothesis, we analyzed data from a survey of 1007 community-dwelling adults. Insomnia was measured using the Insomnia Severity Index (ISI), categorizing items as nighttime disturbances, daytime dysfunction, or self-perceived dissatisfaction. Anxiety symptoms were measured with the Generalized Anxiety Disorder 7-item questionnaire (GAD-7). Linear and binomial logistic regression were used and adjusted for covariates. Post hoc forward stepwise analyses determined which components of the insomnia contributed to individual anxiety symptoms. Significant associations between nighttime disturbance (β = 0.88 [0.44, 1.3]), daytime dysfunction (β = 1.30 [0.81, 1.80]), dissatisfaction (β = 1.20 [0.60, 1.7]) and total GAD-7 score were maintained after adjusting for covariates. Nighttime disturbance was associated with excess worrying, restlessness, irritability, and fear of catastrophe. Daytime dysfunction was associated with all symptoms except for fear of catastrophe, and self-perceived dissatisfaction was associated with all symptoms except irritability. Stepwise analyses revealed that daytime dysfunction and dissatisfaction were most consistently related to anxiety symptoms. Greater attention should be paid to daytime dysfunction in patients with insomnia and anxiety, as improving daytime functioning may improve anxiety

    Onset insomnia and insufficient sleep duration are associated with suicide ideation in university students and athletes

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    Background: Previous work has shown that poor sleep is a prospective risk factor for suicide in clinical populations and might contribute to risk in the general population. The present study evaluated whether sleep distress, onset insomnia, and insufficient sleep are associated with suicide ideation in university students and athletes participating in the 2011-2014 National College Health Assessment (NCHA; n = 113,185). Methods: In the NCHA survey, students self-reported the presence or absence of suicide ideation within the past 12 months. SLEEP DISTRESS was assessed with an item indicating that "sleep difficulties" were "particularly traumatic or difficult to handle." ONSET INSOMNIA was assessed as at least 3 nights per week where survey participants reported an "extremely hard time falling asleep." INSUFFICIENT SLEEP was operationalized as the number of days per week where the participants felt they did not get "enough sleep to feel rested." All variables were yes/no except INSUFFICIENT SLEEP, which was categorized as 0-1 (reference), 2-3, 4-5, or 6-7 nights. Binary logistic regression analyses examined suicide ideation as the outcome and sleep variable as a predictor, adjusted for age, sex, year in school, recent depressed mood, and survey year. Associations within student-athletes were likewise assessed. Results: 7.4% of students reported suicide ideation within the past 12 months. In adjusted models, this was significantly associated with SLEEP DISTRESS (OR = 3.01, 95% CI [2.86, 3.16], p < 0.0001), ONSET INSOMNIA (OR = 1.95, 95% CI [1.86, 2.04], p < 0.0001), as well as INSUFFICIENT SLEEP (4-5 nights, OR = 1.41, 95% CI [1.28, 1.56], p < 0.0001; 6-7 nights, OR = 1.92, 95% CI [1.74, 2.13], p < 0.0001). Although suicide ideation was less common among athletes, ORs were similar for athletes for all sleep variables of interest. Conclusion: Sleep distress, onset insomnia, and insufficient sleep were all strongly related to suicide ideation among university students. These relationships were the same among collegiate athletes, even though this group reported less overall suicide ideation. Our findings suggest that university students may benefit from educational materials linking sleep disruption to maladaptive thinking and suicide ideation.12 month embargo; available online 24 May 2020This item from the UA Faculty Publications collection is made available by the University of Arizona with support from the University of Arizona Libraries. If you have questions, please contact us at [email protected]
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