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Delirium is a heterogeneous syndrome primarily characterized by fluctuations in attention and awareness. Sleep–wake disturbances are a common and significant feature of delirium and can manifest as circadian rhythm inversion, sleep fragmentation, and reduced rapid eye movement (REM) and slow‐wave sleep. Some literature suggests that the relationship between sleep disruption and delirium is reciprocal wherein the two reinforce one another and may share an underlying etiology. As there are no FDA‐approved medications for delirium or delirium‐related sleep disturbances, management is primarily focused on addressing underlying medical concerns and promoting physiologic circadian patterns with non‐pharmacological behavioral interventions. In practice, however, medications are often used, albeit with limited evidence to support their use. This literature review explores the pharmacology and pharmacokinetics of several medications with literature investigating their use in delirium: melatonin, ramelteon, dual orexin receptor antagonists (DORAs), and dexmedetomidine. Current evidence suggests a possible benefit of ramelteon or melatonin, dexmedetomidine for patients in the ICU setting, and DORAs as therapeutic options for the re‐regulation of sleep–wake cycle disruption in delirium. We discuss pertinent pharmacokinetic and pharmacodynamic factors that may influence clinical decision‐making regarding these interventions. [ABSTRACT FROM AUTHOR]

Abstract Background In bluegill sunfish, the melanin-containing pigment granules of the retinal pigment epithelium undergo cyclic movements in response both to ambient lighting and circadian cues. Pigment granules aggregate into the cell body at night (in the dark), and disperse into apical processes during the day (in the light). Regulation of pigment granule aggregation in a number of fishes depends on modulating the intracellular levels of cyclic adenosine monophosphate. Results Here we show isolated RPE takes up cyclic adenosine monophosphate (cAMP) in a saturable manner, exogenously applied cAMP induces pigment granule aggregation in retinal pigment epithelium isolated from bluegill, and aggregation induced in this manner is inhibited by treatment with probenecid, an organic anion transport inhibitor. Conclusion Our results raise the possibility that cAMP functions as a messenger secreted from the neural retina to signal darkness to the RPE, which takes it up. It further suggests that organic anion transport systems are the route by which cAMP crosses RPE cell membranes since probenecid inhibits extracellular cAMP from causing pigment granule aggregation.

Background: The effects of gender, headaches, and their interaction on sleep health (sleep duration, sleep onset and continuity, and indications of hypersomnolence) have not been well studied. Materials and Methods: For American adolescents, we contrasted sleep health variables between males (n = 378) and females (n = 372) and between individuals with chronic headaches (n = 102 females and 60 males) and without chronic headaches (n = 270 females and 318 males) using data from surveys. Results: Not all measures of sleep health differed between groups, but the following patterns were observed for the measures that did differ. Females reported shorter sleep durations on school nights ( p = 0.001), increased likelihood of sleepiness on school days ( p < 0.05), and higher hypersomnolence scores compared with males ( p = 0.005). Individuals with headaches reported shorter sleep durations on weekends ( p = 0.009) and higher hypersomnolence scores ( p = 0.009) than individuals without headaches. Interestingly, females with headaches reported worse sleep health than females without headaches for multiple measures. Males with headaches did not differ from males without headaches, except for greater waking at night ( p = 0.04). Conclusions: These results are consistent with other studies of gender-based differences in sleep health and emphasize the importance of recognizing the risk of headache in female adolescents and treating that condition to prevent additional sleep health issues. [ABSTRACT FROM AUTHOR]

Background: In bluegill sunfish, the melanin-containing pigment granules of the retinal pigment epithelium undergo cyclic movements in response both to ambient lighting and circadian cues. Pigment granules aggregate into the cell body at night (in the dark), and disperse into apical processes during the day (in the light). Regulation of pigment granule aggregation in a number of fishes depends on modulating the intracellular levels of cyclic adenosine monophosphate. Results: Here we show isolated RPE takes up cyclic adenosine monophosphate (cAMP) in a saturable manner, exogenously applied cAMP induces pigment granule aggregation in retinal pigment epithelium isolated from bluegill, and aggregation induced in this manner is inhibited by treatment with probenecid, an organic anion transport inhibitor. Conclusion: Our results raise the possibility that cAMP functions as a messenger secreted from the neural retina to signal darkness to the RPE, which takes it up. It further suggests that organic anion transport systems are the route by which cAMP crosses RPE cell membranes since probenecid inhibits extracellular cAMP from causing pigment granule aggregation. [ABSTRACT FROM AUTHOR]