Repeated Administration Effects on Psychomotor Vigilance Test Performance.

Study Objectives: The Psychomotor Vigilance Test (PVT) is reported to be free of practice effects that can otherwise confound the effects of sleep loss and circadian misalignment on performance. This differentiates the PVT from more complex cognitive tests. To the best of our knowledge, no study has systematically investigated practice effects on the PVT across multiple outcome domains, depending on administration interval, and in ecologically more valid settings. Methods: We administered a validated 3-minute PVT (PVT-B) 16 times in 45 participants (23 male, mean ± SD age 32.6 ± 7.3 years, range 25-54 years) with administration intervals of ≥10 days, ≤5 days, or 4 times per day. We investigated linear and logarithmic trends across repeated administrations in 10 PVT-B outcome variables. Results: The fastest 10% of response times (RT; plin = .0002), minimum RT (plog = .0010), and the slowest 10% of reciprocal RT (plog = .0124) increased while false starts (plog = 0.0050) decreased with repeated administration, collectively decreasing RT variability (plog = .0010) across administrations. However, the observed absolute changes were small (e.g., -0.03 false starts per administration, linear fit) and are probably irrelevant in practice. Test administration interval did not modify the effects of repeated administration on PVT-B performance (all p > .13 for interaction). Importantly, mean and median RT, response speed, and lapses, which are among the most frequently used PVT outcomes, did not change systematically with repeated administration. Conclusions: PVT-B showed stable performance across repeated administrations. Combined with its high sensitivity, this corroborates the status of the PVT as the de facto gold standard measure of the neurobehavioral effects of sleep loss and circadian misalignment.

Inter-individual Differences in the Effects of Aircraft Noise on Sleep Fragmentation.

STUDY OBJECTIVES: Environmental noise exposure disturbs sleep and impairs recuperation, and may contribute to the increased risk for (cardiovascular) disease. Noise policy and regulation are usually based on average responses despite potentially large inter-individual differences in the effects of traffic noise on sleep. In this analysis, we investigated what percentage of the total variance in noise-induced awakening reactions can be explained by stable inter-individual differences. METHODS: We investigated 69 healthy subjects polysomnographically (mean ± standard deviation 40 ± 13 years, range 18-68 years, 32 male) in this randomized, balanced, double-blind, repeated measures laboratory study. This study included one adaptation night, 9 nights with exposure to 40, 80, or 120 road, rail, and/or air traffic noise events (including one noise-free control night), and one recovery night. RESULTS: Mixed-effects models of variance controlling for reaction probability in noise-free control nights, age, sex, number of noise events, and study night showed that 40.5% of the total variance in awakening probability and 52.0% of the total variance in EEG arousal probability were explained by inter-individual differences. If the data set was restricted to nights (4 exposure nights with 80 noise events per night), 46.7% of the total variance in awakening probability and 57.9% of the total variance in EEG arousal probability were explained by inter-individual differences. The results thus demonstrate that, even in this relatively homogeneous, healthy, adult study population, a considerable amount of the variance observed in noise-induced sleep disturbance can be explained by inter-individual differences that cannot be explained by age, gender, or specific study design aspects. CONCLUSIONS: It will be important to identify those at higher risk for noise induced sleep disturbance. Furthermore, the custom to base noise policy and legislation on average responses should be re-assessed based on these findings.

The DNA damage response in filamentous fungi.

The mechanisms used by fungal cells to repair DNA damage have been subjects of intensive investigation for almost 50 years. As a result, the model yeasts Schizosaccharomyces pombe and Saccharomyces cerevisiae have led the way in yielding critical insights into the nature of the DNA damage response. At the same time, largely through the efforts of Etta Kafer, Hirokazu Inoue, and colleagues, a substantial collection of Aspergillus nidulans and Neurospora crassa DNA repair mutants has been identified and characterized in detail. As the analysis of these mutants continues and increasing amounts of annotated genome sequence become available, it is becoming readily apparent that the DNA damage response of filamentous fungi possesses several features that distinguish it from the model yeasts. These features are emphasized in this review, which describes the genes, regulatory networks, and processes that compose the fungal DNA damage response. Further characterization of this response will likely yield general insights that are applicable to animals and plants. Moreover, it may also become evident that the DNA damage response can be manipulated to control fungal growth.