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In Cohort 1, an additional polymorphism (variable-number tandem repeat in per3) was also determined.Adjusting for multiple tests, none of the candidate gene SNPs were significantly associated with the amount of wake time after sleep onset (WASO), a marker of sleep consolidation.
Such an unexpected relationship raises a number of new questions about the relationship of wake time to subsequent REM sleep and/or how REM sleep time effects subsequent wake time.
The third phenotype was characterised by a longer Total Sleep Time, shorter REM Latencies, and a higher percentage of REM and lower percentage of wake time.
The final phenotype had the shortest Total Sleep Time and the highest percentage of wake time and wake after sleep onset.
Additionally, this group demonstrated the shortest Sleep Onset and REMLs, lowest WASO and percentages of wake time and stage 1 sleep, and the lowest number of awakenings.
Apart from a significant, albeit minor increase in the percentage of wake time after sleep onset in the obese group, all polysomnographic variables were not significantly different between the obese and non-obese cohorts (Additional file 1, Table S4).
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This applies to the more than 15 hours of waking time not spent exercising.
It is intriguing that the increased locomotor intensity, during the dark period and the very beginning of light period, did not continue during the remaining light period although a substantial amount of waking time still occurred.
Objective measures of waking time using accelerometers or other devices are also helpful in ensuring the accuracy of sample timing (Dockray et al., 2008).
Although self-reports of wake-time, or activity and sleep monitors may provide evidence of waking, they do not denote the actual timing of saliva samples post-waking.
In addition, sensitivity and specificity tests were conducted for a range of wake-time severity cutoffs based on 2-week mean sleep-log data.
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