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A particular form of sleep disturbance, delayed sleep phase, is often observed in young people with depression: actigraphy measurements have demonstrated that habitual sleep onset later than 1 00 a.m. is seen in 30% of young people with unipolar depression compared to only 10% of age-matched healthy controls [ 5].
In a sleep polysomnography study of depressed children and adolescents, decreased sleep efficiency and delayed sleep onset predicted recurrences within one year [ 17].
Obviously, when the sender has only one forwarding node, before it transmits data, the expected length of time required to wait for the receiver to wake up (called sleep delay) is half of the length of its sleeping time.
Polymorphisms of clock genes such as Per2 and Per3 have been associated with advanced sleep phase disorder, delayed sleep phase disorder, and diurnal preference [20] [23].
The most common adolescent sleep disorder is delayed sleep phase syndrome (5-10%) [ 16].
These findings suggest the bioregulatory mechanisms controlling sleep in adolescents delay sleep onset (sleep phase delay) and hence normal sleep times are truncated by societal requirements such as early school schedules.
Also, if a node suffers relatively less load, it can reduce the sleep delay by increasing its duty cycle.
The sleep delay of a path is the accumulated sleep delays of all edges in the path.
Therefore, sleep delay is an important component of end-to-end delay and plays an important role in it.
Therefore, when the sender is awake, its candidate relays are also awake, thus greatly reducing the sleep delay.
The most direct way to reduce the sleep delay is to increase the duty cycle of nodes.
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Justyna Jupowicz-Kozak
CEO of Professional Science Editing for Scientists @ prosciediting.com