Controlled, experimental studies on the effects of acute sleep loss in humans have shown that mediators of inflammation are altered by sleep loss. Elevations in these mediators have been found to occur in healthy, rigorously screened individuals undergoing experimental vigils of more than 24 hours, and have also been seen in response to various durations of sleep restricted to between 25 and 50% of a normal 8 hour sleep amount. While these altered profiles represent small changes, such sub-clinical shifts in basal inflammatory cytokines are known to be associated with the future development of metabolic syndrome disease in healthy, asymptomatic individuals. Although the mechanism of this altered inflammatory status in humans undergoing experimental sleep loss is unknown, it is likely that autonomic activation and metabolic changes play key roles.

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Stress often co-occurs with inadequate sleep duration, and both are believed to impact mood and emotion. It is not yet known whether inadequate sleep simply increases the intensity of subsequent stress responses or interacts with stressors in more complicated ways. To address this issue, we investigated the effects of one night of total sleep deprivation on subjective stress and mood in response to low-stress and high-stress cognitive testing conditions in healthy adult volunteers in two separate experiments (total N = 53). Sleep was manipulated in a controlled, laboratory setting and stressor intensity was manipulated by changing difficulty of cognitive tasks, time pressure, and feedback about performance. Sleep-deprived participants reported greater subjective stress, anxiety, and anger than rested controls following exposure to the low-stressor condition, but not in response to the high-stressor condition, which elevated negative mood and stress about equally for both sleep conditions. These results suggest that sleep deprivation lowers the psychological threshold for the perception of stress from cognitive demands but does not selectively increase the magnitude of negative affect in response to high-stress performance demands.

Pain can be both a cause and a consequence of sleep deficiency. This bidirectional relationship between sleep and pain has important implications for clinical management of patients, but also for chronic pain prevention and public health more broadly. The review that follows will provide an overview of the neurobiological evidence of mechanisms thought to be involved in the modulation of pain by sleep deficiency, including the opioid, monoaminergic, orexinergic, immune, melatonin, and endocannabinoid systems; the hypothalamus-pituitary-adrenal axis; and adenosine and nitric oxide signaling. In addition, it will provide a broad overview of pharmacological and non-pharmacological approaches for the management of chronic pain comorbid with sleep disturbances and for the management of postoperative pain, as well as discuss the effects of sleep-disturbing medications on pain amplification.

Liver allograft provided renal graft immunoprotection if both organs are transplanted simultaneously (immunogenetic identity), but not for kidneys transplanted subsequently.

Despite a growing body of literature demonstrating a positive relationship between sleep and optimal performance, athletes often have low sleep quality and quantity. Insufficient sleep among athletes may be due to scheduling constraints and the low priority of sleep relative to other training demands, as well as a lack of awareness of the role of sleep in optimizing athletic performance. Domains of athletic performance (e.g., speed and endurance), neurocognitive function (e.g., attention and memory), and physical health (e.g., illness and injury risk, and weight maintenance) have all been shown to be negatively affected by insufficient sleep or experimentally modeled sleep restriction. However, healthy adults are notoriously poor at self-assessing the magnitude of the impact of sleep loss, underscoring the need for increased awareness of the importance of sleep among both elite athletes and practitioners managing their care. Strategies to optimize sleep quality and quantity in athletes include approaches for expanding total sleep duration, improving sleep environment, and identifying potential sleep disorders.

Data indicate that young adult cancer survivors have some unique needs (e.g., multiple competing demands of young adulthood) and preferences (e.g., comfort with remotely delivered interventions) that differentiate them from older cancer survivors. Thus, young survivors would be best served by interventions designed to specifically target this population.

Cognitive behavioral therapy for insomnia is an effective treatment for prenatal insomnia disorder.