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Acute sleep loss increases pro-inflammatory and synaptic plasticity-related molecules in the brain, including interleukin-1 beta (IL-1β), tumor necrosis factor-alpha (TNF-α), and brain-derived neurotrophic factor (BDNF). These molecules enhance non-rapid eye movement sleep slow wave activity (SWA), also known as electroencephalogram delta power, and(More)
Previous findings of time-of-day differences in athletic performance could be confounded by diurnal fluctuations in environmental and behavioral "masking" factors (e.g., sleep, ambient temperature, and energy intake). The purpose of this study was to examine whether there is a circadian rhythm in swim performance that is independent of these masking(More)
Symptoms commonly associated with sleep loss and chronic inflammation include sleepiness, fatigue, poor cognition, enhanced sensitivity to pain and kindling stimuli, excess sleep and increases in circulating levels of tumor necrosis factor α (TNF) in humans and brain levels of interleukin-1 β (IL1) and TNF in animals. Cytokines including IL1 and TNF partake(More)
Cytokines such as tumor necrosis factor alpha (TNFα) and interleukin-1 beta (IL1β) play a role in sleep regulation in health and disease. TNFα or IL1β injection enhances non-rapid eye movement sleep. Inhibition of TNFα or IL1β reduces spontaneous sleep. Mice lacking TNFα or IL1β receptors sleep less. In normal humans and in multiple disease states, plasma(More)
Sleep is dependent upon prior brain activities, e.g., after prolonged wakefulness sleep rebound occurs. These effects are mediated, in part, by humoral sleep regulatory substances such as cytokines. However, the property of wakefulness activity that initiates production and release of such substances and thereby provides a signal for indexing prior waking(More)
Electroencephalographic (EEG) δ waves during non-rapid eye movement sleep (NREMS) after sleep deprivation are enhanced. That observation eventually led to the use of EEG δ power as a parameter to model process S in the two-process model of sleep. It works remarkably well as a model parameter because it often co-varies with sleep duration and intensity.(More)
Interleukin (IL)-1β is involved in several brain functions, including sleep regulation. It promotes non-rapid eye movement (NREM) sleep via the IL-1 type I receptor. IL-1β/IL-1 receptor complex signaling requires adaptor proteins, e.g., the IL-1 receptor brain-specific accessory protein (AcPb). We have cloned and characterized rat AcPb, which shares(More)
24 25 Sleep is dependent upon prior brain activities, e.g. after prolonged wakefulness sleep 26 rebound occurs. These effects are mediated, in part, by humoral sleep regulatory 27 substances such as cytokines. However, the property of wakefulness activity that 28 initiates production and release of such substances and thereby provides a signal for 29(More)
The effects of chronic moderate sleep restriction and exercise training on carcinogenesis were examined in adenomatous polyposis coli multiple intestinal neoplasma (APC Min(+/-)) mice, a genetic strain which is predisposed to developing adenomatous polyposis. The mice were randomized to one of four 11 week treatments in a 2×2 design involving sleep(More)