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1 The hippocampus is particularly sensitive to sleep loss.
2 etes risk and inflammation, independently of sleep loss.
3 reased, indicating a homeostatic response to sleep loss.
4 in sleep timing and homeostatic responses to sleep loss.
5 nd memory deficits comparable to those after sleep loss.
6 higher level of arousal despite the similar sleep loss.
7 d differently in males and females following sleep loss.
8 cesses with regard to trait vulnerability to sleep loss.
9 rom it may require more time than from acute sleep loss.
10 multiplicative effect on performance during sleep loss.
11 , and associates with EEG differences during sleep loss.
12 siological sleepiness in response to chronic sleep loss.
13 out the cellular adaptations that occur with sleep loss.
14 eep and learning impairments associated with sleep loss.
15 campus-related cognitive deficits induced by sleep loss.
16 may be involved in regulating sensitivity to sleep loss.
17 prevented cognitive deficits associated with sleep loss.
18 orted believing that they had adapted to the sleep loss.
19 ial feature of performance impairment due to sleep loss.
20 on of psychomotor vigilance as a function of sleep loss.
21 ndicative of a homeostatic response to acute sleep loss.
22 n the brain and body of animals experiencing sleep loss.
23 generalize to conditions of chronic partial sleep loss.
24 chanisms underlying the anxiogenic impact of sleep loss.
25 dicate that the hippocampus is vulnerable to sleep loss.
26 reduced expression of heat-shock genes after sleep loss.
27 esponse variability, which is exacerbated by sleep loss.
28 es compensatory REM sleep in response to REM sleep loss.
29 KC output connections is scaled uniformly by sleep loss.
30 rmance under challenging conditions, such as sleep loss.
31 groups also experienced different effects of sleep loss.
32 f presynaptic scaling in the fly brain after sleep loss.
33 d neocortex after a brief period of sleep or sleep loss.
34 nd are more resistant to negative effects of sleep loss.
35 own about how these patterns are impacted by sleep loss.
36 d is linked to energy deficit accrued during sleep loss.
37 rlies the adaptive evolution of albinism and sleep loss.
38 l to study the evolution and consequences of sleep loss.
39 REM sleep and compensatory changes following sleep loss.
40 ls, also display mitochondrial changes after sleep loss.
41 memory associations after one night of total sleep loss.
42 57 of 151) were non-resilient after moderate sleep loss.
43 uscle Bmal1 reduced the recovery response to sleep loss.
44 might be causal for individual responses to sleep loss.
45 is associated with intermittent hypoxia and sleep loss.
46 ntain daytime sleep in the face of nighttime sleep loss.
47 to maintain normal blood sugar levels during sleep loss.
48 oday's society due to many factors including sleep loss.
49 ic dysfunction, and potential biomarkers for sleep loss.
50 occurs regardless of the approach to achieve sleep loss.
52 c adverse metabolic effects independently of sleep loss, a parallel group design was used to study 26
56 ast, chronic sleep restriction but not acute sleep loss activates microglia, promotes their phagocyti
62 s and nuclear proteomics we investigated how sleep loss affects the cellular composition and molecula
64 addition, experimental studies suggest that sleep loss alters cerebrospinal fluid Abeta dynamics, de
70 -promoting circuits become hyperactive after sleep loss and are associated with increased whole-brain
71 her investigations, the relationship between sleep loss and behavior has the potential to be used as
75 es) to systematically examine the effects of sleep loss and circadian misalignment using a constant r
76 n time to a visual cue is impaired following sleep loss and circadian misalignment, but it has remain
82 significantly impaired when performed after sleep loss and during the biological night, and thus may
83 r to promptly curtail the chronic effects of sleep loss and effectively screen for underlying, potent
84 on on which to consider interactions between sleep loss and emotional reactivity in a variety of clin
88 on of this circuit in young flies results in sleep loss and lasting deficits in adult courtship behav
90 mework for a positive feedback loop, whereby sleep loss and neuronal excitation accelerate the accumu
92 ation (PSD), a condition distinct from total sleep loss and one experienced by millions on a daily an
93 es in cognitive performance and sleep during sleep loss and recovery, as well as a new approach for p
94 omnography was performed to measure baseline sleep loss and responses to isoflurane anesthesia at 1%
95 nt with a body of literature suggesting that sleep loss and sleep fragmentation are associated with b
96 OA) and hippocampal CA2 region, resulting in sleep loss and social memory deficits, respectively.
97 r modern society suffers from both pervasive sleep loss and substance abuse-what may be the indicatio
98 ules may apply across the brain during acute sleep loss and that sleep need may broadly alter excitat
99 miological studies have shown a link between sleep loss and the obesity 'epidemic,' and several obser
100 ents in performance are exaggerated by prior sleep loss and the time of day in which a person awakens
102 exposed to the shifting schedule revealed no sleep loss, and stress measures were not altered in shif
103 ting effects of stimulants in the context of sleep loss, and the conflicting findings of stimulants f
104 r-individual differences in vulnerability to sleep loss, and these inter-individual differences const
111 d, Kv3.1/Kv3.3-deficient mice display severe sleep loss as a result of unstable slow-wave sleep.
113 n hormonal versus hedonic factors underlying sleep-loss-associated weight gain, we rigorously tested
114 multifaceted view on cerebral correlates of sleep loss at night and propose that genetic predisposit
117 nd recovery differ between acute and chronic sleep loss, but the physiological basis for these time c
119 tal animal and human studies have found that sleep loss can impair metabolic control and body weight
126 al variability exists in the degree to which sleep loss compromises learning, the mechanistic reasons
128 different lights as a countermeasure against sleep-loss decrements in alertness, melatonin and cortis
129 ow-frequency brain electrical activity after sleep loss demonstrate that sleep need is homeostaticall
133 reviously appreciated.SIGNIFICANCE STATEMENT Sleep loss-driven changes in transcript and protein abun
136 more complete understanding of the issues of sleep loss during residency training can inform innovati
138 t cause the expected homeostatic response to sleep loss (e.g., increases in sleep time or intensity).
139 in A1AR availability were more resilient to sleep-loss effects than those with a subtle increase.
142 of the sympathetic nervous system (SNS) from sleep loss elevates blood pressure to promote vascular s
143 Bruchpilot (BRP) abundance in the MB lobes; sleep loss elevates BRP while sleep induction reduces BR
146 eep) on neurobehavioral response to moderate sleep loss (evaluated at 20 hours awake two days later)
148 le of a single species with a convergence on sleep loss exhibited by several independently evolved po
149 ictors of individual responses to subsequent sleep loss exposures chronically or intermittently, acro
151 ns in Drosophila melanogaster can dissociate sleep loss from subsequent homeostatic rebound, offering
152 ng mutants with very different mechanisms of sleep loss: fumin (fmn), redeye (rye), and sleepless (ss
153 or driver of AD progression, suggesting that sleep loss further accelerates AD through a vicious cycl
154 To date it is not known whether sleep or sleep loss has any effect on proliferation of cells in t
159 die from one form of sleep deprivation, but sleep loss has not been shown to cause death in well-con
162 However, society-specific consequences of sleep loss have rarely been explored, and no function of
164 These results collectively indicate that sleep loss impairs motivation and cognitive performance,
165 ive and executive functioning-resulting from sleep loss in a healthy, racially-diverse adult populati
167 reinstates hierarchical BOLD dynamics after sleep loss in an independent sleep deprivation study.
170 studies are warranted to better characterize sleep loss in eczema and develop strategies for treatmen
173 ated neural processing of food rewards after sleep loss in reward-processing areas such as the anteri
174 ep regulation to quantify performance during sleep loss in the absence of caffeine and a dose-depende
175 splay elevated calcium levels in response to sleep loss in the morning, but not the evening consisten
179 tudies in humans and rodents also found that sleep loss increases peripheral markers of inflammation,
182 Sleep disorders are common in humans, and sleep loss increases the risk of obesity and diabetes.
184 d the degree of such neural vulnerability to sleep loss: individuals with highest trait anxiety showe
185 mechanisms for the observed changes comprise sleep loss-induced changes in appetite-signaling hormone
186 myo-inositol and glycine levels, suggesting sleep loss-induced modifications downstream of mGluR5 si
187 estigated potential underlying mechanisms of sleep-loss-induced changes in behavior by high-density e
189 PER3 predicts individual differences in the sleep-loss-induced decrement in performance and that thi
191 hat brain-wide dopaminergic pathways control sleep-loss-induced polymodal affective state transitions
200 s for behavioral change), suggesting that if sleep loss is corrected, it could save lives-including B
201 suggest that increased food valuation after sleep loss is due to hedonic rather than hormonal mechan
203 We demonstrate that the anxiogenic impact of sleep loss is linked to impaired medial prefrontal corte
205 Here, we report that postmating nighttime sleep loss is modulated by diet and sleep deprivation, d
211 Even though the overall consensus is that sleep loss leads to metabolic perturbations promoting th
213 ulation and disrupted attention of ELS mice, sleep loss likely underlies cognitive deficits in ELS mi
214 ed on-call workload was associated with more sleep loss, longer shift duration, and a lower likelihoo
217 suggest that increased food valuation after sleep loss might be due to hedonic rather than hormonal
218 These findings demonstrate that sleep and sleep loss modify experience-dependent cortical plastici
219 It is not yet clear how acute and chronic sleep loss modify neuronal activities and lead to adapti
220 ty, longer episode duration, less subjective sleep loss, more guilt, and more work/activity impairmen
224 ruption and anxiety disorders, the impact of sleep loss on affective anticipatory brain mechanisms, a
225 few studies have investigated the effect of sleep loss on aspects of prospect theory, specifically t
226 way may underlie both the adverse effects of sleep loss on cognition and the subsequent changes in co
227 e reviewed studies addressing the effects of sleep loss on cognition, performance, and health in surg
228 he negative effects of shiftwork and chronic sleep loss on health and productivity are now being appr
229 may be involved with the negative effects of sleep loss on health, and highlight the interrelatedness
231 esults delineate the adverse consequences of sleep loss on hippocampal function at the network level
232 omeostatic sleep response and the effects of sleep loss on memory, previous studies have not determin
234 e a novel framework underlying the impact of sleep loss on pain and, furthermore, establish that the
240 leep and affective regulation, the impact of sleep loss on the discrimination of complex social emoti
243 noninferiority trial showed no more chronic sleep loss or sleepiness across trial days among interns
244 ty in caudate, which was not attributable to sleep loss or so-called social jet lag, whereas physical
245 conclude that circadian disruption, but not sleep loss or stress, are associated with jet lag-relate
246 ble from the energy-balance perturbations of sleep loss or the potentially stressful effects of the f
248 However, during sleep restriction (partial sleep loss) performance predictions based on such models
250 We defined each participant's response-to-sleep-loss phenotype based on the number of attentional
251 ly central accumulation of fat indicate that sleep loss predisposes to abdominal visceral obesity.
254 lesion size were associated with cumulative sleep loss (r=0.77 and r=0.62, respectively), and cumula
258 plicating studies, here, we demonstrate that sleep loss represents one previously unrecognized factor
260 ults may also provide insight for predicting sleep loss responses in patients with schizophrenia and
262 Specific to the central nervous system, sleep loss results in impaired synaptogenesis and long-t
263 use and effect association are still scarce, sleep loss seems to be an appealing target for the preve
265 understand the association between workload, sleep loss, shift duration, and the educational time of
266 memory and cognitive deficits that accompany sleep loss.SIGNIFICANCE STATEMENT The lack of sufficient
267 correlations in neurobehavioral responses to sleep loss suggest that these trait-like differences are
268 sed to a similar extent after short and long sleep loss, suggesting that astrocytic phagocytosis may
269 nificant increase after prolonged and severe sleep loss, suggesting that it may promote the housekeep
270 beta' GABAA and GABABR3 receptors results in sleep loss, suggesting these receptors are the sleep-rel
271 tes these EB neurons are highly sensitive to sleep loss, switching from spiking to burst-firing modes
272 This resilience may be due to a less extreme sleep loss than in previous studies, but also indicates
274 ay be more susceptible to weight gain during sleep loss than women due to a larger increase in daily
276 y insult, these results suggest that chronic sleep loss, through microglia priming, may predispose th
277 osure, sex differences in recovery from NREM-sleep loss; thus, suggesting an underlying sex-differenc
278 ind that increased mGluR5 availability after sleep loss tightly correlates with behavioral and electr
279 stress as a novel mechanism linking chronic sleep loss to adverse health outcomes-and perhaps for li
282 mechanisms linking circadian dysfunction and sleep loss to neurodegenerative diseases, with a focus o
283 urbance numerical rating scale (range, 0 [no sleep loss] to 10 [unable to sleep at all]) at week 4 (3
285 First, at an individual level, 1 night of sleep loss triggers the withdrawal of help from one indi
287 ment of cognitive performance in response to sleep loss was significantly greater in the PER3(5/5) in
288 77 and r=0.62, respectively), and cumulative sleep loss was the strongest predictor of high sensitivi
289 e indeed costs associated with resiliency to sleep loss, we challenged natural allelic variants of th
290 ve CSR that mimics a common pattern of human sleep loss, we quantified a new procedure of sleep disru
291 To characterize effects of learning and sleep loss, we quantified activity-dependent phosphoryla
292 The mania-like behaviors, including the sleep loss, were reversed by valproate, and re-emerged w
293 nd sufficient to suppress starvation-induced sleep loss when animals encounter nutrient-poor food sou
294 r, this mutation in oca2 fails to complement sleep loss when surface fish harboring this engineered m
295 s, enter a catabolic state during periods of sleep loss, which consequently disrupts physiological fu
296 onfer protection against the consequences of sleep loss while simultaneously allowing for the increas
297 xhibited attenuated female-induced nighttime sleep loss yet normal daytime courtship, which suggests