ライフサイエンスコーパス: sleep loss

1 , and associates with EEG differences during sleep loss.

2 siological sleepiness in response to chronic sleep loss.

3 out the cellular adaptations that occur with sleep loss.

4 eep and learning impairments associated with sleep loss.

5 campus-related cognitive deficits induced by sleep loss.

6 may be involved in regulating sensitivity to sleep loss.

7 prevented cognitive deficits associated with sleep loss.

8 ial feature of performance impairment due to sleep loss.

9 on of psychomotor vigilance as a function of sleep loss.

10 ndicative of a homeostatic response to acute sleep loss.

11 n the brain and body of animals experiencing sleep loss.

12 generalize to conditions of chronic partial sleep loss.

13 dicate that the hippocampus is vulnerable to sleep loss.

14 reduced expression of heat-shock genes after sleep loss.

15 es compensatory REM sleep in response to REM sleep loss.

16 is associated with intermittent hypoxia and sleep loss.

17 ntain daytime sleep in the face of nighttime sleep loss.

18 to maintain normal blood sugar levels during sleep loss.

19 ic dysfunction, and potential biomarkers for sleep loss.

20 occurs regardless of the approach to achieve sleep loss.

21 uscle Bmal1 reduced the recovery response to sleep loss.

22 The hippocampus is particularly sensitive to sleep loss.

23 etes risk and inflammation, independently of sleep loss.

24 reased, indicating a homeostatic response to sleep loss.

25 in sleep timing and homeostatic responses to sleep loss.

26 nd memory deficits comparable to those after sleep loss.

27 might be causal for individual responses to sleep loss.

28 higher level of arousal despite the similar sleep loss.

29 d differently in males and females following sleep loss.

30 rom it may require more time than from acute sleep loss.

31 multiplicative effect on performance during sleep loss.

32 Sleep loss, a costly challenge of modern society, has pr

33 c adverse metabolic effects independently of sleep loss, a parallel group design was used to study 26

34 h is predicted by the subjective severity of sleep loss across participants.

35 ast, chronic sleep restriction but not acute sleep loss activates microglia, promotes their phagocyti

36 Sleep loss adversely affects certain types of cognitive

37 addition, experimental studies suggest that sleep loss alters cerebrospinal fluid Abeta dynamics, de

38 Therefore, we suggest that sleep loss alters emotional reactivity by lowering the t

39 Nevertheless, it remains unknown how sleep loss alters the dynamics of brain and behavioral r

40 Here, we demonstrate that sleep loss amplifies preemptive responding in the amygda

41 nts underlie the hyperexcitability caused by sleep loss and Abeta expression.

42 Both sleep loss and amyloid beta increase neural excitability

43 Chronic sleep loss and circadian misalignment enhance developmen

44 Sleep loss and circadian misalignment may disrupt reward

45 racts with early school start times to cause sleep loss and circadian misalignment.

46 Difficulties with jet lag because of sleep loss and decreased performance are emphasised.

47 r to promptly curtail the chronic effects of sleep loss and effectively screen for underlying, potent

48 on on which to consider interactions between sleep loss and emotional reactivity in a variety of clin

49 Recent studies, however, suggest that sleep loss and fatigue result in significant neurobehavi

50 Sleep loss and insufficient sleep are risk factors for c

51 on of this circuit in young flies results in sleep loss and lasting deficits in adult courtship behav

52 academic year were associated with the most sleep loss and longest shift durations.

53 mework for a positive feedback loop, whereby sleep loss and neuronal excitation accelerate the accumu

54 emiological evidence supports a link between sleep loss and obesity.

55 ation (PSD), a condition distinct from total sleep loss and one experienced by millions on a daily an

56 es in cognitive performance and sleep during sleep loss and recovery, as well as a new approach for p

57 omnography was performed to measure baseline sleep loss and responses to isoflurane anesthesia at 1%

58 nt with a body of literature suggesting that sleep loss and sleep fragmentation are associated with b

59 miological studies have shown a link between sleep loss and the obesity 'epidemic,' and several obser

60 echanism that underlies the relation between sleep loss and weight gain.

61 exposed to the shifting schedule revealed no sleep loss, and stress measures were not altered in shif

62 e homeostatic factors that impel sleep after sleep loss are imperfectly understood.

63 d, Kv3.1/Kv3.3-deficient mice display severe sleep loss as a result of unstable slow-wave sleep.

64 multifaceted view on cerebral correlates of sleep loss at night and propose that genetic predisposit

65 It reflects every-day sleep loss better than acute sleep deprivation, but its

66 We demonstrate that sleep loss, but not sleep fragmentation, in healthy mice

67 nd recovery differ between acute and chronic sleep loss, but the physiological basis for these time c

68 tal animal and human studies have found that sleep loss can impair metabolic control and body weight

69 Sleep loss can modify energy intake and expenditure.

70 Sleep loss can severely impair the ability to perform, y

71 We conclude that the sleep loss caused by ablation of VLPO neurons sensitizes

72 Sleep loss causes profound cognitive impairments and inc

73 al variability exists in the degree to which sleep loss compromises learning, the mechanistic reasons

74 Sleep loss decreased the expression of genes encoding ch

75 different lights as a countermeasure against sleep-loss decrements in alertness, melatonin and cortis

76 ow-frequency brain electrical activity after sleep loss demonstrate that sleep need is homeostaticall

77 Sleep loss/disruption has been shown to suppress adult h

78 more complete understanding of the issues of sleep loss during residency training can inform innovati

79 in A1AR availability were more resilient to sleep-loss effects than those with a subtle increase.

80 he most widely consumed stimulant to counter sleep-loss effects.

81 Importantly, these data reveal that sleep loss exacerbates Abeta-induced hyperexcitability a

82 le of a single species with a convergence on sleep loss exhibited by several independently evolved po

83 ictors of individual responses to subsequent sleep loss exposures chronically or intermittently, acro

84 The reduced HCVR after sleep loss found in previous studies may have been affec

85 To date it is not known whether sleep or sleep loss has any effect on proliferation of cells in t

86 g prevalence of obesity and type 2 diabetes, sleep loss has become common in modern societies.

87 Consistently, sleep loss has been linked to behavioral and attention p

88 die from one form of sleep deprivation, but sleep loss has not been shown to cause death in well-con

89 acteristics, sleep duration, and response to sleep loss have been identified.

90 Brief periods of sleep loss have long-lasting consequences such as impair

91 However, society-specific consequences of sleep loss have rarely been explored, and no function of

92 ive and executive functioning-resulting from sleep loss in a healthy, racially-diverse adult populati

93 emory consolidation deficits associated with sleep loss in an object-location task.

94 Sleep loss in attending physicians has an unclear effect

95 studies are warranted to better characterize sleep loss in eczema and develop strategies for treatmen

96 ep regulation to quantify performance during sleep loss in the absence of caffeine and a dose-depende

97 tudies in humans and rodents also found that sleep loss increases peripheral markers of inflammation,

98 Sleep disorders are common in humans, and sleep loss increases the risk of obesity and diabetes.

99 d the degree of such neural vulnerability to sleep loss: individuals with highest trait anxiety showe

100 mechanisms for the observed changes comprise sleep loss-induced changes in appetite-signaling hormone

101 myo-inositol and glycine levels, suggesting sleep loss-induced modifications downstream of mGluR5 si

102 estigated potential underlying mechanisms of sleep-loss-induced changes in behavior by high-density e

103 Despite sleep-loss-induced cognitive deficits, little is known a

104 PER3 predicts individual differences in the sleep-loss-induced decrement in performance and that thi

105 The reversibility of mild sleep-loss-induced pain by wake-promoting agents reveals

106 Sleep loss is an adaptive response to nutrient deprivati

107 In humans, acute sleep loss is associated with increased appetite and ins

108 Significance statement: Sleep loss is known as a robust modulator of emotional r

109 to perform, yet the ability to recover from sleep loss is not well understood.

110 Similar resistance to sleep loss is observed with Notch(spl-1) gain-of-functio

111 e molecular mechanisms underlying effects of sleep loss is only in its nascent stages.

112 Moderate daily repeated sleep loss leads to a progressive accumulation of sleep

113 Even though the overall consensus is that sleep loss leads to metabolic perturbations promoting th

114 Because chronic sleep loss leads to performance decrements, our findings

115 ed on-call workload was associated with more sleep loss, longer shift duration, and a lower likelihoo

116 We propose that sleep loss may be one of the ways that inflammatory proc

117 These findings demonstrate that sleep and sleep loss modify experience-dependent cortical plastici

118 It is not yet clear how acute and chronic sleep loss modify neuronal activities and lead to adapti

119 ty, longer episode duration, less subjective sleep loss, more guilt, and more work/activity impairmen

120 Sleep loss negatively impacts performance, mood, memory,

121 euronal excitability underlie the effects of sleep loss on AD pathogenesis.

122 ruption and anxiety disorders, the impact of sleep loss on affective anticipatory brain mechanisms, a

123 way may underlie both the adverse effects of sleep loss on cognition and the subsequent changes in co

124 e reviewed studies addressing the effects of sleep loss on cognition, performance, and health in surg

125 he negative effects of shiftwork and chronic sleep loss on health and productivity are now being appr

126 may be involved with the negative effects of sleep loss on health, and highlight the interrelatedness

127 We sought to investigate the effects of sleep loss on high-sensitivity C-reactive protein (CRP)

128 omeostatic sleep response and the effects of sleep loss on memory, previous studies have not determin

129 ional notions about the effects of sleep and sleep loss on neurobehavioral performance.

130 In this study, the impact of chronic sleep loss on sleep homeostasis was examined in C57BL/6J

131 leep and affective regulation, the impact of sleep loss on the discrimination of complex social emoti

132 Sleep loss or disturbances are likely to signal an incre

133 conclude that circadian disruption, but not sleep loss or stress, are associated with jet lag-relate

134 ble from the energy-balance perturbations of sleep loss or the potentially stressful effects of the f

135 However, during sleep restriction (partial sleep loss) performance predictions based on such models

136 Sleep loss produces well-characterized cognitive deficit

137 lesion size were associated with cumulative sleep loss (r=0.77 and r=0.62, respectively), and cumula

138 We examined sleep-loss-related attentional vulnerability by consider

139 Our results link higher sleep-loss-related attentional vulnerability to cortical

140 pses, increased after both acute and chronic sleep loss relative to sleep and wake.

141 Across multiple measures, prior sleep loss responses are strong predictors of individual

142 ults may also provide insight for predicting sleep loss responses in patients with schizophrenia and

143 Sleep loss resulting from physiological and pathological

144 use and effect association are still scarce, sleep loss seems to be an appealing target for the preve

145 mmunication may be one detrimental effect of sleep loss shared by social organisms.

146 understand the association between workload, sleep loss, shift duration, and the educational time of

147 correlations in neurobehavioral responses to sleep loss suggest that these trait-like differences are

148 sed to a similar extent after short and long sleep loss, suggesting that astrocytic phagocytosis may

149 nificant increase after prolonged and severe sleep loss, suggesting that it may promote the housekeep

150 beta' GABAA and GABABR3 receptors results in sleep loss, suggesting these receptors are the sleep-rel

151 tes these EB neurons are highly sensitive to sleep loss, switching from spiking to burst-firing modes

152 re susceptible to weight gain resulting from sleep loss than women and whites, respectively.

153 ay be more susceptible to weight gain during sleep loss than women due to a larger increase in daily

154 y insult, these results suggest that chronic sleep loss, through microglia priming, may predispose th

155 ind that increased mGluR5 availability after sleep loss tightly correlates with behavioral and electr

156 Our findings directly link sleep loss to changes in neuronal excitability and Abeta

157 mechanisms linking circadian dysfunction and sleep loss to neurodegenerative diseases, with a focus o

158 ment of cognitive performance in response to sleep loss was significantly greater in the PER3(5/5) in

159 77 and r=0.62, respectively), and cumulative sleep loss was the strongest predictor of high sensitivi

160 e indeed costs associated with resiliency to sleep loss, we challenged natural allelic variants of th

161 ve CSR that mimics a common pattern of human sleep loss, we quantified a new procedure of sleep disru

162 nd sufficient to suppress starvation-induced sleep loss when animals encounter nutrient-poor food sou