ライフサイエンスコーパス: wake

1 alize overall synaptic strength increased by wake.

2 on region that leaves polarized cells in its wake.

3 ists to elucidate the role of TAAR1 in sleep/wake.

4 ticity occur preferentially during sleep vs. wake.

5 wave activity (SWA) is higher after extended wake.

6 n mice is delayed or prevented by subsequent wake.

7 ich provides temporal structure to sleep and wake.

8 of movement-dependent sensory gating during wake.

9 the increased neuronal activity of extended wake.

10 SI) decreased 18% after sleep compared with wake.

11 tes governed by short timescales even during wake.

12 ng either 0.5 (early) or 5.5 (late) hr after wake.

13 and chronic sleep loss relative to sleep and wake.

14 ring sleep and 'desynchronized' state during waking.

15 Consciousness never fades during waking.

16 d fast-gamma (55 to 80 Hz) activity in prior waking.

17 currence of a cortical activation similar to waking accompanied by muscle atonia.

18 ogram (EEG) paradoxically similar to that of wake, accompanied by rapid eye movements and muscle aton

19 ted by sleep pressure, both directly inhibit wake-active hypocretin and GABAergic cells in the latera

20 tive neurons are spatially intermingled with wake-active neurons, making it difficult to target the s

21 ssary for the activation of Hcrt, HA, or ACh wake-active neurons, which may underlie the milder cogni

22 hich shows a robust diurnal pattern of sleep/wake activity, caffeine reduces nighttime sleep behavior

23 nset latency [F3,1042 = 6.01, P < .001], and wake after sleep onset [F3,1042 = 12.68, P < .001]).

24 et latency d = 1.41 [95% CI, 1.15-1.68], and wake after sleep onset d = 0.95 [95% CI, 0.70-1.21]), wi

25 y-derived values for sleep-onset latency and wake after sleep onset, collected prospectively for 10 d

26 SuM(vglut2) neurons decreases and fragments wake, also suppressing theta and gamma frequency EEG act

27 causes impaired TDW maintenance in baseline wake and blunted delta power in SWS, reproducing, respec

28 ptic plasticity and related effects on sleep-wake and circadian systems.

29 ndicate a modulatory role for TAAR1 in sleep/wake and cortical activity and suggest TAAR1 as a novel

30 9 hour phase delay of the light/dark, sleep/wake and meal schedule, which has similarities to flying

31 imulate breathing about equally during quiet wake and non-rapid eye movement (REM) sleep, and to a le

32 shown that cortical activity patterns during wake and NREM sleep are not as global as previously thou

33 and REM sleep, decreased gamma power during wake and NREM, and decreased Tb without affecting LMA; t

34 of SuM(vgat/vglut2) neurons produces minimal wake and optogenetic stimulation of SuM(vgat/vglut2) ter

35 cy of the TAAR1 agonist, RO5256390, on sleep/wake and physiological parameters was determined.

36 Although quiet wake and rapid eye movement (REM) sleep are characterize

37 Although wake and rapid eye movement (REM) sleep exhibit long tim

38 ), a neurotransmitter involved in both sleep-wake and satiety regulation.

39 y disturbed sleep-wake cycle, with very long wake and sleep durations, reaching up to 106-h awake and

40 Reversal of sender/receiver roles across wake and SWS implies that higher- and lower-frequency si

41 n the hippocampus and cerebral cortex across wake and SWS.

42 h cortical activation and muscle tone during waking and because, in their absence, waking with muscle

43 nd we found that their firing increased upon waking and decreased 11% per hour across sleep.

44 at these rapid variations, during both quiet waking and locomotion, are highly correlated with fluctu

45 neurons are similarly more activated during waking and paradoxical sleep (PS; aka REM) than during s

46 In WT mice, RO5263397 increased waking and reduced NREM and REM sleep, decreased gamma p

47 ks among behavioral manifestations of sleep, wake, and sleep deprivation and specific measurable chan

48 sleep reflects synaptic potentiation during wake, and that its homeostatic decrease during the night

49 integrator of arousal and sleep need via the wake- and sleep-promoting neuromodulators, noradrenaline

50 are consistent with the hypothesis that, in waking animals, the koniocellular pathway selectively pa

51 Also, increases in ANS activity during waking, as measured by heart rate variability (HRV), hav

52 n sleep, we asked whether it is specifically wake associated with synaptic plasticity that leads to D

53 ated with pain with eating, weight loss, and waking at night to have a stool.

54 ms (restlessness, difficulty falling asleep, waking at night, trouble getting back to sleep, and earl

55 ficantly higher during PS than during active waking (aWK) similarly in the RSC and hippocampus (HPC)

56 involved in the promotion and maintenance of waking because they discharge in association with cortic

57 calcium and in some cases firing profiles in wake-behaving flies.

58 We measured sleep/wake behavior and cataplexy after injection of saline or

59 ation of BF cholinergic neurons on the sleep-wake behavior and electroencephalogram (EEG) power spect

60 e, two peptides that are important for sleep-wake behavior and food intake.

61 drome (SMS), the dysregulation of both sleep-wake behavior and melatonin production strongly suggests

62 uced between 4 and 10 weeks of age) on sleep-wake behavior in male mice.

63 findings provide new insights into how sleep-wake behavior is programmed during early life and how pe

64 neurons each have distinct effects on sleep/wake behavior, improving our understanding of how the PP

65 ty imposes its long-lasting effects on sleep-wake behavior.

66 Light affects sleep and wake behaviors by providing an indirect cue that entrain

67 tide prokineticin 2 (Prok2) affect sleep and wake behaviors in a light-dependent but circadian-indepe

68 such that light eliminated alert and active-wake behaviors, while leaving time-spent-awake unaffecte

69 standing their role in supporting particular waking behaviors.

70 tion and intensity, but the role of specific waking behaviours remains unclear.

71 only by wake duration, but also by specific waking behaviours.

72 Following the last of the four daily induced wake bouts, we examined the brains and observed a chimer

73 sleep primarily by modulating the length of wake bouts.

74 ature of the sleeping brain, rather than the waking brain, and is slowed in the aging and posttraumat

75 ter systems as they control the state of the waking brain.

76 ngage in phagocytic activity during extended wake, but direct evidence was lacking.

77 , trailing-edge vortices caused by a form of wake capture at stroke reversal, and rotational drag.

78 Putative sleep-wake centers are located in higher-order brain centers t

79 synaptic activity associated with prolonged wake, clearing worn components of heavily used synapses.

80 ave yielded values exceeding those of normal waking consciousness.

81 the Primed condition compared with the Quiet Wake control condition.

82 are implicated in cortical arousal and sleep-wake control.

83 icated in autism spectrum disorder and sleep-wake control.

84 atic impact of Hcrt(ko/ko) mouse spontaneous waking correlates with decreased cortical expression of

85 ficients of 6% for telomere length, 3.4% for waking cortisol levels, and 5.5% for peak cortisol level

86 Participants underwent an ultradian sleep-wake cycle (USW) procedure consisting of 36 cycles of 60

87 The sleep-wake cycle and circadian rhythmicity both contribute to

88 f normal housetraining, and changes in sleep-wake cycle and general activity.

89 (REM) sleep is a recurring part of the sleep-wake cycle characterized by fast, desynchronized rhythms

90 tivity of the basal ganglia across the sleep-wake cycle that contribute to our understanding of RBD.

91 an activity-dependent manner and with sleep-wake cycle, modulating synaptic transmission and short-t

92 tal delay and a dramatically disturbed sleep-wake cycle, with very long wake and sleep durations, rea

93 yloid-beta (Abeta) fluctuates with the sleep-wake cycle.

94 ifted in response to the change in the sleep-wake cycle.

95 ion of astroglial networks impairs the sleep-wake cycle.

96 ion and clearance mechanisms active in sleep-wake cycles and that amyloid deposition may impair norma

97 easible intervention for improving the sleep-wake cycles in patients with PD.

98 luctuations of DRN(DA) activity across sleep-wake cycles with highest activity during wakefulness.

99 ssion, the pupillary light reflex, and sleep/wake cycles.

100 s, notably the feeding, light-dark and sleep-wake cycles.

101 ble across sleep (p = 0.013) with this sleep-wake difference being most pronounced for stimuli with l

102 osis and treatment of circadian rhythm sleep-wake disorders both require assessment of circadian phas

103 the treatment of obesity, anxiety, and sleep/wake disorders.

104 ring poststimulus NREM sleep (but not REM or wake) disrupts coherence between LGN and V1 and also blo

105 Slow-wave activity (SWA) increases with wake duration and declines homeostatically during sleep,

106 s in firing rates are determined not only by wake duration, but also by specific waking behaviours.

107 sleep, with DA signal strength predictive of wake duration.

108 ils to induce a delta power reflecting prior waking duration.

109 In contrast to wake, during sleep there is a complete absence of animal

110 uring acute sleep deprivation (one prolonged wake episode), chronic sleep restriction (multiple night

111 procedure consisting of 36 cycles of 60-min wake episodes alternating with 60-min nap opportunities.

112 dence suggests that cortical dynamics during wake exhibits long-range temporal correlations suitable

113 r the consolidation of hippocampal memory of wake experiences into the neocortex.

114 wer rebound like WT littermates, spontaneous waking fails to induce a delta power reflecting prior wa

115 noma from the Comprehensive Cancer Center of Wake Forest Baptist Medical Center (Winston-Salem, NC, U

116 rk skills for midlevel surgical residents at Wake Forest Baptist Medical Center after they participat

117 nowledge was cross-validated using data from Wake Forest Baptist Medical Center's electronic medical

118 ent mice) can lead to narcoleptic-like sleep-wake fragmentation and sleep structure alterations.

119 driven DRN(DA) activity were associated with waking from sleep, with DA signal strength predictive of

120 mGluR5 exhibit severe dysregulation of sleep-wake homeostasis, including lack of recovery sleep and i

121 e to the molecular machinery governing sleep-wake homeostasis.

122 us coordinates daily rhythms including sleep-wake, hormone release, and gene expression.

123 omen spend a substantial proportion of their waking hours at work, places of employment may be an opp

124 n of the neural systems related to sleep and wake in the basal forebrain, diencephalon, midbrain, and

125 d to the control and regulation of sleep and wake in the basal forebrain, diencephalon, midbrain, and

126 A positron bunch is used to drive the plasma wake in the experiment, though the quasi-linear wake str

127 sleep provides any selective advantage over wake in their repair.

128 Whether Orx neurons discharge during waking in association with particular conditions, notabl

129 he capturing of the injection in a nonlinear wake is demonstrated through 3D PIC simulations as an ex

130 field structure of a highly nonlinear plasma wake is potentially suitable for this purpose but has no

131 Hcrt(ko/ko) mice fully implement TDW when waking is enforced, but spontaneous TDW episode duration

132 As the probe bunch traverses the wake, its momentum is modulated by the electric field of

133 um is modulated by the electric field of the wake, leading to a density variation of the probe after

134 Mind-wandering characterizes much of waking life and is often associated with error-prone, va

135 ng a local population of cortical neurons at wake-like levels during sleep.

136 characterized by membrane depolarization and wake-like tonic firing, and OFF periods, characterized b

137 d eye-movement (REM) sleep, characterized by wake-like, globally 'activated', high-frequency electroe

138 ent even though the bulk of the cortex shows wake-like, paradoxical activation.

139 56390 and partial agonist RO5263397 on sleep/wake, locomotor activity, body temperature, and cataplex

140 roximately 50,000 nights of care-giver sleep/wake logs were collected on school-days for 106 individu

141 ons are maximally active during wakefulness (wake-max).

142 uction later into the morning and that early waking may magnify the diabetes risk conferred by the ri

143 In flies and mice, we find that enriched wake, more than simply time spent awake, induces DSBs, a

144 In all subjects, the majority of waking Motifs (most of which were novel) had more matche

145 ypothesis that in slow-wave sleep, replay of waking neocortical activity under hippocampal guidance l

146 ions between primary brain vigilance states (waking, non-rapid eye movement sleep [NREM] and REM slee

147 n nearly the entire target population in the wake of a disaster are discussed.

148 ly on the excitation of a plasma wave in the wake of a drive beam.

149 ilarly, a depletion of empty micelles in the wake of a droplet swimmer causes negative autochemotaxis

150 In the wake of an epidemic, established immunity against a part

151 potential for societal interventions in the wake of disaster.

152 Nucleosome assembly in the wake of DNA replication is a key process that regulates

153 tem in promoting chromatin reassembly in the wake of elongating RNA polymerase II and transcriptional

154 servation of gene expression patterns in the wake of extensive rewiring is a general feature of trans

155 functional and phylogenetic diversity in the wake of extinctions and introductions across a sample of

156 we find that seasonal flu leaves a transient wake of heterosubtypic immunity that impedes the emergen

157 ty caused by release of self-antigens in the wake of infection.

158 classical view of Mesozoic vicariance in the wake of molecular dating.

159 In the wake of mounting evidence suggesting a lack of benefit t

160 In the wake of policy changes affecting insurance coverage, it

161 In the wake of reconstitution and super-resolution imaging stud

162 ling bunch), as this bunch propagates in the wake of the drive bunch.

163 In the wake of the interaction region, PEPSSI observed suprathe

164 In the wake of the recent outbreak of Ebola virus disease (EVD)

165 In the wake of this rapid growth, clinicians may lack sufficien

166 rally and is increasing in prevalence in the wake of widespread conjugate vaccine use, but no wciG-de

167 ns using 16 years of ocean-color data in the wakes of 141 typhoons in western North Pacific.

168 By identifying the mechanisms by which wake-on neurotransmitters such as ACh modulate RTN chemo

169 tal cortex after 6-8 h of sleep, spontaneous wake, or sleep deprivation (SD) and after chronic ( appr

170 toplankton blooming in tropical-cyclone (TC) wakes over the oligotrophic oceans potentially contribut

171 a 24 h recording to characterize basal sleep/wake parameters, mice were sleep deprived (SD) for 6 h.

172 l modulators of behavioral arousal and sleep-wake patterning.

173 ight administration, whilst monitoring sleep-wake patterns and the urinary 6-sulphatoxymelatonin (aMT

174 lifespan: rhythmic activities such as sleep/wake patterns change markedly as we age, and in many cas

175 ical clock, is associated with altered sleep-wake patterns in response to light.

176 implement a highly coherent reactivation of wake patterns that may support memory consolidation duri

177 Pattern separation deteriorated across the wake period but remained stable across sleep (p = 0.013)

178 cerebral A1AR availability after an extended wake period decreases to a well-rested state after recov

179 iods of active wake, with lengthening of the wake period enhancing firing rate rebound.

180 " were compared between sleeps preceding the waking period ("Sleep-Pre") when the Motifs were identif

181 r towards the end of a spontaneous prolonged waking period.

182 sser extent, by raised blood pressure during wake periods (SBP, +1.6 mmHg; DBP, +1.4 mmHg).

183 function, relative to baseline states during wake periods.

184 widespread cortical regions during complete waking periods.

185 n associated with differences in human sleep-wake phenotypes, and sensitivity to light.

186 ure rises exclusively in TDW rather than all waking, predicts delta power dynamics both in Hcrt(ko/ko

187 ong relativistic electron bunch to probe the wake produced in a plasma by an intense laser pulse or a

188 Modafinil is a wake promoting compound with high potential for cognitiv

189 ivation of LH VGAT(+) neurons was profoundly wake promoting, whereas acute inhibition increased sleep

190 y blocked the behavioral and electrocortical wake-promoting action of armodafinil.

191 ytic, weight-reducing, glucose-lowering, and wake-promoting activities.

192 rsibility of mild sleep-loss-induced pain by wake-promoting agents reveals an unsuspected role for al

193 Caffeine and modafinil, two wake-promoting agents that have no analgesic activity in

194 measured Fos co-expression with markers for wake-promoting cell groups in the lateral hypothalamus (

195 Wake-promoting cell types include hypocretin and GABA (g

196 Thus, the wake-promoting effect of "selective" optogenetic stimula

197 e, we show that dopamine is required for the wake-promoting effect of caffeine in the fly, and that c

198 Thus, our data suggest that the wake-promoting effect of cholinergic stimulation require

199 ts suggest that Prok2 antagonizes the direct wake-promoting effect of light in zebrafish, in part thr

200 olinergic antagonists within BF prevents the wake-promoting effect.

201 Z(Vgat) neurons could attenuate or block the wake-promoting effects of two widely used wake-promoting

202 e-activity; (2) armodafinil cannot exert its wake-promoting effects when PZ(Vgat) neurons are activat

203 Multiple populations of wake-promoting neurons have been characterized in mammal

204 The orexin neurons excite wake-promoting neurons in the basal forebrain (BF), and

205 vo, is expressed non-synaptically in several wake-promoting neurons, and likely couples to a Gi/o het

206 e-specific genetic manipulation silenced the wake-promoting orexin neurons located in the lateral hyp

207 (DA) population is a critical contributor to wake-promoting pathways and is capable of modulating sle

208 he wake-promoting effects of two widely used wake-promoting psychostimulants, armodafinil or caffeine

209 e sleep through selective disfacilitation of wake-promoting systems, whereas benzodiazepine receptor

210 vity and suggest TAAR1 as a novel target for wake-promoting therapeutics.

211 lamus and receive inputs from multiple sleep-wake-regulating neurons.

212 ) availability are supposed to mediate sleep-wake regulation and cognitive performance.

213 rease knowledge on the fundamentals of sleep-wake regulation and to contribute to the development of

214 eptide, play important roles in proper sleep/wake regulation in adult flies.

215 elucidating the 'top-down' pathway of sleep-wake regulation is expected to increase knowledge on the

216 The synaptic homeostasis hypothesis of sleep-wake regulation proposes a homeostatic increase in net s

217 ophila homolog of App, could influence sleep-wake regulation when its function is manipulated in glia

218 in multiple brain functions, including sleep-wake regulation, attention, and learning/memory, but the

219 as of neuroscience research, including sleep/wake regulation, feeding, addiction, reward and motivati

220 ysiological functions, particularly in sleep/wake regulation.

221 scribe a revised integrative model for sleep/wake regulation.

222 tablish NPY as an important vertebrate sleep/wake regulator and link NPY signaling to an established

223 These findings indicate that wake-related changes in firing rates are determined not

224 acological disinhibition of the ECN unmasked wake-related reafference, twitch-related reafference was

225 ivity during sleep nor theta activity during waking rest, likely because of the attenuated electrical

226 ficial lighting at night, inconsistent sleep-wake schedules, and transmeridian air travel, is increas

227 We found that in all states of the wake-sleep cycle, excitatory and inhibitory ensembles ar

228 ay recordings in human and monkey during the wake-sleep cycle.

229 xplanation for how circadian phases, such as wake-sleep onset times, can become unstable in humans, a

230 ify SuM(vglut2) neurons as a key node of the wake-sleep regulatory system.

231 However, murine wake-sleep states may be discriminated from breathing an

232 show that non-invasive discrimination of the wake-sleep states of mice based on visual inspection of

233 e EEG/EMG-based and the WBP-based scoring of wake-sleep states of mice, and provide formal guidelines

234 Wake-sleep states were scored based either on EEG/EMG or

235 y/electromyography (EEG/EMG) to discriminate wake-sleep states.

236 t the drop in functional connectivity during wake-sleep transitions globally holds true at the cellul

237 cretin-producing neurons that regulate sleep-wake stability and are affected in narcolepsy.

238 derstanding the molecular basis of the sleep-wake state-dependent control of breathing.

239 rons are thus linked to the control of sleep-wake state.

240 two distinct conditions: (i) under ordinary waking state and (ii) in an altered state of consciousne

241 in REM sleep compared with movements in the waking state and during NREM sleep.

242 and 2.58 in NonREM to a value of 1.99 in the Waking state.

243 n REM sleep reached levels similar as in the waking state.

244 icobasal ganglia network as movements in the waking state.

245 fferent motor networks than movements in the waking state.

246 pathways and is capable of modulating sleep-wake states according to the outside environment, wherei

247 ysiological and behavioral features of sleep/wake states and the principal neuronal populations invol

248 Sleep and wake states are regulated by a variety of mechanisms.

249 ute cessation of HA neuron activity on sleep-wake states in awake and behaving mice, we examined the

250 es on the neural systems that regulate sleep/wake states in mammals and the circadian mechanisms that

251 The effects of long RT compound 9 on sleep-wake states indicated long RT was translated into sustai

252 tially influence cortical activity and sleep/wake states.

253 he regulation of cortical activity and sleep-wake states.

254 having rats as they cycled between sleep and wake states.

255 sibility is net synaptic potentiation during wake: stronger coupling among neurons would lead to grea

256 e in the experiment, though the quasi-linear wake structure could as easily be formed by an electron

257 more time OFF only after sustained firing in wake, suggesting that fatigue due to sustained firing al

258 play a particularly important role in sleep-wake switching.

259 ion of plasticity-related genes is higher in wake than in sleep, we asked whether it is specifically

260 2 region in SPW-R was more pronounced during waking than sleeping.

261 the other hemisphere as a night watch, which wakes the sleeper up when unfamiliar external signals ar

262 During extended wake, the rapid switching to sleep-like states with shor

263 Orexin neuropeptides regulate sleep/wake through orexin receptors (OX1R, OX2R); OX2R is the

264 ed from the geostrophic flow to submesoscale wakes through anticyclonic vertical vorticity generation

265 The observation of declining LRTCs during wake thus provides additional support for our hypothesis

266 precentral cortex was associated with longer wake time after sleep onset (WASO), and its reduction af

267 In contrast, caffeine increased wake time, NREM gamma power, and LMA in all strains comp

268 ase gene causes a profound decrease in total wake time, owing to an increase in inherent sleep need.

269 f wrist actigraphy and reported habitual bed/wake times from 2010 to 2013.

270 When wake-times are enforced by social constraints, such as w

271 omises synchronisation to the solar day when wake-times are not enforced.

272 s with slow circadian clocks or when imposed wake-times occur after sunrise.

273 ect, an 'indirect' pathway via altered sleep-wake timing has been suggested.

274 0.05), and showed a trend of advanced sleep-wake timing.

275 NP: PER3 (C), PER3 (G)) in relation to sleep-wake timing; ii) the effect of morning light on behaviou

276 odynamic events and enable the sophisticated wake-tracking abilities of these animals.

277 ine clinical features, sleep, abnormal sleep-wake transition and non-sleep disturbances as well as la

278 ion of motor activity during sleep and sleep-wake transitions, and that disruption of these circuit n

279 with whom they traveled over a full day from waking until being assaulted or going to bed.

280 Why do we go to sleep late and struggle to wake up on time?

281 ates inversely with both weekend bedtime and wake up time, and also with poor school performance.

282 as 07:07 +/- 01:31 (bedtime 22:32 +/- 01:27, wake up time: 06:17 +/- 01:25 hh:min), sleep quality sco

283 longitudinal electric field of the unloaded wake up to 83 GV m(-1) to a similar degree of accuracy.

284 reover, some cortical areas can transiently "wake up" [8] in an otherwise sleeping brain.

285 High-frequency firing "wakes up" silent Ib synapses and depresses Is synapses.

286 ses largely on the dates by which the system wakes up.

287 Like falling asleep and waking up, many biological processes in mammals cycle in

288 ence of dengue and chikungunya, constitute a wake-up call for governments, academia, funders, and WHO

289 the three bins examined was associated with wake-up cortisol levels, indicating functional relevance

290 n-label study (NCT01183533) in patients with wake-up stroke (WUS).

291 , inspired and expired sevoflurane fraction, wake-up times, duration of sedation, sevoflurane consump

292 t potentiation should occur primarily during wake, when animals learn, and depression should occur du

293 to recover from the "fatigue" accrued during wake, when overall synaptic activity is higher than in s

294 in physiology and in the regulation of sleep/wake, which has been shown recently to be involved in AD

295 diurnal and circadian variation of sleep and waking while controlling for menstrual cycle phase and h

296 activity due to asthma; number of nights of waking with asthma symptoms; and days of coughing, wheez

297 during waking and because, in their absence, waking with muscle tone cannot be maintained and narcole

298 utonomous set point during periods of active wake, with lengthening of the wake period enhancing firi

299 euronal "fatigue": high, sustained firing in wake would force neurons to recover with more frequent a

300 life are known to be impaired after extended wake, yet, the underlying neuronal correlates have been