ライフサイエンスコーパス: sleep

1 e to the strong behavioral manifestations of sleep.

2 ced wakefulness and increased non-REM (NREM) sleep.

3 creased adiposity is associated with shorter sleep.

4 movement (NREM) and rapid eye movement (REM) sleep.

5 lutamatergic DN1s (gDN1s) paralleled daytime sleep.

6 reases to a well-rested state after recovery sleep.

7 ence associated with postencoding novelty or sleep.

8 anogaster, DAT deficiency results in reduced sleep.

9 ate central nervous system neurons to induce sleep.

10 n cognitive functions and that of MCH in REM sleep.

11 in KO compared with OE mice in NREM and REM sleep.

12 ovelty but in the cortex in association with sleep.

13 efit later memory when it takes place during sleep.

14 text for memory consolidation during non-REM sleep.

15 p deprivation and following 14 h of recovery sleep.

16 e in effective interactions during slow-wave sleep.

17 s re-presented during subsequent REM or NREM sleep.

18 and early awakenings), sleep duration (short sleep 5 hours or less; long sleep greater than 8 hours),

19 mplicated in neurological disorders in which sleep abnormalities are common; for example, variation i

20 sponding epileptic discharges with prominent sleep activation in most cases with loss-of-function mut

21 Insomnia and the inability to sleep affect people's health and well-being.

22 rugs approved for the treatment of insomnia [sleep aids], attention-deficit/hyperactivity disorder dr

23 Surprisingly, most sleep-amount, but not sleep-timing, phenotypes could be

24 Here, we describe sleep and activity in two neighbouring communities, one

25 tedly recorded high-density EEG after normal sleep and after sleep deprivation while participants obs

26 asive high-throughput experiments evaluating sleep and breathing patterns on mouse models of pathophy

27 Conversely, sleep and circadian disruptions are implicated in a vari

28 ces at night increases, leading to disrupted sleep and circadian misalignment (i.e., social jet lag).

29 that CSDS produces persistent disruptions in sleep and circadian rhythmicity, mimicking attributes of

30 in mice produces progressive alterations in sleep and circadian rhythms that resemble features of de

31 ) before CSDS reduced stress effects on both sleep and circadian rhythms, or hastened their recovery,

32 ry, as well as a new approach for predicting sleep and cognitive performance under planned schedules.

33 Ethanol has extensive effects on sleep and daytime alertness, causing premature disabilit

34 wake homeostasis, including lack of recovery sleep and impaired behavioral adjustment to a novel task

35 unction in heterozygote individuals disturbs sleep and might increase the risk for developing mood di

36 priority should be given to the duration of sleep and MVPA.

37 striction (multiple nights with insufficient sleep), and subsequent recovery.

38 l-world physical activity patterns, fitness, sleep, and cardiovascular health.

39 ep, waking at night, trouble getting back to sleep, and early awakenings), sleep duration (short slee

40 a-cell function, for time spent in slow-wave sleep, and for EEG spectral power in the delta, theta, a

41 ng/extinction or utilized peripheral immune, sleep, and noninvasive imaging measures, we argue that t

42 ocortical spindle activity (12-15 Hz) during sleep, and their temporal coordination, are considered c

43 During sleep, animals are disconnected from the external world;

44 e 1990s, estimated prevalence of obstructive sleep apnea (OSA) in the United States is 10% for mild O

45 lth outcomes are associated with obstructive sleep apnea (OSA).

46 ects with high and low risks for obstructive sleep apnea (OSA).

47 ts, is linked to the severity of obstructive sleep apnea (OSA).

48 ular caliber and the severity of obstructive sleep apnea (OSA).

49 ss improvement in ACT scores was obstructive sleep apnea (P = 0.016).

50 Sleep apnea is a common problem affecting daily function

51 Sleep apnea is common in hospitalized heart failure (HF)

52 asthma patients with concomitant obstructive sleep apnea syndrome (OSAS) seems to have a favorable im

53 ing, obesity, diabetes mellitus, obstructive sleep apnea, and elevated blood pressure predispose to A

54 l factors that included obesity, obstructive sleep apnea, higher comorbidity, and use of prescription

55 f the following: CHA2DS2-VASc score of >/=2, sleep apnea, or body mass index >30 kg/m(2).

56 italized HF patients with moderate-to-severe sleep apnea.

57 t necessary for most patients with suspected sleep apnea.

58 ealed increased gray matter with obstructive sleep apnea.

59 a relatively high prevalence of obstructive sleep apnoea (OSA).

60 st, e.g. essential hypertension, obstructive sleep apnoea and heart failure.

61 cause of perinatal mortality in infants and sleep apnoea in adults, but the mechanisms of respirator

62 usitis, gastroesophageal reflux, obstructive sleep apnoea, vocal cord dysfunction, obesity, dysfuncti

63 Older adults do not sleep as well as younger adults.

64 DF projections, ArcLight, GCaMP6 imaging and sleep assays indicate that mir-92a suppresses neuronal e

65 e revisit important experimental findings on sleep-associated memory (i.e., neural activity patterns

66 computational approaches to the analysis of sleep-associated neural codes (SANCs).

67 son mutagenesis strategy based on a two-step Sleeping Beauty (SB) forward genetic screen to identify

68 d mobilization of a single-copy inactivating Sleeping Beauty transposon to Pten disruption within the

69 ng to identify idiopathic rapid eye movement sleep behavior disorder (IRBD) patients at risk for shor

70 resence of probable rapid eye movement (REM) sleep behavior disorder was strongly associated with the

71 Rapid eye movement (REM) sleep behaviour disorder (RBD) is characterised by compl

72 Delivering sounds during sleep biased AC activity patterns, and sound-biased AC p

73 that pattern separation was stabilized after sleep but diminished after wakefulness.

74 d Down states are a defining feature of deep sleep, but their function is not well understood.

75 and waist circumference (WC) was modified by sleep characteristics.This study included cross-sectiona

76 ity or secondary ocular surface disease in a sleep clinic population.

77 The sleep clusters displayed significant differences in prop

78 n-spine interface (ASI) decreased 18% after sleep compared with wake.

79 he incidence of 3 CVD risk factors (obesity, sleep complaints, and depression) was predicted by a lar

80 ticipate in an ancient and central aspect of sleep control.

81 ordings from human STN differentiate between sleep cycle states, and sleep-state specific spectral mo

82 are exposed that directly reflect ultradian sleep cycles and replicate the dynamics of laboratory sl

83 0-350 Hz) that were associated with specific sleep cycles: delta (0-3 Hz) activity during non-rapid e

84 vities are major contributors to the growing sleep deficiency epidemic, as is the high prevalence of

85 roencephalography (EEG), structural MRI, and sleep-dependent memory assessment, we addressed these qu

86 es of sleep (e.g., network oscillations) and sleep-dependent plasticity has been difficult.

87 ased either on EEG/EMG or on WBP signals and sleep-dependent respiratory and cardiovascular estimates

88 hanges in cognitive performance during acute sleep deprivation (one prolonged wake episode), chronic

89 table with repeated exposures to acute total sleep deprivation (TSD) within a short-time interval (we

90 lity in 15 healthy male adults after 52 h of sleep deprivation and following 14 h of recovery sleep.

91 is upregulated already after a few hours of sleep deprivation and shows a further significant increa

92 induced increase in alpha power by means of sleep deprivation increased the average duration of indi

93 Early night, but not late night, sleep deprivation induced a significant phase shift.

94 Sleep deprivation results in a sleep rebound.

95 Recovery from sleep deprivation was associated with a decrease in A1AR

96 igh-density EEG after normal sleep and after sleep deprivation while participants observed a Necker c

97 n of GS and innexin2 are increased following sleep deprivation, indicating that GS and innexin2 genes

98 behavioral adjustment to a novel task after sleep deprivation.

99 in phagocytosis, are upregulated after acute sleep deprivation.

100 arousal in flies counteracts the effects of sleep deprivation.

101 erize basal sleep/wake parameters, mice were sleep deprived (SD) for 6 h.

102 y, and awake after sleep onset, derived from sleep diaries; polysomnography; and symptoms of fatigue,

103 everity (Insomnia Severity Index) and online sleep diary-derived values for sleep-onset latency and w

104 Sleep difficulties might be a contributory causal factor

105 ing evidence suggests an association between sleep-disordered breathing (SDB) and cognitive decline i

106 ights the complex interrelationships between sleep-disordered breathing and cardiovascular disease, p

107 Sleep-disordered breathing is associated with an increas

108 Sleep-disordered breathing was ascertained by apnea-hypo

109 Many genetic variants associated with sleep disorders are also implicated in neurological diso

110 iency epidemic, as is the high prevalence of sleep disorders like insomnia.

111 een healthy adults (age 35-65 years) without sleep disorders underwent 5-14 days of actigraphy, follo

112 genes influencing risk for some neurological sleep disorders.

113 er emerging studies suggest that age-related sleep disruption may be one key factor that renders the

114 Prevalence of sleep disturbance is high in this large Chinese cohort.

115 terest-muscle-related, erectile dysfunction, sleep disturbance, and cognitive impairment-and analysed

116 r patients age 65 to 84 years reported lower sleep disturbance, anxiety, and depression, and better c

117 ple mechanisms have been identified by which sleep disturbances adversely affect cardiovascular struc

118 Chronic sleep disturbances, associated with cardiometabolic dise

119 se events (self-reported breathing problems, sleep disturbances, drowsiness or tiredness, nausea, swe

120 ) have impaired receptor function and showed sleep disturbances.

121 ted mixed effects regression models, shorter sleep duration (per hour less) and greater sleep fragmen

122 etting back to sleep, and early awakenings), sleep duration (short sleep 5 hours or less; long sleep

123 bute substantially to self-reported habitual sleep duration and disruption, these traits are heritabl

124 We assessed sleep duration and quality by 5-7 days of wrist actigrap

125 mental and epidemiologic evidence has linked sleep duration and quality to glucose homeostasis, altho

126 Cross-sectional analyses of adiposity and sleep duration in younger adults suggest that increased

127 factors for changes in objectively assessed sleep duration within a large sample of community-dwelli

128 n = 65), with the former exhibiting reduced sleep duration, earlier sleep offset, and less stability

129 e-wide association analyses of self-reported sleep duration, insomnia symptoms and excessive daytime

130 ated the central neuroendocrine mechanism of sleep during sickness.

131 bserved changes in cognitive performance and sleep during sleep loss and recovery, as well as a new a

132 al studies and big-data approaches assessing sleep dynamics are lacking.

133 l relationships between specific features of sleep (e.g., network oscillations) and sleep-dependent p

134 re but, in contrast to humans, absolute NREM sleep EEG slow-wave activity (SWA, spectral power densit

135 e by decreasing sleep latency and increasing sleep efficiency compared with vehicle.

136 lity; total sleep time, sleep onset latency, sleep efficiency, and awake after sleep onset, derived f

137 previous work has focused on the effects of sleep following fear acquisition, thus neglecting the po

138 n the hippocampus and the BLA during non-REM sleep following training.

139 The consequences of chronic insufficient sleep for health remain uncertain.

140 r sleep duration (per hour less) and greater sleep fragmentation (per 1% more) each associated with g

141 ith hypoxemia, respiratory disturbances, and sleep fragmentation.

142 measures of physical activity, fitness, and sleep from smartphones and to gain insights into activit

143 REM sleep frontal high delta power was a negative correlate

144 duration (short sleep 5 hours or less; long sleep greater than 8 hours), epigenetic age, naive T cel

145 ly related to the adolescents' variations in sleep habits, as its volume correlates inversely with bo

146 pindles during non-rapid-eye-movement (NREM) sleep has been proposed to support memory consolidation.

147 Accordingly, sleep has been suggested as a state characterized by a b

148 Together, these findings indicate that REM sleep has multifaceted functions in brain development, l

149 ms and functions of rapid-eye-movement (REM) sleep have occurred over the past decade.

150 model implies that developmental changes in sleep homeostasis and circadian amplitude make adolescen

151 Sleep homeostasis and circadian function are important m

152 effects of light, circadian rhythmicity and sleep homeostasis to provide a quantitative theoretical

153 euromodulators and acts as a major driver of sleep homeostasis.

154 severity, psychiatric symptom severity, and sleep impairment were significantly worse in patients wi

155 tering the pacemaker's phase-relationship to sleep in a manner that is known to cause switches from d

156 Sleep in flies thus appears to involve at least two dist

157 quency of touchscreen use is associated with sleep in infants and toddlers between 6 and 36 months of

158 ific investigation into the possible role of sleep in memory consolidation began with the early studi

159 a waxing and waning of interest, the role of sleep in memory processing remains controversial and elu

160 of epigenetic age and immune cell aging with sleep in the Women's Health Initiative study (N = 2078;

161 256390 profoundly reduced rapid eye movement sleep in wild-type mice; these effects were eliminated i

162 Testing during quiet natural sleep included tidal breathing, exhaled nitric oxide, an

163 ed oscillatory activity, particularly during sleep induction, followed by desynchronized or decreased

164 We show that an increased need for sleep inhibits male sexual behavior by decreasing the ac

165 udied how two fundamental behaviors, sex and sleep, interact at genetic and neuronal levels in Drosop

166 n 2 experts and between 1 expert and 1 naive sleep investigators gave similar results.

167 Sleep is a dynamic process comprising multiple stages, e

168 Here we show that sleep is also present in Cnidaria [6-8], an earlier-bran

169 ignificantly circadian and dysregulated when sleep is disrupted.

170 sults suggest that coordinated firing during sleep is essential for establishing sparse activation pa

171 Sleep is essential for proper brain function in mammals

172 eep-like states, prompting us to ask whether sleep is present in Cnidaria.

173 During health, animal sleep is regulated by an internal clock and by the durat

174 of hippocampal neural representations during sleep is thought to promote systems consolidation of dec

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

176 s disrupted by methamphetamine by decreasing sleep latency and increasing sleep efficiency compared w

177 en MS1 neurons are activated, isolated males sleep less, and when MS1 neurons are silenced, the norma

178 neglecting the potential effects of baseline sleep levels on the acquisition itself.

179 tor activity to "Locomotor Inactivity During Sleep" (LIDS), movement patterns are exposed that direct

180 t periods of quiescence, a pre-requisite for sleep-like states, prompting us to ask whether sleep is

181 sleep practices of sleep position (supine), sleep location (room sharing without bed sharing), soft

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

183 Sleep loss produces well-characterized cognitive deficit

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

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

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

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

188 chanisms employed in the control of sickness sleep may play a role in correcting cellular homeostasis

189 If this is true, sleep may represent a key modifiable risk factor or ther

190 Both drugs improved activity-based sleep measures disrupted by methamphetamine by decreasin

191 nes involved should improve understanding of sleep, mechanisms linking sleep to disease and developme

192 djusted analyses, mothers receiving the safe sleep mobile health intervention had higher prevalence o

193 e, studies have not examined which aspect of sleep modulates amyloid-beta or other Alzheimer's diseas

194 the current study, we used long-term mobile sleep monitoring and functional neuroimaging (fMRI) to e

195 As expected, older mice slept more but, in contrast to humans, absolute NREM sle

196 s is causally related to reactivation during sleep of previously encoded representations.

197 r exhibiting reduced sleep duration, earlier sleep offset, and less stability in sleep timing.

198 d = 1.41 [95% CI, 1.15-1.68], and wake after sleep onset d = 0.95 [95% CI, 0.70-1.21]), with 56.6% (6

199 f insomnia; sleep quality; total sleep time, sleep onset latency, sleep efficiency, and awake after s

200 ation for how circadian phases, such as wake-sleep onset times, can become unstable in humans, and we

201 alues for sleep-onset latency and wake after sleep onset, collected prospectively for 10 days at each

202 t latency, sleep efficiency, and awake after sleep onset, derived from sleep diaries; polysomnography

203 ifically impacts siesta onset, but not night sleep onset, in response to elevated temperatures.

204 x) and online sleep diary-derived values for sleep-onset latency and wake after sleep onset, collecte

205 Severity Index d = 2.32 [95% CI, 2.01-2.63], sleep-onset latency d = 1.41 [95% CI, 1.15-1.68], and wa

206 d question: do older adults simply need less sleep, or rather, are they unable to generate the sleep

207 The primary sleep outcomes were self-reported online ratings of inso

208 les and replicate the dynamics of laboratory sleep parameters.

209 y provide insight into mechanisms underlying sleep pathophysiology.

210 Changes in sleep pattern are typical for the normal aging process.

211 to explore whether trait-like variations in sleep patterns, measured in advance in both male and fem

212 ion of weakly learned information early in a sleep period.

213 Behavioral arousal in the sleeping period phase shifts the master clock in the sup

214 synchronisation correlates with spindle-rich sleep phases.

215 ation, and socialization, demonstrating that sleep phenotypes are associated with symptom severity in

216 d results provide the necessary quantitative sleep phenotypes for large field studies and outcome ass

217 rightness perception, vigilant attention and sleep physiology.

218 imum sound levels were higher in ICUs with a sleep policy or protocol compared with those without max

219 dherence to 4 infant safe sleep practices of sleep position (supine), sleep location (room sharing wi

220 parately and combined to promote infant safe sleep practices compared with control interventions.

221 nal self-reported adherence to 4 infant safe sleep practices of sleep position (supine), sleep locati

222 Sleep, presumably by neural memory replay, shapes hippoc

223 thoroughly examined the potential effects of sleep prior to conditioning on subsequent acquisition of

224 e SCORAD), symptoms (POEM, VAS pruritus, VAS sleeping problems) and previous treatment of AD were ass

225 ormal evening locomotor activity and daytime sleep profiles, respectively, we suggest that their luci

226 locomotor activity, and the LUC profile from sleep-promoting glutamatergic DN1s (gDN1s) paralleled da

227 n-releasing hormone, and tachykinin 1) label sleep-promoting neurons.

228 pvf-expressing neurons as a novel vertebrate sleep-promoting system and suggest that RFamide neuropep

229 patients had more severe depression, poorer sleep quality and reduced quality of life.

230 nt validity, with perceived stress level and sleep quality for concurrent validity and the receiver o

231 re clinician-assessed remission of insomnia; sleep quality; total sleep time, sleep onset latency, sl

232 lidity (r with perceived stress=0.55, r with sleep quality=0.39) and predictive validity (area under

233 What alterations in sleep quantity and quality occur as we age, and are ther

234 outcome was change in Functional Outcomes of Sleep Questionnaire (FOSQ) score at 4 months.

235 Sleep deprivation results in a sleep rebound.

236 ay be therapeutically effective in improving sleep regularity in this population.

237 sults also associate glutamate recycling and sleep regulation, adding further complexity to the physi

238 Sleep regulatory processes are assumed to lie exclusivel

239 ients are typically characterized by organic sleep related symptoms, rapidly progressive dementia and

240 Sleep remains one of the most mysterious yet ubiquitous

241 imentally induced memory reactivation during sleep renders long-term memories of negative experiences

242 vation (one prolonged wake episode), chronic sleep restriction (multiple nights with insufficient sle

243 e, no study has investigated whether chronic sleep restriction can influence implicit attitudes (e.g.

244 ngle OTU, TM7-3a, was found to increase with sleep restriction of rats.

245 biome is largely resistant to changes during sleep restriction.

246 re time in screen activities (RR = 0.98) and sleeping (RR = 0.96) had the lowest compliance.

247 The association of irregular sleep schedules with circadian timing and academic perfo

248 ivation-based consolidation processes during sleep shape the hippocampal representation itself.

249 Trypanosoma brucei, the causative agent of sleeping sickness (Human African Trypanosomiasis, HAT),

250 ovide different levels of protection against sleeping sickness, but this comes with an increased risk

251 energy metabolism in the causative agent of sleeping sickness, Trypanosoma brucei, with that of huma

252 t for human African trypanosomiasis (HAT) or sleeping sickness.

253 osoma brucei, the causative agent of African sleeping sickness; and Plasmodium spp., the causative ag

254 k factors for infants include prone and side sleeping, soft bedding, bed sharing, inappropriate sleep

255 teraction between slow-wave oscillations and sleep spindles during non-rapid-eye-movement (NREM) slee

256 Sleep spindles promote the consolidation of motor skill

257 it is unclear if invertebrates have distinct sleep stages.

258 n the awake state during behavior and in the sleep state after behavior.

259 ifferentiate between sleep cycle states, and sleep-state specific spectral mosaics may provide insigh

260 /EMG-based and the WBP-based scoring of wake-sleep states of mice, and provide formal guidelines for

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

262 ons interact with the FRU network to mediate sleep suppression by male sex drive.

263 en MS1 neurons are silenced, the normal male sleep suppression in female presence is attenuated and m

264 ng, soft bedding, bed sharing, inappropriate sleep surfaces (including sofas), exposure to tobacco sm

265 storage and memory-guided behavior, whereas sleep SWR reactivation is better suited to support integ

266 Awake and sleep SWRs are associated with memory reactivation and a

267 tal muscle plays a bigger role in regulating sleep than it does in the brain.

268 nificantly fewer brief bouts of activity and sleep than the wild-types.

269 ed memory (i.e., neural activity patterns in sleep that reflect memory processing) and review computa

270 , or rather, are they unable to generate the sleep that they still need?

271 be critical for memory consolidation during sleep, the role spindles play in this interaction is elu

272 nal rhythms of non-rapid-eye-movement (NREM) sleep-the thalamo-cortical spindles, hippocampal ripples

273 Here we show that during sleep there is a rapid cortical-hippocampal-cortical loo

274 ind that FRU(M) regulates male courtship and sleep through distinct neural substrates.

275 Furthermore, we show that the average mid-sleep time of people living in urban areas depends on th

276 remission of insomnia; sleep quality; total sleep time, sleep onset latency, sleep efficiency, and a

277 rse association of either indoor activity or sleeping time with the risk of hyperglycemia among offsp

278 t delays circadian rhythmicity and preferred sleep timing and compromises synchronisation to the sola

279 earlier sleep offset, and less stability in sleep timing.

280 No significant differences were observed in sleep timing/aMT6s rhythms between PER3 (5) /PER3 (5) an

281 Surprisingly, most sleep-amount, but not sleep-timing, phenotypes could be reproduced or rescued

282 e understanding of sleep, mechanisms linking sleep to disease and development of new therapies.

283 ssessment of physical activity, fitness, and sleep using mobile devices may be a useful addition to f

284 e implicated in autism spectrum disorder and sleep-wake control.

285 ader fluctuations of DRN(DA) activity across sleep-wake cycles with highest activity during wakefulne

286 Diagnosis and treatment of circadian rhythm sleep-wake disorders both require assessment of circadia

287 ional mGluR5 exhibit severe dysregulation of sleep-wake homeostasis, including lack of recovery sleep

288 ning light administration, whilst monitoring sleep-wake patterns and the urinary 6-sulphatoxymelatoni

289 (A1AR) availability are supposed to mediate sleep-wake regulation and cognitive performance.

290 owing a 24 h recording to characterize basal sleep/wake parameters, mice were sleep deprived (SD) for

291 we describe a revised integrative model for sleep/wake regulation.

292 ple physiological functions, particularly in sleep/wake regulation.

293 ata establish NPY as an important vertebrate sleep/wake regulator and link NPY signaling to an establ

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

295 Sleep was impaired by troublesome symptoms and nasal obs

296 onsible for the ppDIO-induced alterations in sleep, we focused on the lateral hypothalamus (LH).

297 network dynamics of cortical activity during sleep were obtained by investigating characteristics of

298 oses completely blocked ethanol-induced NREM sleep when administered 30 min prior to (but not after)

299 e properties was preserved across a night of sleep, while memory for both feature types declined over

300 s of hippocampal-neocortical networks during sleep would reveal important circuit mechanisms in memor