ライフサイエンスコーパス: sleep

1 tudies on the mechanisms linking opioids and sleep.

2 on is affected by sensory stimulation during sleep.

3 hargus favors strong RIS activation and thus sleep.

4 eas in non-rapid eye movement (NREM) and REM sleep.

5 ing in larger offline performance gains over sleep.

6 tein waste products, is mostly active during sleep.

7 consciousness was regulated by physiological sleep.

8 ative disease-related changes in arousal and sleep.

9 ion of energy stores, which in turn promotes sleep.

10 ly behaving male rats across wakefulness and sleep.

11 one nostril in non-rapid eye movement (NREM) sleep.

12 larger responses during SWS than during REM sleep.

13 performance, quality of life, and quality of sleep.

14 oring to prevent the adverse effects of poor sleep.

15 delta power, slow oscillatory power, and N3 sleep.

16 the prevalence of insufficient and disrupted sleep.

17 he mechanisms underlying opioid exposure and sleep.

18 tics co-opt the neural mechanisms regulating sleep.

19 maturation of a neural network that controls sleep.

20 er after sleep deprivation than after normal sleep: (30 min [interquartile range [IQR], 17-41] vs. 60

21 of SPD attributable to objectively measured sleep across racial/ethnic groups.

22 d conditions in C. elegans, sleep requires a sleep-active neuron called RIS.

23 ive wake-promoting neurons in turn shut down sleep-active neurons, thus forming a bipartite flip-flop

24 Simulating sleep after new learning reversed the damage and enhance

25 s synchronized during non-rapid eye movement sleep after sleep deprivation at the network and single-

26 s that are reactivated during subsequent REM sleep against a backdrop of overall reduced ABN activity

27 that the brain is in an unconscious state in sleep, akin to general anesthesia (GA), and hence is inc

28 t into behavior than measuring the amount of sleep alone.

29 We propose that mouse nighttime sleep, analogous to the human siesta, is a "hard-wired"

30 tion to brain centers involved in regulating sleep and activity.

31 amework explaining the intimate link between sleep and anxiety and further highlight the prospect of

32 tional relationship between abnormalities in sleep and anxiety-related brain pathways is presented.

33 Sleep and arousability impact health acutely (daytime co

34 ep apnea and other disorders prevent restful sleep and contribute to cognitive, metabolic, and physio

35 n, demographics, body mass, and time between sleep and echocardiographic measurements.

36 G spiking and field potentials during normal sleep and in 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridin

37 causal link between ABN activity during REM sleep and memory consolidation.

38 role of the circadian system and patterns of sleep and motor activity in people with BD.

39 tional feed-forward interaction between poor sleep and opioid use.

40 l signatures of sensory disconnection during sleep and pave the way to understanding the underlying m

41 zation, during non-rapid eye movement (NREM) sleep and rapid eye movement (REM) sleep, in six medicat

42 lculated for each patient and the effects of sleep and seizures on these dynamics were evaluated.

43 effect modifier of the relationship between sleep and severe periodontal disease (OR = 4.8, P < 0.05

44 fect stage, there is a decrease in slow-wave sleep and some limited recovery in REM sleep when indivi

45 support a bidirectional interaction between sleep and synapse pruning after antennal injury: locally

46 d, in the form of cognitive tasks, disrupted sleep and the cortisol awakening response (CAR), dependi

47 al DW coupling was strengthened in post-task sleep and was correlated with performance on the spatial

48 nd explored if these changes were related to sleep and/or gut microbial alpha diversity.

49 ts an effort from editors at 31 respiratory, sleep, and critical care medicine journals to consolidat

50 ocessing in the prefrontal region during REM sleep, and inhibited neural activation in the untrained

51 nd navigation, time-memory for food sources, sleep, and learning/memory processes.

52 appliances that hold the jaw forward during sleep, and surgical modification of the pharyngeal soft

53 ed as a key regulator of behavioral arousal, sleep, and wakefulness and has been an area of intense r

54 The uncovered critical behavior in sleep- and wake-related cortical rhythms indicates a mec

55 lved in circadian control) in agreement with sleep anomalies in all of the individuals.

56 therapeutic interventions for breathing and sleep anomalies.

57 We determine whether obstructive sleep apnea (OSA) increases serum levels of active TGF-b

58 Obstructive sleep apnea (OSA) is a highly prevalent disorder also in

59 Many adults with obstructive sleep apnea (OSA) use device treatments inadequately and

60 ated blood carbon dioxide levels, as seen in sleep apnea [3].

61 However, increased arousals in patients with sleep apnea and other disorders prevent restful sleep an

62 and lifestyle behaviors, severe obstructive sleep apnea associated with increased risk of CKD (hazar

63 apnic COPD undergo screening for obstructive sleep apnea before initiation of long-term NIV (conditio

64 hypertension, emerging risk factors such as sleep apnea or inflammation, and increasingly well-defin

65 ndex (events per hour) to define obstructive sleep apnea severity (normal, <5.0; mild, 5.0-14.9; mode

66 regression was used to estimate obstructive sleep apnea severity with risk of incident CKD, adjustin

67 Obstructive sleep apnea syndrome (OSAS) represents a substantial dis

68 ludes primary snoring through to obstructive sleep apnea syndrome (OSAS), may cause compromise of res

69 ease, migraine, hypotension, and obstructive sleep apnea syndrome.

70 nsion, diagnoses including obesity, alcohol, sleep apnea, diabetes, chronic obstructive pulmonary dis

71 During obstructive sleep apnea, elevation of CO(2) during apneas contribute

72 tus, cardiovascular disease, and obstructive sleep apnea, resulting in significant health care resour

73 hlights the interactions between obstructive sleep apnea-hypopnea syndrome (OSAHS) and cardiovascular

74 simulating a severe condition of obstructive sleep apnea.

75 as shown to be accurate for the diagnosis of sleep apnea; however, studies using the WatchPAT device

76 tension, chronic kidney disease, obstructive sleep apnoea, and metabolic disease including diabetes a

77 ysfunction, atrial fibrillation, obstructive sleep apnoea, osteoporosis and venous thromboembolism.

78 The observed differences in A. cahirinus sleep architecture raise questions about the evolutionar

79 Reserpine induced changes in the sleep architecture with more transitions between states,

80 onic conditions, for which periodontitis and sleep are established risk factors.

81 rcise, psychosocial stress, and insufficient sleep are increasingly prevalent modifiable risk factors

82 wever, the mechanisms by which Abeta affects sleep are unknown.

83 light the prospect of non-rapid eye movement sleep as a therapeutic target for meaningfully reducing

84 sion (GEC(HO-1) rats) were generated using a Sleeping Beauty (SB) transposon system and extent of les

85 Poor sleep behavior appears to have adverse effects on health

86 Rapid eye movement sleep behavior disorder (RBD) is a prodromal synucleinop

87 e prodromal features (eg, rapid eye movement sleep behavior disorder, hyposmia, constipation), charac

88 questions about the evolutionary drivers of sleep behavior.

89 During rapid eye movement (REM) sleep, behavioral unresponsiveness contrasts strongly wi

90 th the poorest activity profile and shortest sleep but also the best diet quality (cluster 2); 3) ano

91 , revealing not only a decrease in Slow Wave Sleep, but also a disinhibition of REM (rapid eye moveme

92 Our results suggest that Mel promotes sleep by activating the BK channel through a specific Me

93 novel regulation of the circadian rhythm and sleep by the miR-375-timeless interaction.

94 arousal (i.e., gentle handling) suggest that sleep can promote synaptic growth and strengthening.

95 Associations of sleep characteristics with mild cognitive impairment (MC

96 MUA responses were considerably increased in sleep compared to waking, with larger responses during S

97 ine the shared and specific effects of three sleep complaints (i.e., trouble falling asleep, early mo

98 exerted almost exclusively through a general sleep complaints factor representing the shared effect a

99 Following adjustments, effects of sleep complaints on this risk were significant and exert

100 or representing the shared effect across all sleep complaints.

101 the end of night), crossed-over with a full sleep condition in a balanced order, followed by a funct

102 The morning after both sleep conditions, we tested cold pressor pain tolerance

103 CSR) is believed to only occur in supine and sleeping conditions, and thus, CSR treatment is applied

104 This study demonstrates that NREM sleep consists of alternating brain states whose tempora

105 chiatric research confirmed a disturbance of sleep continuity in patients with depression, revealing

106 Preserving sleep continuity should be a primary consideration if au

107 ons to mediate nutritional modulation of the sleep-courtship balance.

108 d microphysiological architecture metrics of sleep demonstrated such sensitivity.

109 a disinhibition of REM (rapid eye movement) sleep, demonstrated as a shortening of REM latency, an i

110 ed mechanism that enables Drosophila to form sleep-dependent and sleep-independent memory.

111 -h day to compensate for the well-documented sleep-dependent changes in synaptic excitation.

112 reased spindle density but failed to enhance sleep-dependent procedural memory consolidation.

113 Participants underwent partial sleep deprivation (3 h sleep opportunity at the end of n

114 of serotonin and dopamine in the brain upon sleep deprivation (SD).

115 human cerebrospinal fluid (CSF) and chronic sleep deprivation accelerates the spread of tau protein

116 ed during non-rapid eye movement sleep after sleep deprivation at the network and single-cell level.

117 Partial sleep deprivation caused decreased activation in fusifor

118 ew findings from our group reveal that acute sleep deprivation increases levels of tau in mouse brain

119 Here we show, using flies and mice, that sleep deprivation leads to accumulation of reactive oxyg

120 By contrast, sleep deprivation studies using approaches avoiding nove

121 task failure was significantly shorter after sleep deprivation than after normal sleep: (30 min [inte

122 Furthermore, after sleep deprivation, mice with lesioned VTA(Vgat) neurons

123 In the sleep-deprivation condition, preinspiratory motor potent

124 sleep, even though they were starting from a sleep-deprived baseline, suggesting that sleep homeostas

125 include self-care management strategies for sleep difficulties to ensure retention at work.

126 mance measures compared to sleeping on LR or sleeping directly on spring mattresses without a topper.

127 Individuals with this sleep disorder are also at increased risk for establishe

128 Obstructive sleep-disordered breathing (SDB), which includes primary

129 logical mechanisms underlying the effects of sleep-disordered breathing on the brain.

130 Heart failure has previously been linked to sleep disorders that are often associated with frequent

131 whereas in anti-NMDA receptor encephalitis, sleep disorders vary according to the disease stage alon

132 In anti-IgLON5 disease, sleep disorders were the core symptoms that led to the d

133 billion people worldwide suffer from various sleep disorders.

134 f conditions such as heart, lung, blood, and sleep disorders.

135 ms of hypomania, agitation, impulsivity, and sleeping disorders.

136 ical findings to humans by examining whether sleep disruption alters morphine's analgesic and hedonic

137 c review of all risk factors associated with sleep disruption in the ICU setting.

138 efore arousals suggests its participation in sleep disruption.

139 (US) and two nights of forced awakening (FA) sleep disruption.

140 Patients rated noise and light as the most sleep-disruptive factors.

141 e medication (RR 3.46; 95% CI 2.79 to 4.30), sleep disturbance (MD -7.29; 95% CI -8.23 to -6.35) and

142 haracteristics and physiological features of sleep disturbance in specific DSM anxiety-related disord

143 and anxiety tend to lump different forms of sleep disturbance together.

144 endpoints including cardiovascular disease, sleep disturbance, depression, and psychosocial stress.

145 Our results indicated that sleep disturbances are statistically significant, yet we

146 cient times it is known that melancholia and sleep disturbances co-occur.

147 Limited recovery of sleep disturbances is seen in AUD within the first 30 da

148 es of alcohol craving and mood, anxiety, and sleep disturbances, which are predictive of poor treatme

149 traffic noise is associated with stress and sleep disturbances.

150 for hours, even during a period of elevated sleep drive.

151 vidence has suggested an association between sleep duration and Alzheimer's disease (AD), but it is u

152 Several studies have suggested that reduced sleep duration and quality are associated with an increa

153 tatistically significant association between sleep duration and severe periodontitis.

154 better physical activity profile and longer sleep duration coupled with an average diet quality (clu

155 d marker of earlier puberty with self-report sleep duration in adolescence.

156 Low sleep duration in adults is correlated with psychiatric

157 n the parents was also correlated with short sleep duration in their children.

158 zheimer's disease (AD), but it is unclear if sleep duration is a manifestation of the AD disease proc

159 Short sleep duration might be an early marker of AD.

160 ssed the association of earlier puberty with sleep duration observationally and with validation using

161 ed whether genetic liability for AD predicts sleep duration using a genetic risk score (GRS) for AD (

162 t Charge 2 (FC2), from which sleep duration, sleep duration variability, sleep onset, and sleep onset

163 wed that a higher between-day variability in sleep duration was associated with an increase in HbA1c

164 cipants, after controlling for age, habitual sleep duration was positively related to source memory p

165 older (6-8 years, n = 70) children, habitual sleep duration was related to hippocampal head subfield

166 eased neurotransmitter release and shortened sleep duration, and these effects are nonadditive in dou

167 using the Fitbit Charge 2 (FC2), from which sleep duration, sleep duration variability, sleep onset,

168 U.S. adolescents (12-17 years) self-reported sleep duration, timing, weekday-weekend differences in d

169 trating hormone containing cells to increase sleep duration.

170 fants before imaging to encourage infants to sleep during the scan.

171 as been little progress in understanding how sleep EEG in different brain regions responds to CSR.

172 predicts that memory storage is dynamic, and sleep enables continual learning by combining consolidat

173 d VTA(Vgat) neurons did not catch up on lost sleep, even though they were starting from a sleep-depri

174 ceptor 1) from two independent natural short sleep families.

175 sses [1-3], but it is unclear which specific sleep features are dependent upon this brain structure.

176 Another line of studies has shown that sleep following training also plays a role in facilitati

177 ter appetitive conditioning needed increased sleep for memory consolidation, but flies starved after

178 epresents a substantial disease of recurrent sleep fragmentation, leading to intermittent hypoxia and

179 after sleep onset and latency to persistent sleep from baseline to days 1 and 2 with daridorexant.

180 eep health over time, raising concerns about sleep health disparities emanating from the workplace.

181 ation may contribute to working women's poor sleep health over time, raising concerns about sleep hea

182 m a sleep-deprived baseline, suggesting that sleep homeostasis was bypassed.

183 (<=25 years), higher anxiety level, and poor sleep hygiene.

184 gulates emotional memory, and persistent REM sleep impairment after cocaine withdrawal negatively imp

185 ient for neurotensin exhibited increased REM sleep, implicating the involvement of the neuropeptide i

186 ing natural attentive waking and paradoxical sleep in association with theta activity and could serve

187 ements have occurred in the ability to study sleep in dogs, including development of non-invasive pol

188 We investigated the role of sleep in experience-dependent dendritic spine eliminatio

189 lding upon data suggesting the importance of sleep in learning and memory, we tested a hypothesis tha

190 related metabolic disorders, but the role of sleep in long-term weight loss maintenance (WLM) has not

191 Activation of DA-PB neurons led to reduced sleep in normally fed but not yeast-deprived males.

192 as well tolerated and effective in promoting sleep in people with OSA, which may be therapeutically u

193 e when the internal circadian clock promotes sleep, in many cases resulting in impairments in cogniti

194 nt (NREM) sleep and rapid eye movement (REM) sleep, in six medication-refractory focal epilepsy patie

195 ables Drosophila to form sleep-dependent and sleep-independent memory.

196 ron has previously been suggested to promote sleep independently of RIS.

197 ateral hypothalamus (LH), which regulate REM sleep initiation and maintenance.

198 Sleep is a basic need.

199 Sleep is ubiquitous across animal species, but why it pe

200 ries of demanding cognitive tasks within the sleep laboratory during the following day.

201 nce in the era of the COVID19 epidemic, when sleep labs were closed and most studies were home based.

202 In the UK Biobank, circadian strain markers (sleep length, chronotype, and shift work) are associated

203 am of serotonin in the RN to maintain normal sleep levels.

204 ensin into the fourth ventricle induced NREM sleep-like cortical activity, whereas mice deficient for

205 Perilesional sleep-like off-periods can disrupt network activity but

206 A transcription factor helps young flies to sleep longer by delaying the maturation of a neural netw

207 Sleep loss increases the cerebrospinal fluid concentrati

208 ogressively increased despite of accumulated sleep loss over days.

209 chanisms underlying the anxiogenic impact of sleep loss.

210 recordings along the dorsal CA1-DG axis from sleeping male mice, we detected and classified two types

211 ical evidence that spindles during overnight sleep may act as a physiological mechanism for the restr

212 ent mechanism involving use-dependent, local sleep may be the main driver of response variability.

213 lidation mechanism that is not contingent on sleep may confer an evolutionary advantage.

214 Yet poor sleep may influence opiate use, suggesting a bidirection

215 During both NREM and REM sleep, mice showed large increases in cerebral blood vol

216 uth irritation (n = 4 and n = 0), difficulty sleeping (n = 3 and n = 2), and vivid dreams (n = 3 and

217 osure may be beneficial and that post-trauma sleep needs to be further examined in the context of the

218 During sleep, neurons in the thalamic reticular nucleus (TRN) p

219 We sought to determine which facets of sleep neurophysiology were most strongly linked to cogni

220 Sleeping on HR mattress toppers for four to six weeks im

221 me athletic performance measures compared to sleeping on LR or sleeping directly on spring mattresses

222 01) was found in the reduction of wake after sleep onset and latency to persistent sleep from baselin

223 hips were observed for subjective wake after sleep onset and subjective latency to sleep onset.

224 sleep duration variability, sleep onset, and sleep onset variability were assessed across 14 days clo

225 sleep duration, sleep duration variability, sleep onset, and sleep onset variability were assessed a

226 after sleep onset and subjective latency to sleep onset.

227 nts underwent partial sleep deprivation (3 h sleep opportunity at the end of night), crossed-over wit

228 facilitated by non-rapid eye movement (NREM) sleep or by REM sleep, whether it results from plasticit

229 at reported intervention effects on fatigue, sleep, or performance at work, and on measures of attent

230 Sleep oscillations in the neocortex and hippocampus are

231 ting specific memories associated with local sleep oscillations.

232 the RT group demonstrated an improvement in sleep pattern, redox, inflammatory profiles, and biomark

233 ography; however, basic understanding of dog sleep patterns remains poorly characterized.

234 t that future research should shift focus on sleep, physical/motor activity, or circadian patterns to

235 were formulated by a panel of pulmonary and sleep physicians, respiratory therapists, and methodolog

236 Sleep plays a key role in processing hippocampus-depende

237 risk for developing PTSD; highlighting that sleep potentially plays a role in PTSD's pathology.

238 show that brain structure is associated with sleep problems in children, and that this is related to

239 alcohol may contribute to the prevalence of sleep problems in older age, particularly for men.

240 he hypothalamic neurons that produce it as a sleep-promoting system (Lee et al., 2017).

241 namics in control rats and in rats where the sleep-promoting ventrolateral preoptic nucleus (VLPO) is

242 ning and memory, we tested a hypothesis that sleep protects old memories from being forgotten after n

243 Here, we assessed the extent to which sleep provides a unique memory benefit, above and beyond

244 relations with these patients' self-reported sleep quality and plasma IL-1beta.

245 ating variables include depressive symptoms, sleep quality and processing speed.

246 being married, higher job satisfaction, good sleep quality and regular exercise were positively assoc

247 ever, the relation between those factors and sleep quality are inadequately described.

248 SL (n=20) were evaluated with the Pittsburgh Sleep Quality Index (PSQI), Symptom Checklist 90 (SCL-90

249 Based on the RCSQ results, sleep quality was assessed to be better in the melatonin

250 siological conditions such as stress levels, sleep quality, and emotional states.

251 Measures of depressive symptoms, sleep quality, processing speed, and general cognitive f

252 causing oxyhemoglobin desaturation and poor sleep quality.

253 Notably, rapid eye movement (REM) sleep regulates emotional memory, and persistent REM sle

254 findings identify a widely distributed NREM sleep-regulating circuit in the brainstem with a common

255 within a novel, non-homeostatic paradigm of sleep regulation.SIGNIFICANCE STATEMENT We show that the

256 ompromise of respiratory gas exchange during sleep, related to transient upper airway narrowing disru

257 The hippocampus plays a critical role in sleep-related memory processes [1-3], but it is unclear

258 riate linear regressions were conducted with sleep-related variables as explanatory and subsequent ch

259 nurses and/or midwives that had evaluated a sleep-related/fatigue-management intervention; and (2) s

260 The literature related to sleep-related/fatigue-management interventions for nurse

261 We address two questions: (1) what sleep-related/fatigue-management interventions have been

262 ng many stages and conditions in C. elegans, sleep requires a sleep-active neuron called RIS.

263 Following TSD, two nights of recovery sleep restored hippocampal connectivity to baseline leve

264 recent evidence in human and rodent chronic sleep restriction (CSR) studies suggests that NREM delta

265 ent-Oriented Eczema Measure, pruritus score, sleep score, Dermatology Life Quality Index and IgE.

266 anosoma brucei is a protist parasite causing sleeping sickness and nagana in sub-Saharan Africa.

267 biense human African trypanosomiasis ([gHAT] sleeping sickness) is a vector-borne disease that is typ

268 compounds to treat Chagas disease and human sleeping sickness.

269 ri-infarct zone, randomly distributed during sleep, significantly improved fine motor movements of th

270 nonmotor (eg, constipation, cognition, mood, sleep) signs and symptoms.

271 al for the micro-architecture of spontaneous sleep-stage and arousal transitions within a novel, non-

272 show that the complex micro-architecture of sleep-stage/arousal transitions arises from intrinsic no

273 movement (NREM) and rapid eye movement (REM) sleep, strongly consolidating the waking state for hours

274 differences in the change of TIB devoted to sleep such that students with shorter TIB at baseline be

275 itional PB-projecting neurons regulated male sleep, suggesting several groups of PB-projecting neuron

276 These results suggest that sleep therapeutics immediately following trauma exposure

277 1 (Pgrmc1), while longer Abeta forms induce sleep through a pharmacologically tractable Prion Protei

278 g training enhanced rapid eye movement (REM) sleep time, increased oscillatory activities for reward

279 ncrease of REM density, as well as total REM sleep time.

280 Sleep timing became later by ~50 min during weekdays and

281 s the difference between weekend and weekday sleep timing decreased - hence reducing the amount of so

282 flies starved after training did not require sleep to form memories.

283 ng for genetic variants underlying the short sleep trait, we found two different mutations in the sam

284 Thus, TMR in human sleep transcends global action by selectively promoting

285 rsus placebo after two nights of undisturbed sleep (US) and two nights of forced awakening (FA) sleep

286 y contributes to memory consolidation during sleep using Ca(2+) imaging in freely moving mice.

287 e miR-375 modulated the circadian rhythm and sleep via targeting timeless.

288 nt' between their circadian system and daily sleep-wake behaviors, with negative health consequences,

289 We discovered that sleep-wake brain states and motor behaviors are coregula

290 f the bidirectional relationship between the sleep-wake cycle and tau have not been previously discus

291 ated that FLM can be used to describe normal sleep-wake cycles of healthy adult dogs and the effects

292 Experimental sleep-wake disruption in rodents and humans causally mod

293 DR is associated with circadian outputs and sleep/wake behavior.

294 factors, only mean oxygen saturation during sleep was associated with bilateral volume of hippocampu

295 Objectively measured sleep was collected using the Fitbit Charge 2 (FC2), fro

296 On the postreserpine days, sleep was dominated by slow-wave sleep with fast intrusi

297 Sleep was scored with manual and automated techniques, i

298 -wave sleep and some limited recovery in REM sleep when individuals with AUD stop drinking.

299 on-rapid eye movement (NREM) sleep or by REM sleep, whether it results from plasticity increases or s

300 r neural debris is associated with increased sleep, which is required for efficient active zone remov

301 rpine days, sleep was dominated by slow-wave sleep with fast intrusions and reduced hierarchical coup

302 ded during training becomes effective during sleep, with excited reward processing sending inhibitory