ライフサイエンスコーパス: sleep fragmentation

1 ty (hypoxemia, respiratory disturbances, and sleep fragmentation).

2 ittent hypoxemia, autonomic fluctuation, and sleep fragmentation.

3 e biological subtypes - sleep propensity and sleep fragmentation.

4 s awareness but have a significant effect of sleep fragmentation.

5 wakenings (microarousals, MAs), resulting in sleep fragmentation.

6 uilding, advancing wake time, and increasing sleep fragmentation.

7 ith hypoxemia, respiratory disturbances, and sleep fragmentation.

8 e-movement (REM) sleep, as well as increased sleep fragmentation.

9 long with changes in cerebral blood flow and sleep fragmentation.

10 sed night sleep and day activity and reduced sleep fragmentation.

11 individual, and related this to ante-mortem sleep fragmentation.

12 sive function, and appears to correlate with sleep fragmentation.

13 felong spindle decreases and later life NREM sleep fragmentation.

14 nd separate it from nonrespiratory causes of sleep fragmentation.

15 aviors in the mutants, which correlated with sleep fragmentation.

16 regulated cognitive and motor functions, and sleep fragmentation.

17 central apneas, adding dead space decreased sleep fragmentation: 44 +/- 6 versus 83 +/- 12 arousals

18 Overall, BaYaka exhibited high sleep fragmentation (50.5) and short total sleep time (5

19 al HTT-induced behavioral defects, including sleep fragmentation, a key hallmark of many neurodegener

20 akefulness, narcoleptic mammals also display sleep fragmentation, a less understood phenotype recapit

21 cases showed reduction in total sleep time, sleep fragmentation, abnormal short non-rapid eye moveme

22 of CP-AMPARs in the NAc, whereas increasing sleep fragmentation accelerated NAc CP-AMPAR accumulatio

23 In contrast, experimentally increasing sleep fragmentation after cocaine self-administration ex

24 ent hypoxemia, hemodynamic fluctuations, and sleep fragmentation, all of which could damage cerebral

25 to both increased daytime blood pressure and sleep fragmentation, all participants with an apnea-hypo

26 CIH, but not sleep fragmentation alone, induced an increase in macrop

27 comprised sleep episodes during daytime and sleep fragmentation and a reduction of sleep efficiency

28 hen considering the 2 study groups together, sleep fragmentation and AHI were associated with jeopard

29 While stress commonly leads to sleep fragmentation and arousal in both humans and anima

30 a valuable model for studying age-associated sleep fragmentation and breakdown of rhythm strength, an

31 Obstructive sleep apnea, characterized by sleep fragmentation and chronic intermittent hypoxia (CI

32 to relate pericyte marker gene expression to sleep fragmentation and cognitive decline in the decade

33 ferred from marker gene expression, may link sleep fragmentation and cognitive decline.

34 y a potential role of M-pericytes in linking sleep fragmentation and cognitive trajectories in older

35 ection of respiratory disturbance may reduce sleep fragmentation and excessive daytime sleepiness.

36 , the latter being consistent with decreased sleep fragmentation and increased sleep duration for mic

37 f obstruction of the upper airway leading to sleep fragmentation and intermittent hypoxia during slee

38 t is not responsible for the majority of the sleep fragmentation and may therefore not be as disrupti

39 SD mPrP(0/0) mice showed a larger degree of sleep fragmentation and of latency to enter rapid eye mo

40 Nevertheless, sleep fragmentation and repeated fluctuations of arteria

41 ar target for interventions that may prevent sleep fragmentation and the attendant cardiovascular and

42 g sleep resulting in oxygen desaturation and sleep fragmentation, and associated with increased risk

43 d found reduced neuronal activity, increased sleep fragmentation, and decreased SWS time as compared

44 east active 5-h, mid-point most active 10-h, sleep fragmentation, and efficiency) on HbA1c/glucose in

45 in severe insomnia with delayed sleep onset, sleep fragmentation, and increased wakefulness.

46 Measures of hypoxia, sleep fragmentation, and sleep duration were investigate

47 sturbances (particularly for sleep duration, sleep fragmentation, and sleep-disordered breathing) in

48 of literature suggesting that sleep loss and sleep fragmentation are associated with blunted hypercap

49 apnea, the relative roles of hypoxia versus sleep fragmentation are difficult to separate in apneic

50 s suggest that AHI, nocturnal hypoxemia, and sleep fragmentation are independent determinants of hype

51 llations, and found it to be an indicator of sleep fragmentation (ArI-LHPR(NREM): r=-0.8, p=0.0053; A

52 Measures of sleep fragmentation (arousal index and wake after sleep

53 Sleep fragmentation, as assessed by the distribution of

54 Such sleep fragmentation, as well as abnormalities evident in

55 In adjusted analyses, greater sleep fragmentation associated with increased ESRD risk

56 ework in mouse models of atherosclerosis and sleep fragmentation by showing that expansion of competi

57 Sleep fragmentation caused hyperalgesia in volunteers, w

58 roups increased sleep duration and decreased sleep fragmentation compared with sleeping alone, despit

59 Sleep fragmentation could be transiently overcome with s

60 h the effects of intermittent hypoxaemia and sleep fragmentation, could contribute independently to t

61 characterized by prolonged sleep latencies, sleep fragmentation, decreased sleep efficiency, frequen

62 le hypocretin/orexin (Hcrt/OX) neurons drive sleep fragmentation during aging.

63 pressure score (SPS), a surrogate measure of sleep fragmentation emerged (p = 0.02, r = -0.51) emerge

64 We found that sleep fragmentation enhanced tumor size and weight compa

65 fulness drive can lead to central apneas and sleep fragmentation, especially in patients with heart f

66 Sleep fragmentation exerts a lasting influence on the HS

67 Moreover, DAergic RicQ117L expression caused sleep fragmentation in a DAT-dependent manner but had no

68 treatment increased delta power and reduced sleep fragmentation in APP mice.

69 Sleep fragmentation in focal drug-resistant epilepsy is

70 for pharmacological treatment of age-related sleep fragmentation in humans.

71 e amount of NREM and REM sleep and increased sleep fragmentation in naive mice throughout the light-d

72 termediate nucleus neurons is accompanied by sleep fragmentation in older adults with and without Alz

73 ain neurophysiological mechanisms underlying sleep fragmentations in PD, which can inform new interve

74 We demonstrate that sleep loss, but not sleep fragmentation, in healthy mice increases sensitivi

75 sal index (ArI)-beta(NREM): r=0.9, p=0.0001, sleep fragmentation index (SFI)-beta(NREM): r=0.6, p=0.0

76 Sleep fragmentation index was defined as the sum of the

77 nt sleep stages, correlated with arousal and sleep fragmentation index, and preceded stage transition

78 age 1 sleep divided by the total sleep time (sleep fragmentation index: SFI).

79 Sleep fragmentation is a persistent problem throughout t

80 n-based study, we tested the hypothesis that sleep fragmentation is associated with elevated awake bl

81 Lastly, we show that sleep fragmentation is associated with increased prevale

82 Sleep fragmentation is common in older adults and is ass

83 Sleep duration is decreased, sleep fragmentation is increased, and the timing of slee

84 est fragmentation, a potential surrogate for sleep fragmentation, is independently associated with a

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

86 st that sleep difficulties, specifically REM sleep fragmentation, may play a mechanistic role in post

87 Sleep fragmentation, measured as the number of arousals

88 analysis, we extracted total sleep time and sleep fragmentation metrics over the 22:00 to 06:00 peri

89 similar between ventilator groups, including sleep fragmentation (number of arousals and awakenings/h

90 -reported mean (SD) sleep metrics, including sleep fragmentation (number of overnight awakenings, 1.5

91 geing in diverse organisms, could rescue the sleep fragmentation of ageing Drosophila.

92 esign, we compared mice that were exposed to sleep fragmentation one week before engraftment of synge

93 es 1 and 2) without significant increases in sleep fragmentation or decreases in rapid eye movement (

94 The sleep fragmentation originated from NMDA receptors on GA

95 BDLE further has a unique effect on REM sleep fragmentation (p = 0.0479) over and above that of

96 odone/ L-tryptophan dose-dependently reduced sleep fragmentation, p = 0.03, increased sleep efficienc

97 Sleep fragmentation, particularly reduced and interrupte

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

99 ts, the more aggressive features produced by sleep fragmentation persisted.

100 Sleep fragmentation predicted approximately twice the va

101 Participants within the highest quintile of sleep fragmentation presented a higher prevalence of mul

102 We show that mice subjected to sleep fragmentation produce more Ly-6C(high) monocytes,

103 this study, we examined the hypothesis that sleep fragmentation promotes tumor growth and progressio

104 atergic neurons causes a high degree of NREM sleep fragmentation, promotes state instability with fre

105 0 individuals, we describe a pathway wherein sleep fragmentation raises inflammatory-related white bl

106 th delayed sleep onset latency and increased sleep fragmentation (reduced sleep state percentages, nu

107 influence of nocturnal epileptic activity on sleep fragmentation remains poorly understood.

108 leep time, which is accompanied by increased sleep fragmentation resembling chronic insomnia.

109 TNF-alpha after either sleep deprivation or sleep fragmentation (SF) appear to underlie excessive da

110 Chronic sleep fragmentation (SF) commonly occurs in human popula

111 diovascular disease; thus, understanding how sleep fragmentation (SF) in an obesity setting impacts i

112 Sleep fragmentation (SF) is a common condition among pre

113 Sleep fragmentation (SF) is a highly prevalent condition

114 re, respectively and then exposed to 24-h of sleep fragmentation (SF) or allowed to sleep (control).

115 duced (1) sleep-induced hypoxia (SIH) or (2) sleep fragmentation (SF) without hypoxia for 5 days (12-

116 Sleep fragmentation (SF), a primary feature of obstructi

117 eep disturbance, achieved in mice by chronic sleep fragmentation (SF), enhanced neural activity in th

118 nsions of sleep behaviour (total sleep time, sleep fragmentation, sleep quality, and sleep distributi

119 Males appeared to be more affected by sleep fragmentation than females.

120 en patients, such as degree of hypoxemia and sleep fragmentation, that reflect differences in pathoph

121 Additionally, dysbiosis induces sleep fragmentation through the activation of insulin-pr

122 ated macrophages (TAM) were more numerous in sleep fragmentation tumors, where they were distributed

123 Increased invasiveness was apparent in sleep fragmentation tumors, which penetrated the tumor c

124 lept an average of 6.5 hours per night; mean sleep fragmentation was 21%.

125 In the lateral orbitofrontal cortex, greater sleep fragmentation was also associated with greater com

126 solateral prefrontal cortex, greater average sleep fragmentation was associated with greater expressi

127 with right amygdala volume, and more severe sleep fragmentation was associated with increased thickn

128 Sleep fragmentation was defined as the total number of a

129 e-mortem annual cognitive assessments, while sleep fragmentation was derived from ante-mortem wrist-a

130 , these more aggressive features produced by sleep fragmentation were abolished completely in TLR4(-/

131 the time spent >140 mg/dL or <70 mg/dL, and sleep fragmentation were derived for each week and compa

132 eurons in the parabrachial nucleus prevented sleep fragmentation, whereas pharmacological blockade of

133 stabilized sleep, mimicking aging-associated sleep fragmentation, whereas the KCNQ-selective activato