ライフサイエンスコーパス: OSAS

1 OSAS affected 60% of children with NAFLD; the presence a

2 OSAS did not significantly affect neuropsychological mea

3 OSAS does not seem to affect the cortical processing of

4 OSAS was defined by an apnea/hypopnea index (AHI) greate

5 OSAS, by exposing children to recurrent intermittent hyp

6 5 muV; P = 0.019), and did not improve after OSAS treatment (N350 at Cz pretreatment -25.1 +/- 7.4 vs

7 are obese, we hypothesized that the anatomic OSAS risk factors would be more similar to those in adul

8 association between periodontal disease and OSAS risk in Class III obese patients, but OSAS risk was

9 ers, narcolepsy, restless-legs syndrome, and OSAS.

10 he subjects with AHI >/= 20 were accepted as OSAS.

11 e evaluated the possible association between OSAS and NTG.

12 potential bidirectional relationship between OSAS and periodontal disease.

13 approaches for preventing and treating both OSAS and overweight across the pediatric age range.

14 d OSAS risk in Class III obese patients, but OSAS risk was associated with both NC and PPNC.

15 lectomy as a primary treatment for childhood OSAS.

16 ce, presentation, and treatment of childhood OSAS.

17 ions of the overweight epidemic on childhood OSAS are discussed.

18 We conclude that childhood OSAS is associated with systemic diastolic hypertension.

19 Patients underwent polysomnography to detect OSAS and were prospectively followed up to assess the ri

20 for the metabolite ratios in differentiating OSAS vs. CONTROLS: Positive correlations were found betw

21 The 5 years after initial evaluation for OSAS.

22 res, is the primary anatomic risk factor for OSAS in obese adolescents.

23 ith periodontal disease showed high risk for OSAS (82.9%) and ESS (45.7%).

24 he differences between high and low risk for OSAS groups.

25 ntly larger in the patients at high risk for OSAS than in those at low risk for OSAS.

26 , 81.5% of the patients showed high risk for OSAS, 46.3% had excessive daytime sleepiness, 41.5% were

27 (ESS) were applied to determine the risk for OSAS.

28 risk for OSAS than in those at low risk for OSAS.

29 d be considered as the initial treatment for OSAS in obese adolescents, a group that has poor continu

30 who underwent polysomnography, 67 (75%) had OSAS.

31 ts with NTG and 3 (12.5%) of 24 controls had OSAS (p < 0.05).

32 etical cohort of persons suspected of having OSAS.

33 RREP were blunted in OSAS compared with control subjects (N350 at Cz -27 +/-

34 atory responsiveness to bradykinin exists in OSAS.

35 fluctuations during tidal breathing noted in OSAS at levels 1 through 4 were 317, 422, 785, and 922%,

36 and putamen tCho/Cr and GABA/Cr occurred in OSAS vs healthy subjects (p < 0.05).

37 Auditory evoked potentials were similar in OSAS and control subjects at baseline (N350 at Cz -58 +/

38 4 days to repetitive cycles of CIH mimicking OSAS in humans, or caged with room air (handled controls

39 on-OSAS) group, 17 were in the mild/moderate OSAS group, and 22 were in the severe OSAS group.

40 We conclude that in children with moderate OSAS, the upper airway is restricted both by the adenoid

41 In pediatric NAFLD, OSAS is associated with biochemical, immunohistochemical

42 hirteen individuals were in the control (non-OSAS) group, 17 were in the mild/moderate OSAS group, an

43 h obese and lean control subjects; (2) obese OSAS adolescents had a smaller nasopharyngeal airway tha

44 o the utility of treatment in the absence of OSAS.

45 t polysomnography (PSG) for the diagnosis of OSAS and calculation of Apnea-Hypopnea Index (AHI).

46 home study or no testing in the diagnosis of OSAS compares favorably with that of other procedures fo

47 Bedside diagnosis of OSAS without any testing has also been discussed.

48 demonstrates a likely pathway of effects of OSAS on neurocognitive function in children, as well as

49 yrus mean diffusivity mediates the impact of OSAS on verbal learning capacity.

50 obing depth, CAL measures, and indicators of OSAS severity (P <0.01).

51 g survival analysis based on the presence of OSAS, indication for ventilation treatment with continuo

52 The prevalence of OSAS in patients with NAION and the risk of second eye i

53 The prevalence of OSAS was higher in patients with NTG and the difference

54 IL-6 and IL-33 concentrations regardless of OSAS severity.

55 during sleep that could put them at risk of OSAS recurrence.

56 ren with NAFLD; the presence and severity of OSAS were associated with the presence of NASH (odds rat

57 e was no influence of periodontal disease on OSAS risk.

58 upper airway resistance syndrome [UARS], or OSAS) and four asymptomatic subjects underwent nocturnal

59 ve, the interrelationships between pediatric OSAS and overweight are reviewed, and the implications o

60 nticipated increased prevalence of pediatric OSAS mandates assessment of optimal approaches for preve

61 in patients with mild-to-moderate positional OSAS, taking into account the potential confounding effe

62 A total of 25 adults with positional OSAS (apnea-hypopnea index [AHI]supine:AHInon-supine >/=

63 eater than or equal to 1 event/h, and severe OSAS was defined by an AHI greater than or equal to 5 ev

64 derate OSAS group, and 22 were in the severe OSAS group.

65 tive airway pressure in patients with severe OSAS increased the risk of second eye involvement (hazar

66 ivity above baseline in patients with severe OSAS suggests that some chemical or mechanical compensat

67 dings also suggest that patients with severe OSAS who are nonadherent to ventilation treatment with c

68 active during sleep in patients with severe OSAS; (2) EMGgg reductions are temporally associated wit

69 jects with obstructive sleep apnea syndrome (OSAS) (0.06%), parasomnia (0.7%), restless leg syndrome

70 iated with obstructive sleep apnea syndrome (OSAS) among young children, but strongly associated with

71 Obstructive sleep apnea syndrome (OSAS) and nonalcoholic fatty liver disease (NAFLD) are f

72 ccurs with obstructive sleep apnea syndrome (OSAS) and provokes systemic endothelial dysfunction, whi

73 ldren with obstructive sleep apnea syndrome (OSAS) associated with significant hypoxemia.

74 ldren with obstructive sleep apnea syndrome (OSAS) have more collapsible airways compared with normal

75 ldren with obstructive sleep apnea syndrome (OSAS) have not been established.

76 valence of obstructive sleep apnea syndrome (OSAS) in patients with nonarteritic anterior ischemic op

77 The obstructive sleep apnea syndrome (OSAS) is associated with cardiovascular disease and syst

78 Obstructive sleep apnea syndrome (OSAS) is associated with intermittent hypoxia and sleep

79 pediatric obstructive sleep apnea syndrome (OSAS) is suggested by the observation that obstruction d

80 Obstructive sleep apnea syndrome (OSAS) is usually diagnosed with overnight polysomnograph

81 Obstructive sleep apnea syndrome (OSAS) leads to neurocognitive and autonomic deficits tha

82 g that the obstructive sleep apnea syndrome (OSAS) may compromise optic nerve head perfusion and caus

83 on between obstructive sleep apnea syndrome (OSAS) risk with periodontal disease and anthropometric m

84 oncomitant obstructive sleep apnea syndrome (OSAS) seems to have a favorable impact on asthma, but da

85 Obstructive sleep apnea syndrome (OSAS), a disorder characterized by episodic hypoxia (EH)

86 ients with obstructive sleep apnea syndrome (OSAS), and these two chronic conditions may be linked vi

87 n with the obstructive sleep apnea syndrome (OSAS).

88 tration in obstructive sleep apnea syndrome (OSAS).

89 noring and obstructive sleep apnea syndrome (OSAS).

90 ition, and obstructive sleep apnea syndrome (OSAS).

91 ldren with obstructive sleep apnea syndrome (OSAS; age, 4.3 +/- 2.3 years) and 10 matched control sub

92 actors to obstructive sleep apnoea syndrome (OSAS) has led to a better understanding of this complex

93 We found that OSAS was associated with decreased mean diffusivity of t

94 We hypothesized that OSAS would affect the dentate gyrus, a hippocampal subdi

95 These results suggest that OSAS is common in patients with NAION and that polysomno

96 The present findings suggest that OSAS may have an increasing effect on salivary IL-6 and

97 to bradykinin was significantly lower in the OSAS group (62.1% +/- 26.1%) than in the control group (

98 n to nitroglycerin tended to be lower in the OSAS group (78.6% +/- 31.8%) than the control group (100

99 When six of the OSAS subjects were retested after 60 d of treatment with

100 IL-33 concentrations were similar in the two OSAS groups (P >0.05), which were statistically higher t

101 sal continuous positive airway pressure when OSAS was diagnosed.

102 Whether OSAS and intermittent hypoxia are associated with liver

103 linical studies are needed to assess whether OSAS contributes to endothelial impairment in human pati

104 Because many adolescents with OSAS are obese, we hypothesized that the anatomic OSAS r

105 ts and found that (1) obese adolescents with OSAS had increased adenotonsillar tissue compared with o

106 bnormalities in most of the adolescents with OSAS, the ratio of soft tissue to craniofacial space sur

107 young children, but strongly associated with OSAS in older children and adolescents.

108 r airway structure in 18 young children with OSAS (age 4.8 +/- 2.1 yr; 12 males and 6 females) and an

109 In children with OSAS (n = 11) and control subjects (n = 12; age and sex

110 Twenty-four children with OSAS and 24 control subjects were tested during N3 sleep

111 aximal maneuver, we studied 10 children with OSAS and 6 normal control subjects to determine EMGgg ac

112 Children with OSAS had a significantly higher diastolic BP than those

113 pothesized that, during sleep, children with OSAS have (1) abnormal RREP, (2) normal cortical process

114 Children with OSAS have persistent primary or irreversible respiratory

115 Thirteen children with OSAS repeated testing 4-6 months after adenotonsillectom

116 ucture of the dentate gyrus in children with OSAS that may help explain some of the neurocognitive de

117 ) during polysomnography in 41 children with OSAS, compared to 26 children with primary snoring (PS).

118 the use of supplemental O2 in children with OSAS, we studied 16 children ages 2-8 (mean: 4.28 +/- 2.

119 sivity of the dentate gyrus in children with OSAS, which correlates with a lower verbal learning and

120 eficial temporary treatment in children with OSAS.

121 tional area would be larger in children with OSAS.

122 y marker of brain pathology in children with OSAS.SIGNIFICANCE STATEMENT In this study we investigate

123 16 yr) underwent MRI: obese individuals with OSAS (n = 49), obese control subjects (n = 38), and lean

124 ts at 3 years: 8 (15.4%) of 52 patients with OSAS at 3 years and 2 (9.5%) of 21 patients without OSAS

125 ved that the EMGgg activity in patients with OSAS compared with control subjects was significantly gr

126 CPAP lowered the EMGgg in patients with OSAS during all sleep states.

127 Ggg at sleep onset observed in patients with OSAS is consistent with the relative loss of this reflex

128 pressure (CPAP) (n = 13); (2) patients with OSAS with CPAP (n = 5); and (3) control subjects without

129 three groups of children: (1) patients with OSAS without continuous positive airway pressure (CPAP)

130 In patients with OSAS, the EMGgg for apneic breaths during REM (37 +/- 9%

131 ve the baseline in four of the patients with OSAS.

132 the soft palate was larger in subjects with OSAS (3.5 +/- 1.1 versus 2.7 +/- 1.2 cm(3); p < 0.05).

133 subjects (7.5 +/- 1.6 mm Hg), subjects with OSAS (6.8 +/- 1.2 mm Hg), normotensive subjects with UAR

134 glycerin were obtained from 12 subjects with OSAS and 12 matched control subjects.

135 ft palate) was similar between subjects with OSAS and obese control subjects; (4) although there were

136 g are significantly greater in subjects with OSAS compared with control subjects.

137 We noted the following in subjects with OSAS compared with control subjects: (1) a smaller upper

138 he upper airway was smaller in subjects with OSAS in comparison with control subjects (1.5 +/- 0.8 ve

139 s with insomnia and low BP, 15 subjects with OSAS, and 15 healthy control subjects.

140 ss might exist in the veins of subjects with OSAS.

141 ult asthma patients (mean age 57 years) with OSAS (respiratory disturbance index >/=20).

142 ldren ages 2-8 (mean: 4.28 +/- 2.88 yr) with OSAS secondary to adenotonsillar hypertrophy.

143 wake, normotensive subjects with and without OSAS, using the dorsal hand vein compliance technique.

144 concentrations in patients with and without OSAS.

145 3 years and 2 (9.5%) of 21 patients without OSAS at 3 years; P = .04.