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 children were mostly obese (84%) and 57% had modera

3 OSAS did not significantly affect neuropsychological mea

4 OSAS does not seem to affect the cortical processing of

5 OSAS is relatively common in SCD populations, with hypox

6 OSAS patients revealed an increased PD-1 and PD-L1 expre

7 OSAS was confirmed by polysomnography.

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

9 OSAS, by exposing children to recurrent intermittent hyp

10 In addition, OSAS is considered as low-grade systemic inflammation, w

11 5 muV; P = 0.019), and did not improve after OSAS treatment (N350 at Cz pretreatment -25.1 +/- 7.4 vs

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

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

14 nship between these anatomical landmarks and OSAS could help to stratify treatments, guiding choice t

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

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

17 e evaluated the possible association between OSAS and NTG.

18 s study investigates the association between OSAS in children and secondary osteoporosis.

19 between the 3 groups and correlation between OSAS risk score and vascular changes were calculated.

20 potential bidirectional relationship between OSAS and periodontal disease.

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

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

23 lectomy as a primary treatment for childhood OSAS.

24 ce, presentation, and treatment of childhood OSAS.

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

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

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

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

29 The 5 years after initial evaluation for OSAS.

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

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

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

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

34 , 81.5% of the patients showed high risk for OSAS, 46.3% had excessive daytime sleepiness, 41.5% were

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

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

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

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

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

40 etical cohort of persons suspected of having OSAS.

41 In patients with high OSAS risk, an increase in flow areas (P = .011) and vess

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

43 ions of circulating monocytes and T cells in OSAS patients, which are known to be affected by oxidati

44 ha and MMP-2) and meibomian gland dropout in OSAS.

45 f monocytes and T cells was also elevated in OSAS patients, which indicates a deregulated PD-1/PD-L1

46 atory responsiveness to bradykinin exists in OSAS.

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

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

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

50 increase of both CD16(+) monocyte subsets in OSAS patients that was positively correlated with the bo

51 4 days to repetitive cycles of CIH mimicking OSAS in humans, or caged with room air (handled controls

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

53 d 125 patients divided into mild-to-moderate OSAS (n = 40), severe OSAS (n = 46), and control groups

54 re higher than those in the mild-to-moderate OSAS group (all, p = 0,001).

55 ticipants in the severe and mild-to-moderate OSAS groups were higher than those in the control group

56 ticipants in the severe and mild-to-moderate OSAS groups were higher than those in the control group,

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

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

59 ged 10-17 years: 86 with OSAS and 64 with no OSAS.

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

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

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

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

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

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

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

67 factors involved in the etiopathogenesis of OSAS damage on the ocular surface.

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

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

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

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

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

73 sease (SCD), exhibit a greater prevalence of OSAS.

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

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

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

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

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

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

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

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

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

83 into mild-to-moderate OSAS (n = 40), severe OSAS (n = 46), and control groups (n = 39).

84 ticipants in the mild-to-moderate and severe OSAS groups were significantly higher, and serum desmosi

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

86 and dropout values were higher in the severe OSAS group than those in the control group (p = 0.001) (

87 ire values of the participants in the severe OSAS group were higher than those in the mild-to-moderat

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

89 y obese (84%) and 57% had moderate to severe OSAS.

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

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

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

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

94 (FG) and octenyl succinic anhydride starch (OSAS) composite films loaded with 1, 2, 3 and 4 wt% bact

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

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

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

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

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

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

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

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

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

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

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

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

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

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

109 Obstructive sleep apnea syndrome (OSAS) represents a substantial disease of recurrent slee

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

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

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

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

114 through to obstructive sleep apnea syndrome (OSAS), may cause compromise of respiratory gas exchange

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

116 tration in obstructive sleep apnea syndrome (OSAS).

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

118 noring and obstructive sleep apnea syndrome (OSAS).

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

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

121 a seen in obstructive sleep apnoea syndrome (OSAS) may affect bone metabolism increasing the risk for

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

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

124 ing MRI of the upper airway illustrated that OSAS populations tend to have a greater amount of lympho

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

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

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

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

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

130 ants were divided into 3 groups based on the OSAS risk score.

131 f peripheral monocyte subsets in response to OSAS and its accompanying phenomena.

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

133 sal continuous positive airway pressure when OSAS was diagnosed.

134 Whether OSAS and intermittent hypoxia are associated with liver

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

136 luded 150 children aged 10-17 years: 86 with OSAS and 64 with no OSAS.

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

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

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

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

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

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

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

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

145 gle and multivariate analysis, children with OSAS had a lower mean SoS value, p < 0.001 and p = 0.004

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

147 Children with OSAS had lower SoS suggesting risk for secondary osteopo

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

149 Children with OSAS have persistent primary or irreversible respiratory

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

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

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

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

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

155 tional area would be larger in children with OSAS.

156 eficial temporary treatment in children with OSAS.

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

158 16 yr) underwent MRI: obese individuals with OSAS (n = 49), obese control subjects (n = 38), and lean

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

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

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

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

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

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

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

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

167 ce ocular surface morbidity in patients with OSAS.

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

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

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

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

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

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

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

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

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

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

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

179 y differences between those with and without OSAS, as well as between ethnicities and disease states.

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

181 concentrations in patients with and without OSAS.

182 3 years and 2 (9.5%) of 21 patients without OSAS at 3 years; P = .04.