ライフサイエンスコーパス: OSA

1 OSA and <90% oxyhemoglobin saturation were not associate

2 OSA is an independent predictor for the progression to p

3 OSA is associated with a 2- to 3-fold increased risk of

4 OSA is associated with STDR in patients with type 2 diab

5 OSA is associated with structural and functional atrial

6 OSA is common and the prevalence is increasing with the

7 OSA leads to high cardiovascular morbidity and mortality

8 OSA lends itself to a personalized approach to diagnosis

9 OSA patients intolerant to CPAP have a strong positive c

10 OSA severity was classified based on conventionally acce

11 OSA treatment increased SWA, and SWA was significantly c

12 OSA was assessed using a home-based multichannel cardior

13 asured as regional grey matter volume, in 16 OSA children (8 male, 8.1 +/- 2.2 years, AHI:11.1 +/- 5.

14 was found in FHIA 21 (0.020) starch with 3% OSA and 4-h reaction at room temperature.

15 cinate starch (OS starch) esterified with 3% OSA complexed with magnesium or calcium.

16 , normal and Hylon VII) were treated with 3% OSA solution.

17 he derivation cohort, screening of OSA(>=5), OSA(>=15), and OSA(>=30) revealed that GOAL questionnair

18 OAL questionnaire for screening of OSA(>=5), OSA(>=15), and OSA(>=30) was similar to No-Apnea, STOP-B

19 he validation cohort, screening of OSA(>=5), OSA(>=15), and OSA(>=30), corroborated validation steps

20 Moderate and severe adult OSA patients, who were previously prescribed continuous

21 Since adult OSA manifests MRI evidence of brain injury, and animal m

22 scle responsiveness, zolpidem does not alter OSA severity.

23 Although OSA traits are heritable, few genetic associations have

24 iological feasibility of oral swab analysis (OSA) for the diagnosis of TB.

25 rs (hazard ratio [HR] = 1.030, P < .001) and OSA diagnosis (HR = 1.081, P < .033), and was lower in w

26 ohort, screening of OSA(>=5), OSA(>=15), and OSA(>=30) revealed that GOAL questionnaire achieved sens

27 re for screening of OSA(>=5), OSA(>=15), and OSA(>=30) was similar to No-Apnea, STOP-Bang or NoSAS.

28 ohort, screening of OSA(>=5), OSA(>=15), and OSA(>=30), corroborated validation steps with sensitivit

29 frequency bands between the SS (n = 42) and OSA (n = 129) groups during the non-rapid eye movement (

30 ive Airway Pressure in Patients with ACS and OSA) study, including 1,701 patients admitted for ACS (N

31 son, control patients with paroxysmal AF and OSA who underwent PV isolation alone without ablation on

32 triggers in patients with paroxysmal AF and OSA.

33 0 latency with resolved vs recurrent ICH and OSA.

34 e in vitro digestibility of non-modified and OSA-modified corn starch was studied.

35 In addition, narcolepsy and OSA can occur as comorbid disorders.

36 : A total of 67 individuals with obesity and OSA (AHI >= 10 events/h) underwent a sleep study and upp

37 The link between obesity and OSA is likely to be the deposition of fat in the tongue,

38 airway anatomy in subjects with obesity and OSA.

39 explain the relationship between obesity and OSA.

40 ay soft tissues in subjects with obesity and OSA.

41 igh-risk participants and those with OSA and OSA syndrome.

42 dels with interactions between age, sex, and OSA status to determine patients' risk of developing CSC

43 sputum GeneXpert (1 sample per subject) and OSA (2 samples per subject) were identical at 49/59 (83.

44 k of CSC is higher in men than in women, and OSA increases risk of CSC in both men and women.

45 tive starch with octenyl succinic anhydride (OSA) at levels of 3% or 9%, and afterwards by its comple

46 odification with octenyl succinic anhydride (OSA) helps to control the physicochemical and thermal pr

47 ages compared to octenyl succinic anhydride (OSA)-modified quinoa starch.

48 Obstructive sleep apnea (OSA) affects 17% of women and 34% of men in the US and h

49 Obstructive sleep apnea (OSA) and asthma are highly prevalent chronic respiratory

50 H) in patients with obstructive sleep apnea (OSA) and cutaneous melanoma (CM).

51 rs is important for obstructive sleep apnea (OSA) evaluation.

52 monary disease, and obstructive sleep apnea (OSA) exhibit daily variance.

53 high prevalence of obstructive sleep apnea (OSA) has been reported in Down syndrome (DS) owing to th

54 nce and severity of obstructive sleep apnea (OSA) have been defined by the apnea-hypopnea index (AHI)

55 mated prevalence of obstructive sleep apnea (OSA) in the United States is 10% for mild OSA and 3.8% t

56 Obstructive sleep apnea (OSA) increases risk of dementia, a relationship that may

57 e determine whether obstructive sleep apnea (OSA) increases serum levels of active TGF-beta1 in patie

58 Obstructive sleep apnea (OSA) is a common disorder associated with increased risk

59 Obstructive sleep apnea (OSA) is a common sleep disorder associated with obesity.

60 Obstructive sleep apnea (OSA) is a highly prevalent disorder also involving elast

61 Obstructive sleep apnea (OSA) is a very prevalent disorder.

62 Rationale: Obstructive sleep apnea (OSA) is associated with increased cardiovascular disease

63 Obstructive sleep apnea (OSA) is associated with systemic hypertension.

64 e demonstrated that obstructive sleep apnea (OSA) is associated with the development and evolution of

65 Obstructive sleep apnea (OSA) is linked to increased glaucoma risk in middle-aged

66 Obstructive sleep apnea (OSA) is very common but is frequently undiagnosed.

67 ertension (ICH) and obstructive sleep apnea (OSA) on optic nerve function in children with craniosyno

68 moderate and severe obstructive sleep apnea (OSA) patients requires elucidation.

69 Many adults with obstructive sleep apnea (OSA) use device treatments inadequately and remain untre

70 Moderate or severe obstructive sleep apnea (OSA) was defined as a respiratory event index >=15, and

71 rk manifestation of obstructive sleep apnea (OSA), a widespread disorder of breathing.

72 ), 21 patients with obstructive sleep apnea (OSA), and 19 healthy volunteers).

73 both narcolepsy and obstructive sleep apnea (OSA).

74 gical treatment for obstructive sleep apnea (OSA).

75 es of patients with obstructive sleep apnea (OSA).

76 and the severity of obstructive sleep apnea (OSA).

77 are associated with obstructive sleep apnea (OSA).

78 h and low risks for obstructive sleep apnea (OSA).

79 to the severity of obstructive sleep apnea (OSA).

80 ary risk factor for obstructive sleep apnea (OSA).

81 somnia disorder and obstructive sleep apnea (OSA).

82 Obstructive sleep apnoea (OSA) is a heterogeneous and complex disease; however, di

83 Obstructive sleep apnoea (OSA) is characterised by intermittent hypoxia and system

84 liance therapy for obstructive sleep apnoea (OSA) is that therapeutic responses remain unpredictable.

85 in contributors to obstructive sleep apnoea (OSA) pathogenesis.

86 Some patients with obstructive sleep apnoea (OSA) respond well to oral appliance therapy, whereas oth

87 e with and without obstructive sleep apnoea (OSA).

88 high prevalence of obstructive sleep apnoea (OSA).

89 SS and those with obstructive sleep apnoea (OSA).

90 Managing asymptomatic OSA to reduce cardiovascular and cerebrovascular events

91 To evaluate the association between OSA and quantitative markers of eyelid laxity or seconda

92 ere fit to determine the association between OSA severity and uncontrolled BP or resistant hypertensi

93 , little is known about associations between OSA and glaucoma-related optic disc parameters in young

94 ted adjusting for known associations between OSA and sex, age, body mass index, and medical comorbidi

95 Initial correlation between OSA and ocular surface and eyelid markers was calculated

96 thin a single test population categorized by OSA severity.

97 Fetal perturbations by OSA during pregnancy impose long-term detrimental effect

98 lar consequences.Objectives: To characterize OSA symptom subtypes and assess their association with p

99 the excessively sleepy subtype.Conclusions: OSA symptom subtypes are reproducible and associated wit

100 After adjustment for confounders, OSA remained independently associated with STDR (odds ra

101 Conversely, OSA has not been shown to increase recurrent cardiovascu

102 was insufficient to systematically decrease OSA severity as measured by the apnoea-hypopnoea index.

103 sults, 178 participants (21.0%) demonstrated OSA: 150 with mild OSA, 26 with moderate OSA, and 2 with

104 propose a control panel tool that describes OSA in four domains: disease severity, biological activi

105 Twenty-five OSA patients underwent upper airway endoscopy during nat

106 istic curve yielded a sensitivity of 90% for OSA with a specificity of 71.4%.

107 nefit from specific treatment approaches for OSA.

108 er male patients, may be good candidates for OSA evaluation following a CSC diagnosis.

109 ntermittent hypoxia, a widely used model for OSA.

110 can be considered as a treatment option for OSA and other motorneuron disorders.

111 nd can serve as an experimental platform for OSA research.

112 s with an increased pre-test probability for OSA.

113 points (>=2 points indicating high risk for OSA).

114 OSA group as well as in the combined group (OSA + SS).

115 ex thresholds: >=5.0/h (OSA(>=5)), >=15.0/h (OSA(>=15)), and >=30.0/h (OSA(>=30)).

116 A(>=5)), >=15.0/h (OSA(>=15)), and >=30.0/h (OSA(>=30)).

117 ed apnea/hypopnea index thresholds: >=5.0/h (OSA(>=5)), >=15.0/h (OSA(>=15)), and >=30.0/h (OSA(>=30)

118 Among the sample, 25.7% had OSA, which was untreated in 94% of participants.

119 sis with CSC, and defined patients as having OSA if they had a diagnosis following a sleep study.

120 Weight loss improves OSA, but the mechanism is unknown.Objectives: To determi

121 In OSA patients, MDK levels correlated with nocturnal hypox

122 In OSA patients, TGF-beta1 levels correlated with mitotic i

123 to evaluate circulating HMW-HA and HYAL-1 in OSA.

124 dominant cause of daytime increases in BP in OSA.

125 atory events measured with the 3-D-camera in OSA patients (r = 0.823; p < 0.001).

126 y behavioural and neurostructural changes in OSA.

127 a trend for reduced HMW-HA concentrations in OSA (31.63/18.11-59.25/ng/mL vs. 46.83/25.41-89.95/ng/mL

128 tially leading to endothelial dysfunction in OSA.

129 ss or sleepiness, or overnight hypoxaemia in OSA.

130 ated to the degree of nocturnal hypoxemia in OSA.

131 Greater improvement in OSA was associated with greater decreases in Abeta.

132 xia, or the recurrent arousals that occur in OSA, could cause the daytime increases in blood pressure

133 ls of IH patterned after O2 profiles seen in OSA.

134 ssive, anxious and anorexiolytic symptoms in OSA.

135 Increasing OSA severity is independently associated with retinal ar

136 Like OSA, NAFLD is a prevalent disorder associated with major

137 , nasal mask and pneumotachograph to measure OSA severity, arousal threshold and upper airway muscle

138 a (OSA) in the United States is 10% for mild OSA and 3.8% to 6.5% for moderate to severe OSA; current

139 uped into no OSA (AHI < 5 events/hour), mild OSA (AHI >= 5 and <15 events/hour), moderate OSA (AHI >=

140 rate-severe OSA patients vs. non-OSA or mild OSA patients with CM.

141 s were higher in severe OSA compared to mild OSA or non-OSA patients, whereas no differences in VEGF

142 ants (21.0%) demonstrated OSA: 150 with mild OSA, 26 with moderate OSA, and 2 with severe OSA.

143 animals, intermittent hypoxia (IH) mimicking OSA promotes tumor malignancy both directly and via host

144 OSA (AHI >= 5 and <15 events/hour), moderate OSA (AHI >= 15 and <30 events/hour), or severe OSA (AHI

145 ted OSA: 150 with mild OSA, 26 with moderate OSA, and 2 with severe OSA.

146 I results, participants were grouped into no OSA (AHI < 5 events/hour), mild OSA (AHI >= 5 and <15 ev

147 er in severe OSA compared to mild OSA or non-OSA patients, whereas no differences in VEGF levels emer

148 ear localization of gammaH2AX & p16 than non-OSA individuals (20.1 +/- 10.8% vs. 10.3 +/- 2.7%, P(adj

149 and/or RAS inhibitors was comparable to non-OSA individuals.

150 ased in moderate-severe OSA patients vs. non-OSA or mild OSA patients with CM.

151 nosis in patients with OSA compared with non-OSA controls (OR, 1.27; 95% confidence interval [CI], 1.

152 d an increased risk of XFS compared with non-OSA controls with HTN (OR, 2.67; 95% CI, 2.06-3.46; P <

153 s only associate with leptin levels in obese OSA patients.

154 d to TGF-beta1 levels in obese and non-obese OSA patients.

155 line in 3 areas: diagnosis and assessment of OSA and chronic insomnia disorder, treatment and managem

156 ized on the basis of the underlying cause of OSA; patients could better understand which symptoms and

157 These tools can address the complexity of OSA and guide a physician's course of action on the basi

158 quivalent were used to define a diagnosis of OSA (ICD-9 327.23) and a diagnosis of XFS (ICD-9 365.52

159 have in predicting a subsequent diagnosis of OSA.

160 could suggest that the deleterious effect of OSA and its contribution to CVD could depend on specific

161 ofiles.Objectives: To evaluate the effect of OSA on cardiovascular risk for patients with different A

162 The effect of OSA on recurrent cardiovascular event risk was evaluated

163 the no-previous-CVD phenotype, the effect of OSA showed an adjusted hazard ratio (95% confidence inte

164 or the previous-CVD phenotype, the effect of OSA showed an adjusted hazard ratio of 0.69 (0.46-1.04;

165 conducted to gain insights on the effect of OSA-treatment on in vitro digestibility.

166 ces in optic disc measures between groups of OSA severity.

167 Intermittent hypoxia, a hallmark of OSA, could impose significant long-term effects on somat

168 of intermittent hypoxia (IH), a hallmark of OSA, on senescence in human white preadipocytes.

169 History of OSA was determined by polysomnography and associated con

170 History of OSA, in addition to recurrent ICH, is associated with gr

171 ; and group 4, recurrent ICH with history of OSA.

172 SA; group 3, recurrent ICH absent history of OSA; and group 4, recurrent ICH with history of OSA.

173 ups: group 1, resolved ICH absent history of OSA; group 2, resolved ICH with history of OSA; group 3,

174 f OSA; group 2, resolved ICH with history of OSA; group 3, recurrent ICH absent history of OSA; and g

175 logists should encourage early management of OSA as well as ICH to optimize ophthalmic outcomes.

176 d has also facilitated routine management of OSA by primary care providers.

177 somnia disorder, treatment and management of OSA, and treatment and management of chronic insomnia di

178 ty, posing a challenge for the management of OSA.

179 intermittent hypoxia, a key manifestation of OSA, to shed light on the mechanisms by which OSA may gi

180 vernight polysomnography-derived measures of OSA and the optic disc in young adults.

181 OX-2 specific inhibitor in a murine model of OSA bearing Lewis lung carcinoma (LLC1) tumors.

182 timodal imaging in this established model of OSA, a discernible neuroinflammatory response was demons

183 ment, contributing to the pathophysiology of OSA and potentially other diseases that involve hypoxia.

184 vealed glass-transition and melting peaks of OSA-starch and a cold-crystallization peak corresponding

185 clinical manifestation (i.e., phenotype) of OSA in an individual are not well described by the AHI.

186 The PPV of CSC diagnosis as a predictor of OSA was highest in the fifth decade of life.

187 To evaluate the presence of OSA (apnea-hypopnea index >= 15 events . h(-1)), all pat

188 In the derivation cohort, screening of OSA(>=5), OSA(>=15), and OSA(>=30) revealed that GOAL qu

189 ility of GOAL questionnaire for screening of OSA(>=5), OSA(>=15), and OSA(>=30) was similar to No-Apn

190 In the validation cohort, screening of OSA(>=5), OSA(>=15), and OSA(>=30), corroborated validat

191 In this first admixture mapping study of OSA, novel associations with variants in the iron/heme m

192 (or endotypes) that help define subtypes of OSA and identify the potential use of genetics to furthe

193 The most common presenting symptom of OSA is excessive sleepiness, although this symptom is re

194 gammaH2AX & p16 nuclei in adipose tissue of OSA patients receiving statin, aspirin, and/or RAS inhib

195 an update on the diagnosis and treatment of OSA.

196 ibilities for the pharmacologic treatment of OSA.

197 sion; however, randomized clinical trials of OSA treatment have not demonstrated significant benefit

198 This more detailed understanding of OSA pathogenesis should influence clinical treatment dec

199 etine) and an antimuscarinic (oxybutynin) on OSA severity (apnea-hypopnea index [AHI]; primary outcom

200 ught to determine the effects of zolpidem on OSA severity, upper airway physiology and next-day sleep

201 Overall, OSA treatment induced the formation of more complex star

202 In conclusion, in CM patients, OSA severity is associated with higher MDK levels, which

203 In CM patients, OSA was associated with higher TGF-beta1 levels and grea

204 In many patients, OSA can be diagnosed with home sleep apnea testing, whic

205 Pediatric OSA is associated with cognitive risk.

206 lead to regional neuronal losses, pediatric OSA patients may also be affected.

207 Thus, pediatric OSA subjects show extensive regionally-demarcated grey m

208 patients with ACS and a specific phenotype, OSA is associated with an increased risk of recurrent ca

209 Admixture mapping analysis of the primary OSA traits identified local African ancestry at the chro

210 e applied admixture mapping on three primary OSA traits [the apnea hypopnea index (AHI), overnight av

211 zolpidem may stabilise breathing and reduce OSA severity without CPAP.

212 pairing pharyngeal muscle activity to reduce OSA severity, with variable success.

213 ly before bedtime on 1 night greatly reduced OSA severity.

214 sed awareness of obstructive sleep apnoea's (OSA) links to Alzheimer's disease and major psychiatric

215 ortable monitor testing for detecting severe OSA syndrome (AHI >/=30 and ESS score >10) was AUC 0.80

216 MDK levels were higher in severe OSA compared to mild OSA or non-OSA patients, whereas no

217 indicates moderate and >30 indicates severe OSA) and the Epworth Sleepiness Scale (ESS; range, 0-24;

218 TGF-beta1 was increased in moderate-severe OSA patients vs. non-OSA or mild OSA patients with CM.

219 CM patients and increased in moderate-severe OSA.

220 A (AHI >= 15 and <30 events/hour), or severe OSA (AHI >= 30 events/hour).

221 unders, participants with moderate or severe OSA had a 2.0 times higher odds of resistant hypertensio

222 nary study of adults with moderate or severe OSA in whom conventional therapy had failed, combined pa

223 Adults with symptomatic moderate or severe OSA in whom conventional treatments had failed were enro

224 Untreated moderate or severe OSA is associated with increased odds of resistant hyper

225 thdrawal in patients with moderate to severe OSA.

226 OSA and 3.8% to 6.5% for moderate to severe OSA; current prevalence may be higher, given the increas

227 is trial, we randomized patients with severe OSA and no overt cardiovascular disease to receive 2 mon

228 OSA, 26 with moderate OSA, and 2 with severe OSA.

229 endothelial function in patients with severe OSA.

230 octenyl succinic anhydride modified starch (OSA), water soluble soy polysaccharides (WSSP)) and gela

231 Hence, it's plausible that OSA could play a role in the pathogenesis of sight-threa

232 We previously showed that OSA may impair Abeta clearance and affect the relationsh

233 s abdominal adipose tissue which showed that OSA patients had a significantly higher percentage of ce

234 In vitro digestibility tests showed that OSA treatment reduced the fraction of fastly digestible

235 Emerging evidence suggest that OSA increases the risk of cardiovascular morbidity and m

236 Together, our data suggest that OSA may be considered as a senescence-related disorder.

237 This suggests that OSA could be acting as a cross-linking agent between sta

238 ter solubility and intrinsic viscosity, that OSA addition changed physicochemical properties of starc

239 The OSA-based system offered the fastest release of AP and,

240 positively correlated with beta power in the OSA group as well as in the combined group (OSA + SS).

241 e periodontitis prevalence was higher in the OSA group than control group.

242 ta power during NREM sleep were found in the OSA group than in the SS group, and beta power was corre

243 the beta and delta bands were higher in the OSA group than in the SS group.

244 The specificity of the OSA was 91.5%.

245 por permeability and tensile strength of the OSA-based carrier.

246 t has emerged from these studies is that the OSA-NAFLD association is related to the degree of noctur

247 tors that predispose patients with asthma to OSA.

248 factors predisposing patients with asthma to OSA.

249 This review is focused on EDS due to OSA and narcolepsy and addresses some of the challenges

250 n approach could also be readily exported to OSA.

251 which symptoms and outcomes will respond to OSA treatment and by how much; and researchers could sel

252 versely, undiagnosed or inadequately treated OSA adversely affects asthma control, partly via effects

253 in influencing respiratory traits underlying OSA.

254 Untreated OSA can show polysomnographic findings that are similar

255 These results suggest that untreated OSA may contribute to inadequate BP control in blacks.

256 We propose a model whereby OSA treatment may affect both Abeta release and clearanc

257 SA, to shed light on the mechanisms by which OSA may give rise to the complex metabolic disturbances

258 To identify genetic regions associated with OSA and improve statistical power, we applied admixture

259 ts with OSA, TGF-beta1 levels correlate with OSA severity and leptin levels, whereas only associate w

260 A cohort of 81 735 patients diagnosed with OSA at ages 50 to 90 years was identified from medical r

261 k already may be present in individuals with OSA since young adulthood.

262 Retrospective study in individuals with OSA who were intolerant to continuous positive airway pr

263 Incidence was higher in women and men with OSA (17.2 and 40.8 per 100,000).

264 CSF Abeta were measured in participants with OSA before and 1 to 4 months after treatment.

265 n the unadjusted analyses, participants with OSA on average showed thinner peripapillary RNFL at the

266 Study.Methods: Data from 1,207 patients with OSA (apnea-hypopnea index >= 15 events/h) were used to e

267 We recruited 68 patients with OSA and 40 control volunteers.

268 asets comprising 353 untreated patients with OSA and 444 healthy controls were included.

269 ents by HTN diagnosis history, patients with OSA and HTN exhibited an increased risk of XFS compared

270 most common symptoms, but many patients with OSA are asymptomatic.

271 s were significantly higher in patients with OSA compared to controls (0.59/0.31-0.88/ng/mL vs. 0.31/

272 ed risk of an XFS diagnosis in patients with OSA compared with non-OSA controls (OR, 1.27; 95% confid

273 Whether patients with OSA have an increased risk of diagnosis of XFS compared

274 Patients with OSA may be at an increased risk of XFS compared with pat

275 Of the 15/20 patients with OSA on placebo (AHI > 10 events/hr), AHI was lowered by

276 and systemic vascular risk in patients with OSA requiring further comprehensive investigation.

277 STDR prevalence was higher in patients with OSA than in those without OSA (42.9% vs. 24.1%; P = 0.00

278 edman tongue position (FTP) in patients with OSA through drug-induced sleep endoscopy (DISE).

279 Patients with OSA who are asymptomatic, or whose symptoms are minimall

280 clinician screen for NAFLD in patients with OSA, and vice versa?

281 Moreover, in non-obese patients with OSA, TGF-beta1 levels correlate with OSA severity and le

282 irway surgery for treatment of patients with OSA.

283 e fat should be considered for patients with OSA.

284 stimate regional GM changes in patients with OSA.

285 F IL-1beta and serum hs-CRP in patients with OSA.

286 to estimate the risk of XFS in patients with OSA.

287 ay be therapeutically useful for people with OSA and comorbid insomnia.

288 ~10%, which may be beneficial in people with OSA and insomnia.

289 orted by as few as 15% to 50% of people with OSA in the general population.

290 Nineteen people with OSA with low-to-moderate arousal threshold received 10 m

291 effective in promoting sleep in people with OSA, which may be therapeutically useful for people with

292 nsiveness (secondary outcome) in people with OSA.

293 ongue fat is increased in obese persons with OSA, and may explain the relationship between obesity an

294 ampled high-risk participants and those with OSA and OSA syndrome.

295 culating MDK in CM patients with and without OSA, and their relationship with tumor aggressiveness, w

296 gnosis of XFS compared with controls without OSA.

297 When compared with individuals without OSA (apnea-hypopnea index < 5), significantly increased

298 d risk of XFS compared with patients without OSA, particularly in patients with a history of HTN.

299 r in patients with OSA than in those without OSA (42.9% vs. 24.1%; P = 0.004).

300 0.008) segments compared with those without OSA.