ライフサイエンスコーパス: OSA

1 OSA is an independent predictor for the progression to p

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

3 OSA is associated with structural and functional atrial

4 OSA leads to high cardiovascular morbidity and mortality

5 OSA lends itself to a personalized approach to diagnosis

6 OSA patients showed increased nerve fiber indicator (NFI

7 OSA rice and tapioca starches were analyzed using micros

8 OSA severity was defined by the apnea-hypopnea index (AH

9 OSA severity was defined by using established clinical c

10 OSA was assessed using a home-based multichannel cardior

11 OSA was independently associated with hs-TnT among women

12 OSA was not significantly associated with the prevalence

13 OSA, assessed in midlife, is independently associated wi

14 e, case-control, parallel-design study (2:1; OSA/no-OSA), all patients began treatment with an angiot

15 with an AHI greater than or equal to 20 (10 OSA; 5 CSA) participated.

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

17 Esterification with 3% OSA results in starch that has OSA substituted mainly on

18 paraaminohippurate clearance technique in 31 OSA subjects (respiratory disturbance index, 51 +/- 25 h

19 le of this cross-sectional study included 40 OSA patients and 45 age-matched controls, consecutively

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

21 opectin changed significantly (P<0.05) after OSA esterification.

22 All OSA-related variables collected from the sleep study wer

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

24 triggers in patients with paroxysmal AF and OSA.

25 e patients with newly revascularized CAD and OSA (apnea-hypopnea index >/=15/h) without daytime sleep

26 9 dB and -1.43 +/- 2.3 dB in the control and OSA groups, respectively (p = 0.01).

27 tcomes were compared between the control and OSA groups.

28 suboptimally controlled type 2 diabetes and OSA, CPAP treatment for 6 months resulted in improved gl

29 13.29 and from 14.87 to 12.47 in native and OSA rice and tapioca starches, respectively.

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

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

32 an 84-miRNA array among patients with RH and OSA at baseline and after 3 months of adherent CPAP use.

33 es to CPAP treatment in patients with RH and OSA.

34 STDR and OSA prevalence rates were 36.1% and 63.9%, respectively.

35 5 or positive airway pressure treatment) and OSA concomitant with habitual daytime sleepiness were es

36 fine structure of octenylsuccinic anhydride (OSA) starch would lead to a better understanding of func

37 Octenylsuccinic anhydride (OSA)-modified starches with a low (0.018) and high (0.09

38 and cleaves B-band LPS (O-specific antigen, OSA) of Pseudomonas aeruginosa PAO1.

39 d, both obstructive and central sleep apnea (OSA and CSA) are common.

40 Obstructive sleep apnea (OSA) affects 8-10% of the population, is characterized b

41 association between obstructive sleep apnea (OSA) and Alzheimer's disease is OSA leading to decreased

42 Obstructive sleep apnea (OSA) and nocturnal hypoxemia are associated with chronic

43 Risk factors for obstructive sleep apnea (OSA) and the development of subsequent cardiovascular (C

44 tment is needed for obstructive sleep apnea (OSA) because untreated OSA can result in serious health

45 urgical success for obstructive sleep apnea (OSA) depends on identifying sites of obstruction in the

46 n periodontitis and obstructive sleep apnea (OSA) has been suggested.

47 An adverse role for obstructive sleep apnea (OSA) in cancer epidemiology and outcomes has recently em

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

49 Mild obstructive sleep apnea (OSA) is a highly prevalent disorder in adults; however,

50 Obstructive sleep apnea (OSA) is a known risk factor for atherosclerosis.

51 Obstructive sleep apnea (OSA) is a risk factor for type 2 diabetes that adversely

52 Obstructive sleep apnea (OSA) is a sleep disorder characterized by disruptions of

53 Obstructive sleep apnea (OSA) is a worldwide disease whose prevalence is increasi

54 Obstructive sleep apnea (OSA) is associated with atrial remodeling, atrial fibril

55 Obstructive sleep apnea (OSA) is associated with hypertension.

56 Although obstructive sleep apnea (OSA) is associated with impaired glucose tolerance and d

57 RATIONALE: Obstructive sleep apnea (OSA) is associated with several pathophysiological defic

58 Obstructive sleep apnea (OSA) is characterized by recurrent upper airway obstruct

59 Obstructive sleep apnea (OSA) is common in patients with coronary artery disease

60 Obstructive sleep apnea (OSA) is common in people with hypertension, particularly

61 Obstructive sleep apnea (OSA) is more common among patients with asthma; whether

62 PSG) for diagnosing obstructive sleep apnea (OSA) is unclear.

63 rging evidence that obstructive sleep apnea (OSA) may cause metabolic disturbances independently of o

64 The effect of obstructive sleep apnea (OSA) syndrome in the peripapillary retinal nerve fiber l

65 risk for developing obstructive sleep apnea (OSA), and both of these conditions are associated with a

66 hildhood asthma and obstructive sleep apnea (OSA), both disorders of airway inflammation, were associ

67 pertension (RH) and obstructive sleep apnea (OSA), the blood pressure response to continuous positive

68 eyelid syndrome and obstructive sleep apnea (OSA), the diagnostic criteria of floppy eyelid syndrome

69 are associated with obstructive sleep apnea (OSA).

70 e for patients with obstructive sleep apnea (OSA).

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

72 ts with symptomatic obstructive sleep apnea (OSA).

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

74 treatment used for obstructive sleep apnea (OSA).

75 d ten patients with obstructive sleep apnea (OSA).

76 ajor determinant of obstructive sleep apnea (OSA).

77 athology underlying obstructive sleep apnea (OSA).

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

79 moderate to severe obstructive sleep apnoea (OSA) syndrome have been established in middle-aged peopl

80 on profiles during obstructive sleep apnoea (OSA), have been shown to exhibit a heightened carotid bo

81 on profiles during obstructive sleep apnoea (OSA), have been shown to exhibit a heightened carotid bo

82 ) in patients with obstructive sleep apnoea (OSA), yet its effects on the other traits responsible fo

83 high prevalence of obstructive sleep apnoea (OSA).

84 high prevalence of obstructive sleep apnoea (OSA).

85 ce bran oil and incorporated into an aqueous OSA-ST solution.

86 eports of an independent association between OSA and metabolic dysfunction, and suggested that this a

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

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

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

90 ustment, no association was observed between OSA severity and an eyelid laxity score (regression coef

91 ifferences exist in the relationship between OSA and CV disease.

92 To assess the relationship between OSA and DR in patients with type 2 diabetes and to asses

93 We hypothesize that the relationship between OSA and high-sensitivity troponin T (hs-TnT), cardiac st

94 ion of asthma with 4-year incidences of both OSA (AHI of >/=5 or positive airway pressure treatment)

95 Thus, perturbations to fetal environment by OSA during pregnancy can have long-term detrimental effe

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

97 nd sleep duration (P = 0.06 for ethnicity-by-OSA severity interaction).

98 Although childhood OSA is effectively treated by adenotonsillectomy (AT), i

99 AT, the first line of therapy for childhood OSA, would be associated with improved asthma outcomes a

100 he apnea-hypopnea index was used to classify OSA as none (0-4.9/h), mild (5-14.9/h), or moderate to s

101 For example, different clinical OSA subtypes likely benefit from therapy in different wa

102 After adjustment for confounders, OSA remained an independent predictor of progression to

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

104 CPAP corrected OSA and hypoxemia (RDI: 42 +/- 4 vs. 4 +/- 1 h(-1), P <

105 A total of 30 newly diagnosed OSA patients with no history of cardiovascular diseases

106 y normotensive, nondiabetic, newly diagnosed OSA subjects (15 men, 5 women, 50 +/- 2 yr, respiratory

107 aged 65 years or older with newly diagnosed OSA syndrome were eligible to join the trial.

108 hook peptide 3 KRGRGRPRK [M + 2H](+2) during OSA-TIMS-FT-ICR MS.

109 Eleven OSA subjects underwent a night of polysomnography during

110 g participants without an incident CV event, OSA assessed in midlife was independently associated wit

111 re-relevant evidence on screening adults for OSA, test accuracy, and treatment of OSA, to inform the

112 All models controlled for OSA events during non-REM sleep, either by statistical a

113 ld signal-to-noise increase was observed for OSA-TIMS when compared with SA-TIMS during the PAH analy

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

115 There is no effective pharmacotherapy for OSA.

116 effects on the other traits responsible for OSA remain unknown.

117 nefits, and potential harms of screening for OSA in asymptomatic adults seen in primary care, includi

118 rce (USPSTF) recommendation on screening for OSA in asymptomatic adults.

119 lance of benefits and harms of screening for OSA in asymptomatic adults.

120 de of the benefits or harms of screening for OSA or whether there is a net benefit or harm to screeni

121 Multiple treatments for OSA reduce AHI, ESS scores, and blood pressure.

122 medical subject headings and text words for OSA in adults as well as by hand searches.

123 ation with 3% OSA results in starch that has OSA substituted mainly on amylose chains or possibly on

124 nt a home sleep study (55 were found to have OSA; 36 were not).

125 e, closely mimicking the chronicity of human OSA, increased accumulation and proliferation of pro-inf

126 ies and respiratory-related abnormalities in OSA.

127 nt grey matter volume reductions appeared in OSA throughout areas of the superior frontal and prefron

128 Losartan reduced BP in OSA, but the reductions were less than in no-OSA.

129 graphy and lumbar puncture were performed in OSA and control groups.

130 e in the adverse cancer outcomes reported in OSA.

131 a thickness (CCA-IMT) with snoring sounds in OSA patients.

132 d hypoxia alter four physiological traits in OSA patients.

133 n [95% CI, 1.02-1.13], P = .01) and incident OSA with habitual sleepiness (RR, 1.18 [95% CI, 1.07-1.3

134 Asthma duration was related to both incident OSA (RR, 1.07 per 5-year increment in asthma duration [9

135 , 17%-37%]) with asthma experienced incident OSA over their first observed 4-year follow-up interval

136 with asthma experienced 45 cases of incident OSA during 167 4-year intervals (27% [95% CI, 20%-34%])

137 out asthma experienced 160 cases of incident OSA during 938 4-year intervals (17% [95% CI, 15%-19%]);

138 to have any respiratory disorder (including OSA) were excluded.

139 Increasing OSA severity is independently associated with retinal ar

140 ontrolling for multiple confounders, initial OSA severity and its physiologic consequences predicted

141 sleep apnea (OSA) and Alzheimer's disease is OSA leading to decreased slow wave activity (SWA), incre

142 mass spectrometry analyses of degraded LPS (OSA) fragments show an O5 serotype-specific polysacchari

143 ere were 41 severe, 35 moderate, and 25 mild OSA patients and 14 controls.

144 tent regarding the relationship between mild OSA and daytime sleepiness.

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

146 hould focus on clarifying the effect of mild OSA and impact of effective treatment on other neurocogn

147 There is evidence that treatment of mild OSA in individuals who demonstrate subjective sleepiness

148 s, evaluate whether or not treatment of mild OSA is effective at preventing or reducing these adverse

149 However, treatment of mild OSA may improve sleepiness in patients who are sleepy at

150 pertaining to the impact of therapy of mild OSA on neurocognition, mood, vehicle accidents, cardiova

151 cant differences were found between the mild OSA and moderate-to-severe OSA groups.

152 iovascular outcomes are attributable to mild OSA in adults, evaluate whether or not treatment of mild

153 nt disorder in adults; however, whether mild OSA has significant neurocognitive and cardiovascular co

154 e incongruent in their definitions of "mild" OSA.

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

156 ents with paroxysmal AF (43 with >/=moderate OSA [apnea-hypopnea index >/=15] and 43 without OSA [apn

157 OSA, but the reductions were less than in no-OSA.

158 -control, parallel-design study (2:1; OSA/no-OSA), all patients began treatment with an angiotensin I

159 18 females and 65 males) with OSA and 80 non-OSA individuals (23 females and 57 males) as controls.

160 of CPAP to patients with CAD with nonsleepy OSA did not significantly reduce long-term adverse cardi

161 this population may provide clues for novel OSA interventions.

162 The analytical advantages of OSA-TIMS over SA-TIMS were illustrated for the analysis

163 roof-of-principle for further application of OSA-TIMS-FT-ICR MS for the unsupervised analysis of comp

164 In the case of OSA-TIMS-FT-ICR MS, the TIMS operation sequence, trappin

165 asthma is associated with the development of OSA is unknown.

166 ribed above may explain the disappearance of OSA and the emergence of central sleep apnoea in conditi

167 ible participants were identified as free of OSA (apnea-hypopnea index [AHI] of <5 events/h and not t

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

169 Intermittent hypoxia (IH), a hallmark of OSA, could impose significant long-term effects on somat

170 Intermittent hypoxia (IH), a hallmark of OSA, enhances melanoma growth and metastasis in mice.

171 l studies are needed to assess the impact of OSA treatment on STDR.

172 g glucose after considering the influence of OSA.

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

174 overload contributes to the pathogenesis of OSA and CSA in ESRD, and that fluid removal by UF attenu

175 overload is involved in the pathogenesis of OSA and CSA in this condition.

176 The pathogenesis of OSA has been linked to a defect in neuromuscular control

177 ssociation was found between the presence of OSA and the rate of progression of CKD or all-cause mort

178 Here, we hypothesized that the presence of OSA would be associated with higher risk of mortality an

179 analyze the association between severity of OSA and the prevalence/severity of periodontitis.

180 icial effect of hyperoxia on the severity of OSA is primarily based on its ability to reduce LG.

181 The presence and severity of OSA were determined from polysomnography results.

182 associated with the presence or severity of OSA.

183 Although weight loss and treatment of OSA by adenotonsillectomy improve endothelial function,

184 nt evidence on screening for or treatment of OSA in asymptomatic adults or adults with unrecognized s

185 is clinically relevant because treatment of OSA is often limited to the first half of the sleep peri

186 ce on the benefits and harms of treatment of OSA on intermediate and final health outcomes.

187 lts for OSA, test accuracy, and treatment of OSA, to inform the US Preventive Services Task Force.

188 wo-stage model of eGFR change including only OSA as a variable.

189 Asthma was also associated with new-onset OSA with habitual sleepiness (RR, 2.72 [95% CI, 1.26-5.8

190 sociated with an increased risk of new-onset OSA.

191 Among other OSA-related variables, AHI in rapid eye movement sleep a

192 Pediatric OSA is associated with cognitive risk.

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

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

195 g this association and the value of periodic OSA evaluation in patients with asthma are warranted.

196 we can focus efforts to predict and prevent OSA on an individual level.

197 ere repeated at 4-year intervals to quantify OSA.

198 OSA, mandibular advancement therapy reduced OSA severity and related symptoms but had no effect on e

199 was reduced only in REM sleep, allowing REM OSA to recur.

200 Severe OSA is associated with increased all-cause mortality, ca

201 Severe OSA was related to a reduction of the RNFL thickness ass

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

203 In severe OSA subjects (n = 22), NFI and AHI had a Spearman correl

204 ncrease in severity with increasingly severe OSA because both disease entities share common inflammat

205 In women with moderate or severe OSA, 3 months of CPAP therapy improved QoL, mood state,

206 opnea index (AHI): mild, moderate, or severe OSA.

207 tive women diagnosed with moderate to severe OSA (apnea-hypopnea index, >/=15) in 19 Spanish sleep un

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

209 between the mild OSA and moderate-to-severe OSA groups.

210 o subjects without apnea, moderate-to-severe OSA was significantly associated with abnormal fasting g

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

212 In moderately sleepy patients with severe OSA, mandibular advancement therapy reduced OSA severity

213 endothelial function in patients with severe OSA.

214 Similarly, OSA was associated with incident heart failure or death

215 Since OSA disease duration in our subjects is unknown, these f

216 to explore the association between REM sleep OSA and prevalent hypertension in the entire cohort (n =

217 umulation Trapped Ion Mobility Spectrometry (OSA-TIMS) when coupled to ultrahigh resolution mass anal

218 Octenyl succinic anhydride modified starch (OSA-ST) was used to encapsulate coenzyme Q10 (CoQ10).

219 Compared with control subjects, OSA subjects demonstrated decreased renovascular sensiti

220 Consecutive women referred for suspected OSA and free of previous stroke and CHD were analyzed.

221 ut previous diabetes referred with suspected OSA who underwent a diagnostic sleep study at St.

222 (n = 406) aged 25 to 80 years with suspected OSA.

223 First-line treatment for symptomatic OSA is continuous positive airway pressure (CPAP), but i

224 ose and amylopectin fractions indicated that OSA substitution was present only in amylose fractions o

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

226 ariability may lie with the recognition that OSA is a multifactorial disorder and that OAs may affect

227 of pure amylopectin fractions suggested that OSA groups were not present in the amylopectin portion o

228 decreased in the OSA group, suggesting that OSA may affect the interaction between interstitial and

229 The OSA group was divided into 3 sub-groups based on the apn

230 The OSA responder group exhibited blood pressure decreases e

231 Prevalence of periodontitis in the OSA group (96.4%) was significantly higher than in the c

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

233 ot total protein, were also decreased in the OSA group, suggesting that OSA may affect the interactio

234 ctedly, amyloid-beta-40 was decreased in the OSA group.

235 a-40 among controls and was decreased in the OSA group.

236 en, randomized, parallel-design study of the OSA group, all subjects continued to receive losartan an

237 The test group was classified according to OSA severity.

238 lar disease risk in children with underlying OSA and/or obesity, and identify therapeutic targets.

239 lar event was separately assessed, untreated OSA showed a stronger association with incident stroke (

240 tructive sleep apnea (OSA) because untreated OSA can result in serious health problems.

241 The untreated OSA group showed a greater incidence rate of the composi

242 In women, untreated OSA is associated with increased incidence of serious ca

243 During 13-year follow-up, OSA was associated with incident heart failure or death

244 n cross sections (<1%) can be measured using OSA-TIMS-FT-ICR MS with high mobility resolving powers (

245 ced changes may not be reversible with usual OSA treatment.

246 f AngII challenge (mean +/- SD; all P values OSA vs. control).

247 s with type 2 diabetes and to assess whether OSA is associated with its progression.

248 We sought to investigate whether OSA increases the incidence of a composite of stroke or

249 own risk factors, it remains unclear whether OSA is associated with incident diabetes.

250 nce and diabetes, it remains unclear whether OSA treatment with continuous positive airway pressure (

251 in whom other comorbidities associated with OSA may play a more important role.

252 unction, not every obese child or child with OSA develops ED.

253 her obese children or nonobese children with OSA were primarily derived from endothelial cell sources

254 ater than or equal to 10 were diagnosed with OSA and classified as CPAP-treated (adherence >/= 4 h/d)

255 (without OSA: 12.6, 7.2, and 9.0 mm Hg; with OSA: 9.8, 5.7, and 6.1 mm Hg).

256 3 individuals (18 females and 65 males) with OSA and 80 non-OSA individuals (23 females and 57 males)

257 t improves quality of life (QoL) in men with OSA, but its role in women has not yet been assessed.

258 th 25 overweight/obese matched patients with OSA (apnea-hypopnea index >/= 15 events per hour) and 11

259 In this model patients with OSA (eGFR versus time was -0.93 ml/min/1.73 m(2)/yr(95%C

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

261 r cardiovascular disease among patients with OSA and RH.

262 randomized clinical trial, 50 patients with OSA and type 2 diabetes and two HbA1c levels equal to or

263 randomized crossover study, 14 patients with OSA attended two sleep studies with and without their OA

264 revalence between controls and patients with OSA by assessing clinical periodontal parameters and gin

265 Patients with OSA exhibited high levels of SNA when awake, during norm

266 s; however, after PV isolation patients with OSA had increased incidence of additional extra-PV trigg

267 Patients with OSA had lower atrial voltage amplitude (right atrial, P=

268 ody mass index, sex, and race, patients with OSA had significantly reduced glucose uptake in the geni

269 tive airway pressure (CPAP) of patients with OSA on renal hemodynamics at baseline and in response to

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

271 be offered routinely to older patients with OSA syndrome.

272 s were significantly higher in patients with OSA than in controls (P = 0.001).

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

274 d morphometry (VBM) studies of patients with OSA to identify their brain abnormalities.

275 up of 43.0 (37.0-51.0) months, patients with OSA were more likely than patients without OSA to develo

276 Thirty-five adult patients with OSA were prospectively enrolled.

277 educed significantly in the 13 patients with OSA who used CPAP at least 4 hours per night.

278 mass index (BMI) and age among patients with OSA, and GM reductions in the SFG (medial rostral part)

279 ed sleep airway obstruction in patients with OSA.

280 ent to control hypertension in patients with OSA.

281 omputed tomography (DI-SCT) in patients with OSA.

282 coherence tomography (OCT) in patients with OSA.

283 pful when planning surgery for patients with OSA.

284 on independently of obesity in patients with OSA.

285 imary therapeutic approach for patients with OSA.

286 n tongue EMG activity in obese patients with OSA.

287 (EMG) activity is increased in patients with OSA.

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

289 s were significantly higher in patients with OSA.

290 stimate regional GM changes in patients with OSA.

291 Among people with OSA, and controlling for multiple confounders, initial O

292 ther therapies that can work for people with OSA.

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

294 [apnea-hypopnea index >/=15] and 43 without OSA [apnea-hypopnea index <5]), right atrial and left at

295 as similar between patients with and without OSA (83.7% and 81.4%, respectively; P=0.59).

296 tion rate(eGFR) in patients with and without OSA were compared using a two-stage model of eGFR change

297 and mean arterial BP in both groups (without OSA: 12.6, 7.2, and 9.0 mm Hg; with OSA: 9.8, 5.7, and 6

298 h OSA were more likely than patients without OSA to develop preproliferative/proliferative DR (18.4%

299 imilar slope as compared to patients without OSA(eGFR versus time was -1.24 ml/min/1.73 m(2)/yr(95%CI

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