ライフサイエンスコーパス: CPAP

1 CPAP (centrosomal protein 4.1-associated protein) was pr

2 CPAP (MCPH6) and STIL (MCPH7) are required for centriole

3 CPAP adherence did not differ between the groups.

4 CPAP adherence was ensured by continuous supervision.

5 CPAP corrected OSA and hypoxemia (RDI: 42 +/- 4 vs. 4 +/

6 CPAP improved objective sleepiness (p=0.024), mobility (

7 CPAP is an important therapy in OSA patients undergoing

8 CPAP is safe and improves respiratory rate in a non-tert

9 CPAP machines were allocated to one hospital during each

10 CPAP or no therapy while maintaining usual blood pressur

11 CPAP reduced baseline mean arterial pressure (94 +/- 2 v

12 CPAP reduced ESS by 2.1 points (95% CI -3.0 to -1.3; p<0

13 CPAP reduced GFR (124 +/- 8 ml/min vs. 110 +/- 6 ml/min,

14 CPAP therapy resulted in higher AF-free survival rate (7

15 CPAP therapy was associated with improved renal hemodyna

16 CPAP tracking systems are able to reliably track CPAP ad

17 CPAP treatment improves quality of life (QoL) in men wit

18 CPAP treatment is accompanied by changes in cardiovascul

19 CPAP usage can be reliably determined from CPAP tracking

20 CPAP was associated with modest improvement in sleep-rel

21 CPAP was more efficacious than MAD in reducing AHI (CPAP

22 CPAP with surfactant but without any positive pressure v

23 CPAP-30 worsened markers of potential epithelial cell da

24 52 protein interacts with Sak/Plk4 and Sas-4/CPAP and is required for centriole duplication, although

25 nd SAS-5/Ana2/STIL, which then recruit SAS-4/CPAP, which in turn helps assemble the outer centriole m

26 by either bubble CPAP (5 L/min starting at a CPAP level of 5 cm H2O), standard low-flow nasal cannula

27 ether, our results indicate that CEP120 is a CPAP-interacting protein that positively regulates centr

28 tations [Y254L/T257A (YLTA) and C186P/A220P (CPAP)] stabilize the naturally occuring AR domain of hum

29 Additionally, CPAP treatment significantly altered a total of 47 plasm

30 Adequate CPAP treatment seems to reduce this risk.

31 ovascular death in the elderly, and adequate CPAP treatment may reduce this risk.

32 cardiovascular death in women, and adequate CPAP treatment may reduce this risk.

33 A at baseline and after 3 months of adherent CPAP use.

34 eding the observed median (>4.5 mm Hg) after CPAP, which were not present in the nonresponder group (

35 se abnormalities significantly improve after CPAP therapy.

36 fferent than in the control group only after CPAP compliance adjustment.

37 s more efficacious than MAD in reducing AHI (CPAP AHI, 4.5 +/- 6.6/h; MAD AHI, 11.1 +/- 12.1/h; P < 0

38 definitions of these parameters differ among CPAP manufacturers.

39 of CEP135(full) binding proteins (SAS-6 and CPAP) and the pericentriolar localization of gamma-tubul

40 how that centrobin interacts with CEP152 and CPAP, and the centrobin-CPAP interaction is critical for

41 s including PLK4, CEP192, CEP152, CEP63, and CPAP.

42 ffer significantly between the high-flow and CPAP groups (15.5% and 11.5%, respectively; risk differe

43 n, adherence to a regimen of weight loss and CPAP may result in incremental reductions in blood press

44 ere similar after 1 month of optimal MAD and CPAP treatment in patients with moderate-severe OSA.

45 c parameters improved similarly with NIV and CPAP relative to the control.

46 NIV and CPAP were more effective than lifestyle modification in

47 condary effects were similar between NIV and CPAP.

48 invited, based on their expertise in OSA and CPAP monitoring.

49 determine the independent impact of OSA and CPAP treatment on cardiovascular mortality.

50 effects of nocturnal supplemental oxygen and CPAP on markers of cardiovascular risk.

51 termittent positive pressure ventilation and CPAP, both when used as primary support and as postextub

52 nt and WT proteins reveals that the YLTA and CPAP consensus mutations cause unexpected long-range eff

53 ts with obesity and obstructive sleep apnea, CPAP combined with a weight-loss intervention did not re

54 10 were diagnosed with OSA and classified as CPAP-treated (adherence >/= 4 h/d) or untreated (adheren

55 Patients with OSA were classified as CPAP-treated (adherence >/= 4 h/d) or untreated (adheren

56 Patients with OSA were classified as CPAP-treated (adherence >/=4 hours per day) or untreated

57 nd leak data are not as easy to interpret as CPAP usage and the definitions of these parameters diffe

58 Here we show that Cenpj, also known as CPAP, a microcephaly gene, is a transcriptional target o

59 ibility was quantified as the ventilation at CPAP of 0 cmH2O.

60 ibility was quantified as the ventilation at CPAP=0.

61 reatment or a healthy habit assessment, auto-CPAP titration (for CPAP indication), health-related qua

62 There was no significant difference between CPAP and MADs in their association with change in SBP (-

63 patients with obstructive sleep apnea, both CPAP and MADs were associated with reductions in BP.

64 in pulmonary acute lung injury, whereas both CPAP-30 and STEP-30/30 yielded endothelial injury in ext

65 Children who received oxygen by bubble CPAP had significantly lower rates of death than the chi

66 Oxygen therapy delivered by bubble CPAP improved outcomes in Bangladeshi children with very

67 children to receive oxygen therapy by bubble CPAP, 67 (30%) to low-flow oxygen therapy, and 79 (35%)

68 a to receive oxygen therapy by either bubble CPAP (5 L/min starting at a CPAP level of 5 cm H2O), sta

69 in district hospitals and to improve bubble CPAP delivery technology.

70 Use of bubble CPAP oxygen therapy could have a large effect in hospita

71 ldren, of whom five (6%) had received bubble CPAP, 16 (24%) had received low-flow oxygen therapy, and

72 ure was noted between patients in the bubble CPAP and those in the high-flow oxygen therapy group (RR

73 Significantly fewer children in the bubble CPAP group had treatment failure than in the low-flow ox

74 the low-flow oxygen group than in the bubble CPAP group, and we acknowledge that the early cessation

75 Three (4%) children died in the bubble CPAP group, ten (15%) children died in the low-flow oxyg

76 to test the feasibility of scaling up bubble CPAP in district hospitals and to improve bubble CPAP de

77 owever, there are no standards for capturing CPAP adherence data, scoring flow signals, or measuring

78 he CPAP binding site, could restore cellular CPAP levels in centrobin-depleted cells, indicating that

79 ly protein Cep63, required to localize CENPJ/CPAP/Sas-4, a final common target.

80 d cells restored the cellular and centriolar CPAP expression, suggesting its ubiquitination and prote

81 cells led to the reappearance of centriolar CPAP.

82 Hence, we conclude that centrobin-CPAP interaction is critical for the recruitment of CPAP

83 acts with CEP152 and CPAP, and the centrobin-CPAP interaction is critical for centriole duplication.

84 ed MADs with an inactive control, 1 compared CPAP with an MAD, and 3 compared CPAP, MADs, and an inac

85 1 compared CPAP with an MAD, and 3 compared CPAP, MADs, and an inactive control.

86 in the analysis (4888 patients), 44 compared CPAP with an inactive control, 3 compared MADs with an i

87 Compared with an inactive control, CPAP was associated with a reduction in SBP of 2.5 mm Hg

88 Conversely, CPAP was undetectable in centrobin-depleted cells, sugge

89 or on treatment with MAD compared with CPAP (CPAP-MAD difference, 0.2 mm Hg [95% confidence interval,

90 95% CI, 1.01-1.75), among those who declined CPAP therapy (1.96; 95% CI, 1.44-2.66), and among those

91 4.82-6.86) in patients with OSA who declined CPAP therapy, 5.12 (95% CI, 3.76-6.47) in patients with

92 at loss of centrobin expression destabilizes CPAP and triggers its degradation to restrict the centri

93 ly higher rate of treatment failure than did CPAP.

94 respiratory functional improvements than did CPAP.

95 ther via a thin endotracheal catheter during CPAP-assisted spontaneous breathing (intervention group)

96 premature infants randomly assigned to early CPAP or early surfactant administration and to a lower o

97 ys and 27 weeks 6 days of gestation to early CPAP with a limited ventilation strategy or early surfac

98 Women were randomized to receive effective CPAP therapy (n = 151) or conservative treatment (n = 15

99 e and mean arterial pressure than did either CPAP or weight loss alone.

100 group) or, in addition to education, either CPAP or nocturnal supplemental oxygen.

101 (1:1) into parallel groups to receive either CPAP with best supportive care (BSC) or BSC alone for 12

102 -to-treat analysis, although adjustments for CPAP and NIV compliance were also analyzed.

103 eater among patients with OSA ineligible for CPAP therapy (1.33; 95% CI, 1.01-1.75), among those who

104 85-3.82) in patients with OSA ineligible for CPAP therapy, 5.84 (95% CI, 4.82-6.86) in patients with

105 y habit assessment, auto-CPAP titration (for CPAP indication), health-related quality-of-life questio

106 CPAP usage can be reliably determined from CPAP tracking systems, but the residual events (apnea/hy

107 alt balance pre- and post-CPAP therapy (>4 h CPAP use/night for 1 mo).

108 nd 24 patients (2%) in the control group had CPAP-related adverse events, such as vomiting, aspiratio

109 e effect was greater in patients with higher CPAP usage or higher baseline ESS.

110 atients with OSA and resistant hypertension, CPAP treatment for 12 weeks compared with control result

111 ate in their own care, and doing so improves CPAP compliance.

112 n and explain how a microcephaly mutation in CPAP compromises complex formation.

113 AF recurrence following PVI in CPAP nonuser patients was significantly higher (HR: 2.4,

114 Depletion of CEP120 inhibited CPAP-induced centriole elongation and vice versa, implyi

115 In extrapulmonary acute lung injury, CPAP-30 and STEP-30/30 increased vascular cell adhesion

116 In pulmonary acute lung injury, CPAP-30 yielded lower surfactant protein-B and higher ty

117 roviders need to understand how to interpret CPAP adherence tracking data.

118 ASQ score (-17.8 vs. -24.7; P = 0.018), less CPAP use (4.5 vs. 5.3 hours per night; P = 0.04), and lo

119 A 1-hour-per-night increase in mean CPAP use was associated with an additional reduction in

120 eshold were determined using multiple 3 min 'CPAP pressure drops': pharyngeal anatomy/collapsibility

121 cannulae was noninferior to the use of nasal CPAP, with treatment failure occurring in 52 of 152 infa

122 cannulae (5 to 6 liters per minute) or nasal CPAP (7 cm of water) after extubation.

123 with either nasal high-flow therapy or nasal CPAP.

124 ed with 180 of 490 infants assigned to nasal CPAP (36.7%) (adjusted odds ratio, 1.09; 95% confidence

125 eated with nasal CPAP; infants in whom nasal CPAP failed were reintubated.

126 pport with nasal IPPV as compared with nasal CPAP.

127 cannulae failed could be treated with nasal CPAP; infants in whom nasal CPAP failed were reintubated

128 Newer CPAP machines can track adherence, hours of use, mask le

129 CPAP throughout, whereas on the other night, CPAP was reduced only in REM sleep, allowing REM OSA to

130 and were randomly assigned to either nightly CPAP as add-on therapy or no CPAP.

131 ly assigned to receive either 8-hour nightly CPAP (n = 26) or oral placebo (n = 13).

132 In patients with prediabetes, 8-hour nightly CPAP treatment for 2 weeks improves glucose metabolism c

133 o determine the comparative efficacy of NIV, CPAP, and lifestyle modification (control group) using d

134 6.5% were randomized to CPAP (n = 26) or no CPAP (control; n = 24), while their usual medication for

135 omly assigned to receive CPAP (n = 98) or no CPAP (control; n = 96).

136 either nightly CPAP as add-on therapy or no CPAP.

137 of centrioles due to massive accumulation of CPAP in the cell.

138 ls of CEP152, it caused the disappearance of CPAP from both the preexisting and newly formed centriol

139 f centrobin also caused the disappearance of CPAP from both the preexisting and newly synthesized cen

140 We show that the TCP domain of CPAP constitutes a novel proline recognition domain that

141 , we compared the effects of 1 month each of CPAP and MAD treatment on cardiovascular and neurobehavi

142 ized clinical trials comparing the effect of CPAP or MADs (vs each other or an inactive control) on B

143 Common adverse effects of CPAP and MADs included oral or nasal dryness, irritation

144 characteristics and the reported effects of CPAP vs inactive control.

145 ults may be explained by greater efficacy of CPAP being offset by inferior compliance relative to MAD

146 ficant positive correlation between hours of CPAP use and the decrease in 24-hour mean blood pressure

147 However, the impact of CPAP therapy on PVI outcome in patients with OSA is poor

148 e examined asthma outcomes after 6 months of CPAP in 99 adult asthma patients (mean age 57 years) wit

149 men with moderate or severe OSA, 3 months of CPAP therapy improved QoL, mood state, anxiety and depre

150 Interestingly, exogenous overexpression of CPAP in the centrobin-depleted cells did not restore CPA

151 ughter centrioles and for the persistence of CPAP on preexisting mother centrioles.

152 pleted cells, indicating that persistence of CPAP requires its interaction with centrobin.

153 hout daytime sleepiness, the prescription of CPAP compared with usual care did not result in a statis

154 Routine prescription of CPAP to patients with CAD with nonsleepy OSA did not sig

155 AF recurrence rate of CPAP-treated patients was similar to a group of patients

156 teraction is critical for the recruitment of CPAP to procentrioles to promote the elongation of daugh

157 Our study indicates that regulation of CPAP levels on the centrioles by centrobin is critical f

158 h-flow nasal cannulae was similar to that of CPAP as respiratory support for very preterm infants aft

159 e a pressure-time product similar to that of CPAP-30; and 3) stepwise airway pressure increase (5 cm

160 Trials of CPAP and other treatments have not established whether t

161 ATION: In the unadjusted analysis the use of CPAP did not decrease all-cause 2-week mortality in chil

162 Add-on CPAP therapy resulted in no significant changes in 24-ho

163 Add-on CPAP treatment had no significant changes in 24-hour BP

164 Forced overexpression of either CEP120 or CPAP not only induced the assembly of overly long centri

165 ssure (CPAP), a weight-loss intervention, or CPAP plus a weight-loss intervention for 24 weeks.

166 tions as compared with either weight loss or CPAP alone.

167 ptimally controlled type 2 diabetes and OSA, CPAP treatment for 6 months resulted in improved glycemi

168 Post-CPAP demonstrated a blunted GFR response (-9 +/- 3 ml/mi

169 e studied in high-salt balance pre- and post-CPAP therapy (>4 h CPAP use/night for 1 mo).

170 erular pressure) were measured pre- and post-CPAP using inulin and para-aminohippurate clearance tech

171 A singular pre-CPAP treatment cluster of 3 plasma miRNAs predicts blood

172 Continuous positive airway pressure (CPAP) and mandibular advancement device (MAD) therapy ar

173 lthough continuous positive airway pressure (CPAP) can mitigate these risks, effectiveness can be red

174 nd that continuous positive airway pressure (CPAP) compared with sham was significantly associated wi

175 (SASQ), continuous positive airway pressure (CPAP) compliance, and physician decision making.

176 fits of continuous positive airway pressure (CPAP) for moderate to severe obstructive sleep apnoea (O

177 o nasal continuous positive airway pressure (CPAP) for noninvasive respiratory support of very preter

178 nt with continuous positive airway pressure (CPAP) has metabolic benefits.

179 bubble continuous positive airway pressure (CPAP) improved outcomes compared with standard low-flow

180 Continuous positive airway pressure (CPAP) in asthma patients with concomitant obstructive sl

181 Continuous positive airway pressure (CPAP) is considered the treatment of choice for obstruct

182 Continuous positive airway pressure (CPAP) is the first-line treatment for patients with symp

183 Continuous positive airway pressure (CPAP) is the treatment of choice in patients with sympto

184 apeutic continuous positive airway pressure (CPAP) levels.

185 tolerate continous positive airway pressure (CPAP) machines or intraoral devices.

186 fect of continuous positive airway pressure (CPAP) of patients with OSA on renal hemodynamics at base

187 fect of continuous positive airway pressure (CPAP) on glycemic control in patients with diabetes.

188 ts with continuous positive airway pressure (CPAP) preserves surfactant and keeps the lung open but i

189 Continuous positive airway pressure (CPAP) reduces blood pressure, but adherence is often sub

190 Continuous positive airway pressure (CPAP) therapy is the most common treatment used for obst

191 fect of continuous positive airway pressure (CPAP) therapy on atrial fibrillation (AF) recurrence in

192 te that continuous positive airway pressure (CPAP) therapy reduces blood pressure in patients with hy

193 scribed continuous positive airway pressure (CPAP) therapy to manage OSA and were identified via accr

194 olonged continuous positive airway pressure (CPAP) therapy with supplemental oxygen was also associat

195 onse to continuous positive airway pressure (CPAP) treatment is highly variable and could be associat

196 fect of continuous positive airway pressure (CPAP) treatment on blood pressure in patients with resis

197 role of continuous positive airway pressure (CPAP) treatment on this association.

198 making, continuous positive airway pressure (CPAP) treatment or a healthy habit assessment, auto-CPAP

199 IV) and continuous positive airway pressure (CPAP) use in patients with OHS, information regarding ef

200 f nasal continuous positive airway pressure (CPAP) when used as postextubation support in neonates.

201 mine if continuous positive airway pressure (CPAP), a form of non-invasive ventilation, decreases all

202 nt with continuous positive airway pressure (CPAP), a weight-loss intervention, or CPAP plus a weight

203 OSA is continuous positive airway pressure (CPAP), but its value in patients without daytime sleepin

204 tion of continuous positive airway pressure (CPAP), which remains a primary therapeutic approach for

205 r nasal continuous positive airway pressure (CPAP)--at the time of the first use of noninvasive respi

206 rapy of continuous positive airway pressure (CPAP).

207 nt with continuous positive airway pressure (CPAP).

208 and Klebsiella OTUs) and need for prolonged CPAP oxygen signal increased risk of NEC in presymptomat

209 The microcephaly protein CPAP (also known as MCPH6) promotes procentriole growth,

210 centrosomal protein 4.1-associated protein (CPAP), achieved by its degradation at mitosis, is consid

211 Centrosomal protein 4.1-associated protein (CPAP), centrosomal protein of 152 kDa (CEP152), and cent

212 y in patients who did versus did not receive CPAP (18.1% vs. 22.1%; hazard ratio, 0.80; 95% confidenc

213 4 patients were randomly assigned to receive CPAP (n = 98) or no CPAP (control; n = 96).

214 Patients were allocated to receive CPAP treatment or no active intervention.

215 140 patients were allocated to and received CPAP plus BSC and 138 were allocated to and received BSC

216 ing below an altitude of 800 m and receiving CPAP therapy who underwent studies at a university hospi

217 changes were observed in the group receiving CPAP alone.

218 tervention group than in the group receiving CPAP only, but there were no significant differences in

219 at 12 weeks was lower in the group receiving CPAP than in the control group (-2.4 mm Hg; 95% confiden

220 igh-flow therapy failed could receive rescue CPAP; infants in whom CPAP failed were intubated and mec

221 the centrobin-depleted cells did not restore CPAP localization to the centrioles.

222 Restricting CPAP withdrawal to REM through real-time monitoring of t

223 cluding spindle assembly defective-4 (SAS4) (CPAP/CENPJ), is required for centriole biogenesis.

224 ous positive airway pressure for 30 seconds (CPAP-30); 2) stepwise airway pressure increase (5 cm H2O

225 In older people with OSA syndrome, CPAP reduces sleepiness and is marginally more cost effe

226 annulae are noninferior to or no better than CPAP when used to support preterm infants after extubati

227 he basis of these results, we recommend that CPAP treatment should be offered routinely to older pati

228 Here we show that CPAP levels and centriole elongation are regulated by ce

229 e OSA group, 0.93 (CI, 0.46 to 1.89) for the CPAP-treated group, and 1.38 (CI, 0.73 to 2.64) for the

230 group, and 0.91 (95% CI, 0.43-1.95) for the CPAP-treated group.

231 A group; and 0.19 (CI, 0.02 to 1.67) for the CPAP-treated, mild to moderate OSA group.

232 e OSA group; 0.55 (CI, 0.17 to 1.74) for the CPAP-treated, severe OSA group; 1.60 (CI, 0.52 to 4.90)

233 Compared with the control group, the CPAP group achieved a significantly greater improvement

234 ment occurred in 27.9% of the infants in the CPAP group (173 of 621 infants), versus 29.9% of those i

235 ower in the nasal-cannulae group than in the CPAP group (P=0.01), but there were no significant diffe

236 roup and in 38 of 286 infants (13.3%) in the CPAP group (risk difference, 12.3 percentage points; 95%

237 roup and in 39 of 151 infants (25.8%) in the CPAP group (risk difference, 8.4 percentage points; 95%

238 100 person-years (95% CI, 7.36-11.04) in the CPAP group and 11.02 per 100 person-years (95% CI, 8.96-

239 Final analysis included 1021 patients in the CPAP group and 1160 patients in the control group.

240 28 patients (3%) in the CPAP group and 24 patients (2%) in the control group had

241 not receive allocated treatment); 357 in the CPAP group and 366 in the control group were included in

242 , IL-6, and adiponectin also improved in the CPAP group compared with the control group after 6 month

243 at the 12-week follow-up was greater in the CPAP group than in the control group (35.9% vs 21.6%; ad

244 In the CPAP group there were 68 patients with new hypertension

245 , the odds ratio for 2-week mortality in the CPAP group versus the control group was 0.4 in children

246 important variables, 2-week mortality in the CPAP group versus the control group was significantly de

247 37 serious adverse events occurred in the CPAP group, and 22 in BSC group; all were independently

248 ortality was ten (3%) of 374 patients in the CPAP group, and 24 (7%) of 359 patients in the control g

249 r enrolment, 26 (3%) of 1021 patients in the CPAP group, and 44 (4%) of 1160 patients in the control

250 In the CPAP group, PaCO2 improvement was significantly differen

251 iod were compared between groups by ITT, the CPAP group achieved a greater decrease in 24-hour mean b

252 obin, but not its mutant form that lacks the CPAP binding site, could restore cellular CPAP levels in

253 After 6 months, the CPAP group achieved a greater decrease in HbA1c levels c

254 be performed examining the usefulness of the CPAP tracking systems and how these systems affect OSA o

255 Moreover, exogenous expression of the CPAP-binding fragment of centrobin also caused the disap

256 Nomenclature on the CPAP adherence tracking reports needs to be standardized

257 timescale, compared to either the WT or the CPAP mutant IkappaBalphas.

258 ts in human disease and also reveal that the CPAP-STIL interaction constitutes a conserved key step i

259 to the control group but not relative to the CPAP group.

260 ormally consolidated with use of therapeutic CPAP throughout, whereas on the other night, CPAP was re

261 Thus, CPAP treatment may be beneficial for metabolic risk redu

262 score <10) were randomized to auto-titrating CPAP (n = 122) or no positive airway pressure (n = 122).

263 d difficulty either accepting or adhering to CPAP therapy.

264 al and no significant harm was attributed to CPAP use.

265 site of microtubule nucleation and binds to CPAP for triplet microtubule formation [13, 14].

266 ntify patients who will respond favorably to CPAP treatment.

267 , 1.44-2.66), and among those nonadherent to CPAP therapy (1.78; 95% CI, 1.23-2.58), whereas the HR w

268 76-6.47) in patients with OSA nonadherent to CPAP therapy, and 3.06 (95% CI, 2.70-3.41) in patients w

269 qual to or exceeding 6.5% were randomized to CPAP (n = 26) or no CPAP (control; n = 24), while their

270 such a favorable blood pressure response to CPAP (area under the curve: 0.92; p = 0.01).

271 miRNAs predicts blood pressure responses to CPAP treatment in patients with RH and OSA.

272 les that predict blood pressure responses to CPAP treatment.

273 imilar amounts, although MAD was superior to CPAP for improving four general quality-of-life domains.

274 tracking systems are able to reliably track CPAP adherence.

275 me-independent accumulation of ubiquitinated CPAP and abnormal, ubiquitin-positive, elongated centrio

276 that centrobin interacts with ubiquitinated CPAP and prevents its degradation for normal centriole e

277 25590163

278 icantly in the 13 patients with OSA who used CPAP at least 4 hours per night.

279 diovascular risk reduction in those who used CPAP for >/=4 versus <4 hours per night or did not recei

280 24-hour BP measures except in patients using CPAP efficiently.

281 The percentage of patients using CPAP for 4 or more hours per day was 72.4%.

282 5 cm of water pressure was delivered via CPAP nasal prongs.

283 er on MAD (MAD, 6.50 +/- 1.3 h per night vs. CPAP, 5.20 +/- 2 h per night; P < 0.00001).

284 Secondary outcomes were changes in weight, CPAP adherence, and functional status.

285 "CPAP users" the remaining 30 patients were "CPAP nonusers." The recurrence of any atrial tachyarrhyt

286 While 32 patients were "CPAP users" the remaining 30 patients were "CPAP nonuser

287 d could receive rescue CPAP; infants in whom CPAP failed were intubated and mechanically ventilated.

288 fidence interval, 0.03-1.52]; P = 0.04) with CPAP as compared with placebo.

289 he treatment of obstructive sleep apnea with CPAP, but not nocturnal supplemental oxygen, resulted in

290 serum triglyceride levels when combined with CPAP.

291 inferior on treatment with MAD compared with CPAP (CPAP-MAD difference, 0.2 mm Hg [95% confidence int

292 gulated protein that directly interacts with CPAP and is required for centriole duplication.

293 alth-care costs were marginally reduced with CPAP (- pound35, -390 to 321; p=0.847).

294 and 24-hour blood pressure were reduced with CPAP as compared with placebo.

295 nce results improved more with NIV than with CPAP.

296 Severe OSA not treated with CPAP is associated with cardiovascular death in the elde

297 r in patients with OSA who were treated with CPAP therapy (0.71; 95% CI, 0.53-0.94).

298 ith untreated OSA, and in those treated with CPAP therapy according to national guidelines.

299 -3.41) in patients with OSA and treated with CPAP therapy.

300 nnulae failed were successfully treated with CPAP without reintubation.

301 In patients treated with CPAP, mean nocturnal oxygen saturation and baseline IL-1

302 mited value to OSA patients not treated with CPAP.

303 cident hypertension; however, treatment with CPAP therapy was associated with a lower risk of hyperte