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 was ensured by continuous supervision.

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

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

6 CPAP is an important therapy in OSA patients undergoing

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

8 CPAP machines were allocated to one hospital during each

9 CPAP or no therapy while maintaining usual blood pressur

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

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

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

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

14 CPAP therapy was associated with improved renal hemodyna

15 CPAP tracking systems are able to reliably track CPAP ad

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

17 CPAP treatment is accompanied by changes in cardiovascul

18 CPAP usage can be reliably determined from CPAP tracking

19 CPAP was associated with modest improvement in sleep-rel

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

21 CPAP with surfactant but without any positive pressure v

22 CPAP-30 worsened markers of potential epithelial cell da

23 52 protein interacts with Sak/Plk4 and Sas-4/CPAP and is required for centriole duplication, although

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

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

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

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

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

29 Adequate CPAP treatment seems to reduce this risk.

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

31 tile range, -31.0 to -16.3; P < 0.001) after CPAP withdrawal.

32 come was the change in home morning BP after CPAP withdrawal for 14 nights, oxygen versus air.

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

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

35 oxygen virtually abolished the BP rise after CPAP withdrawal and, compared with air, significantly re

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

37 definitions of these parameters differ among CPAP manufacturers.

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

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

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

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

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

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

44 the effectiveness of three years of NIV and CPAP on structural and functional echocardiographic chan

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

46 NIV and CPAP therapies similarly improved left ventricular diast

47 NIV and CPAP were more effective than lifestyle modification in

48 condary effects were similar between NIV and CPAP.

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

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

51 es the stable incorporation of both STIL and CPAP into the centriole.

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

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

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

55 10 were diagnosed with OSA and classified as CPAP-treated (adherence >/= 4 h/d) or untreated (adheren

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

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

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

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

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

61 to determine the differential effect between CPAP and NIV.Measurements and Main Results: A total of 1

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

80 cells led to the reappearance of centriolar CPAP.

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

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

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

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

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

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

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

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

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

90 ly higher rate of treatment failure than did CPAP.

91 respiratory functional improvements than did CPAP.

92 ally abolished the rise in morning BP during CPAP withdrawal.

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

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

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

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

97 (1:1) into parallel groups to receive either CPAP with best supportive care (BSC) or BSC alone for 12

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

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

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

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

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

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

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

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

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

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

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

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

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

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

112 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

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

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

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

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

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

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

119 pport with nasal IPPV as compared with nasal CPAP.

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

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

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

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

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

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

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

127 6.5% were randomized to CPAP (n = 26) or no CPAP (control; n = 24), while their usual medication for

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

146 Genetic and chemical perturbation of CPAP-tubulin interaction activates extra centrosomes to

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

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

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

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

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

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

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

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

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

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

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

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

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

160 o treatment with either high-flow therapy or CPAP.

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

162 Screening for compounds that perturb CPAP-tubulin interaction led to the identification of CC

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

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

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

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

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

168 o nasal continuous positive airway pressure (CPAP) as a means of respiratory support for newborn infa

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

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

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

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

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

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

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

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

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

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

179 apeutic continuous positive airway pressure (CPAP) levels.

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

181 d using continuous positive airway pressure (CPAP) manipulations indicated that the hypnotic zolpidem

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

183 NIV) or continuous positive airway pressure (CPAP) on cardiac structure and function assessed by echo

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

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

186 AP), 3) continuous positive airway pressure (CPAP) rather than noninvasive ventilation be offered as

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

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

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

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

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

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

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

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

195 rant to continuous positive airway pressure (CPAP) treatment, submitted to DISE between June 1, 2013,

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

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

198 , after continuous positive airway pressure (CPAP) withdrawal in patients with moderate to severe OSA

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

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

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

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

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

204 rapy of continuous positive airway pressure (CPAP).

205 nt with continuous positive airway pressure (CPAP).

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

207 by interacting with the centrosomal protein CPAP, negatively regulates CPAP-dependent peri-centriola

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

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

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

211 whom high-flow therapy failed could receive CPAP.

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).

214 140 patients were allocated to and received CPAP plus BSC and 138 were allocated to and received BSC

215 changes were observed in the group receiving CPAP alone.

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

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

218 ntrosomal protein CPAP, negatively regulates CPAP-dependent peri-centriolar material recruitment, and

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

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

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

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

223 The Tetrahymena Sas4/CPAP protein is enriched at assembling BBs, localizing t

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 y higher incidence of treatment failure than CPAP when used in nontertiary special care nurseries as

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

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

230 ion of CCB02, which selectively binds at the CPAP binding site of tubulin.

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

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

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

234 roup and in 38 of 373 infants (10.2%) in the CPAP group (risk difference, 10.3 percentage points; 95%

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

236 group and in 27 of 338 infants (8.0%) in the CPAP group (risk difference, 6.5 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 Final analysis included 1021 patients in the CPAP group and 1160 patients in the control group.

239 28 patients (3%) in the CPAP group and 24 patients (2%) in the control group had

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

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

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

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

244 37 serious adverse events occurred in the CPAP group, and 22 in BSC group; all were independently

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

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

247 In the CPAP group, PaCO2 improvement was significantly differen

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

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

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

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

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

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

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

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

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

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

258 continuous positive airway pressure therapy (CPAP) but were dissatisfied with it (n = 56), were studi

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

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

261 d difficulty either accepting or adhering to CPAP therapy.

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

263 erved site, S428, to promote STIL binding to CPAP.

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

265 ntify patients who will respond favorably to CPAP treatment.

266 OSA patients intolerant to CPAP have a strong positive correlation between the FTP

267 w therapy was not shown to be noninferior to CPAP and resulted in a significantly higher incidence of

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

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

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

271 les that predict blood pressure responses to CPAP treatment.

272 tion of S428 promotes the binding of STIL to CPAP, linking the cartwheel to microtubules of the centr

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

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

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

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

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

289 serum triglyceride levels when combined with CPAP.

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

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

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

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

294 nce results improved more with NIV than with CPAP.

295 atients were analyzed: 102 were treated with CPAP and 94 were treated with NIV.

296 nnulae failed were successfully treated with CPAP without reintubation.

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

298 mited value to OSA patients not treated with CPAP.

299 e to 35.3 +/- 1.33 mm Hg at three years with CPAP, and from 41.5 +/- 1.56 mm Hg to 35.5 +/- 1.42 with

300 se breathing and reduce OSA severity without CPAP.