ライフサイエンスコーパス: apnoea

1 rome, type 2 diabetes, and obstructive sleep apnoea.

2 ay motor disorders such as obstructive sleep apnoea.

3 death syndrome (SIDS) and obstructive sleep apnoea.

4 x evoked exaggerated increases in SNA during apnoea.

5 spiratory chemosensitivity and central sleep apnoea.

6 impaired in patients with obstructive sleep apnoea.

7 ertension in patients with obstructive sleep apnoea.

8 ry activity, with intense activation causing apnoea.

9 inical problem of cyclical obstructive sleep apnoea.

10 sm linking hypertension to obstructive sleep apnoea.

11 O2 -7 +/- 1 mmHg vs. baseline) occurred post-apnoea.

12 rostimulation in patients with central sleep apnoea.

13 r disease in patients with obstructive sleep apnoea.

14 seline blood pressure, and severity of sleep apnoea.

15 ising therapeutic approach for central sleep apnoea.

16 ast three breaths prior to each hypopnoea or apnoea.

17 th a prolonged reflexively evoked expiratory apnoea.

18 ory neurons were excited in REM sleep during apnoea.

19 ly used as a treatment for obstructive sleep apnoea.

20 be baroreflex mediated, and disappear during apnoea.

21 ypoxic response which we refer to as central apnoea.

22 cardiopulmonary instability caused by sleep apnoea.

23 s not influenced significantly by hypocapnic apnoea.

24 ated startle reflexes, muscle hypertonia and apnoea.

25 /=45%) treated for predominant central sleep apnoea.

26 ia and hypercapnia associated with prolonged apnoea.

27 severe hypoxaemia associated with prolonged apnoea.

28 oxygen deprivation associated with prolonged apnoea.

29 developed specifically for obstructive sleep apnoea.

30 ertension, angina, MI, and obstructive sleep apnoea.

31 ormal sleep behaviours and obstructive sleep apnoea.

32 tion also results in unstable breathing with apnoeas.

33 e markedly reduced the occurrence of central apnoeas.

34 28 (95% CI 0.10-0.74); and obstructive sleep apnoea, 0.55 (95% CI 0.40-0.87).

35 ubjects performing repetitive end-expiratory apnoeas (20 s) every minute for 30 min during intermitte

36 a-MeATP were: bradycardia 14.6 +/- 3.8 nmol; apnoea 47.1 +/- 8.5 nmol; hyperventilation 23.3 +/- 6.0

37 1 mmHg-1), or the CFV responses to voluntary apnoea (+51 +/- 19 vs. +50 +/- 18 %).

38 mittent hypoxia (CIH) is a hallmark of sleep apnoea, a condition associated with diverse clinical dis

39 Obstructive sleep apnoea, a syndrome that leads to recurrent intermittent

40 The assessment of how obstructive sleep apnoea affects cognition depends on the specificity and

41 and hypercapnia, it is unknown if repetitive apnoeas also elicit LTF.

42 d by approximately 29% at the termination of apnoea, although there was no change in the non-oxidativ

43 sorders, including cerebral ischaemia, sleep apnoea, Alzheimer's disease, multiple sclerosis, amyotro

44 bited hypertension, irregular breathing with apnoeas, an augmented CB chemosensory reflex as indicate

45 Thirteen participants with sleep apnoea and 13 controls completed two trials.

46 CBD) chemoreceptors would reduce SNA, reduce apnoea and arrhythmia incidence and improve ventricular

47 bited hypertension, irregular breathing with apnoea and augmented the CB chemosensory reflex, with al

48 Typically, postictal apnoea and bradycardia progress to asystole and death.

49 a consequence of increased obstructive sleep apnoea and cardiovascular disease.

50 as many undesirable side effects (sedation, apnoea and dependence) by binding to and activating the

51 hypoxia (CIH) occurs in patients with sleep apnoea and has adverse effects on multiple physiological

52 g. essential hypertension, obstructive sleep apnoea and heart failure.

53 in both adults and children during untreated apnoea and hypopnoea, along with changes in cerebral blo

54 of RTN neurons probably underlies the sleep apnoea and lack of chemoreflex that characterize congeni

55 inspiration after swallow, prolonged swallow apnoea and multiple swallows per bolus.

56 ut the association between obstructive sleep apnoea and myocardial infarction, stroke, and congestive

57 The prevalence of central apnoea and periodic breathing is increased in the elderl

58 fic physiological sleep disorders--eg, sleep apnoea and periodic limb movement disorder--are essentia

59 lmonary C fibre receptor stimulation elicits apnoea and rapid shallow breathing, but the effects on t

60 ically during cardiopulmonary C fibre-evoked apnoea and rapid shallow breathing, displaying increased

61 ring cardiopulmonary C fibre receptor-evoked apnoea and rapid shallow breathing.

62 on the association between obstructive sleep apnoea and stroke reviewing both the epidemiological dat

63 of the association between obstructive sleep apnoea and the brain.

64 region of the pons reduced the incidence of apnoea and the respiratory irregularity of Rett female m

65 Obstructive sleep apnoea and type 2 diabetes are common medical disorders

66 receptors in the nasal mucosa caused reflex apnoea and vasoconstriction in muscle.

67 T respiratory phenotype of recurrent central apnoeas and prolonged post-inspiratory activity.

68 n premature infants who suffer from frequent apnoeas and respiratory depression.

69 Central apnoeas and respiratory irregularity are a common featur

70 n (MI), stroke, fractures, obstructive sleep apnoea, and cancer; mortality; and resolution of hyperte

71 aroreflex mediated, that they persist during apnoea, and that autonomic responses to apnoea result fr

72 enotypes including ptosis, obstructive sleep apnoea, and the occurrence of seizures.

73 usual breathing frequencies disappear during apnoea, and thus cannot provide evidence for the existen

74 Features include snoring, witnessed apnoeas, and sleepiness.

75 elated disorders including obstructive sleep apnoea (apnea), REM sleep behaviour disorder (RBD) and n

76 CIH and sleep apnoea are characterized by increased reactive oxygen sp

77 uggest that responses of healthy subjects to apnoea are driven importantly, and possibly prepotently,

78 Although repetitive apnoeas are a frequent natural occurrence producing brie

79 reatening breathing irregularity and central apnoeas are highly prevalent in children suffering from

80 REM sleep could explain why certain central apnoeas are less frequent during this sleep stage.

81 esis that repeated, brief ventilator-induced apnoeas are sufficient to induce serotonin-dependent phr

82 activity should emerge out of the background apnoea as a manifestation of the drive.

83 vements and behaviours and obstructive sleep apnoea, as confirmed by polysomnography.

84 e study cohort was an episode of significant apnoea at presentation, found to have been recorded in 7

85 ss, startles and stumbles' of hyperekplexia, apnoea attacks (50 of 89) and delayed development (47 of

86 c outcomes for affected cases such as severe apnoea attacks, learning difficulties and developmental

87 O2 ) will be reduced near the termination of apnoea, attributed in part to the hypercapnia.

88 of the phrenic motor nucleus prior to neural apnoea blocked long-lasting iPMF (2 +/- 8% baseline; P >

89 nary chemoreflex responses, characterized by apnoea, bradycardia and hypotension.

90 in the cerebral metabolic reduction near the apnoea breakpoint.

91 rtly explain the reduction in CMRO2 near the apnoea breakpoint.

92 sleep apnoea than those who had less severe apnoea, but was independent of the baseline blood pressu

93 CFV increased during apnoeas (by 42 +/- 3 %) and decreased below baseline (by

94 Obstructive sleep apnoea can be diagnosed on the basis of characteristic h

95 agmatic activity emerged out of a background apnoea caused by mechanical hyperventilation an average

96 t study, endogenous drive was studied during apnoea caused by mechanical hyperventilation.

97 Obstructive sleep apnoea causes sleepiness, road traffic accidents, and pr

98 iciency in diverse conditions, such as sleep apnoea, cervical spinal injury or amyotrophic lateral sc

99 1, Cohen's d = 1.18) near the termination of apnoea compared to baseline, although non-oxidative meta

100 l of therapeutic NCPAP for obstructive sleep apnoea compared with a control group on subtherapeutic N

101 ontrolled and random frequency breathing and apnoea, conceived to perturb their autonomic function an

102 ses, such as sleep-disordered breathing with apnoea, congestive heart failure and essential hypertens

103 rain hypoperfusion such as obstructive sleep apnoea, congestive heart failure, cardiac arrhythmias, a

104 The subjects' responses to apnoea could not be attributed to changes of central che

105 ived normal subjects and patients with sleep apnoea could react differently.

106 bnormalities in those with obstructive sleep apnoea could reduce cardiovascular disease risk and impr

107 e discussed, management of obstructive sleep apnoea could soon transition from a so-called one size f

108 The post-apnoea decrease in CFV did not occur when hyperventilati

109 Men with obstructive sleep apnoea, defined as an Epworth sleepiness score of 10 or

110 f oxyhaemoglobin desaturation caused by 20 s apnoea did not affect CFV.

111 Dips suggestive of obstructive sleep apnoea did not predict CNS events, and adenotonsillectom

112 Fourteen elite apnoea-divers performed a maximal apnoea (range 3 min 36

113 In addition to altering baseline V(I) and apnoea duration, DNE is associated with subtle but signi

114 In six subjects who demonstrated spontaneous apnoeas during sleep, apnoea per se did not alter burst

115 decreased the number of sighs and post-sigh apnoeas during wakefulness in both the light and the dar

116 Thus, brief ventilator apnoeas elicit phrenic and XII LTF.

117 d pressure in 118 men with obstructive sleep apnoea (Epworth score > 9, and a > 4% oxygen desaturatio

118 carotid bodies were made during a period of apnoea evoked reflexly by electrical stimulation of both

119 Patients with obstructive sleep apnoea experience chronic intermittent hypoxia-hypercapn

120 iated with an abnormal pattern (i.e. swallow apnoeas followed by inspiration) and to clarify whether

121 If the latter, any apnoea following ablation of the pre-Botzinger complex m

122 ted pathologies, including obstructive sleep apnoea, heart failure and diabetes.

123 d below baseline (by 20 +/- 2 %) during post-apnoea hyperventilation.

124 the P(CO2) required to produce hypopnoea or apnoea (hypopnoea/apnoeic threshold) in sleeping humans.

125 iable adjustment, the upper quartile for the apnoea-hypopnoea index (>20.6 events per h) was associat

126 (11 men, 11 women) with OSA (mean +/-s.e.m., apnoea-hypopnoea index (AHI) 48.9 +/- 5.9 events h(-1))

127 Oscillatory breathing was quantified as the apnoea-hypopnoea index (AHI) and respiratory rate variab

128 Eligible patients with an apnoea-hypopnoea index (AHI) of at least 20 events per h

129 The apnoea-hypopnoea index (AHI)was assessed on separate nig

130 The median apnoea-hypopnoea index was 6.9 events per h (IQR 2.7-14.

131 coefficient of variation of tidal volume and apnoea-hypopnoea index were increased in CHF-sham animal

132 ured by plethysmography and quantified by an apnoea-hypopnoea index, respiratory rate variability ind

133 sleep-disordered breathing, assessed by the apnoea-hypopnoea index.

134 d SNP were significantly correlated with the apnoea/hypopnoea index (AHI) (P = 0.035, 0.042 and 0.026

135 Obstructive sleep apnoea/hypopnoea syndrome, depression and anxiety were i

136 5% (13/53); five of these patients had sleep apnoea/hypopnoea syndrome, six had depression and five a

137 ively] a marked increase in the incidence of apnoeas/hypopnoeas (20.2 +/- 4.0 vs. 9.7 +/- 2.6 events

138 observed in patients with obstructive sleep apnoea (i.e. reflex compensation for an anatomically sma

139 ) not influenced significantly by hypocapnic apnoea, (ii) decreased by hyperthermia, which increased

140 on of Piezo2(+) vagal sensory neurons causes apnoea in adult mice.

141 of perinatal mortality in infants and sleep apnoea in adults, but the mechanisms of respiratory cont

142 ce of OSA and the emergence of central sleep apnoea in conditions such as high altitude.

143 Prolonged apnoea in humans is reflected in progressive hypoxaemia

144 The swallow apnoea in patients with brain, spinal cord and periphera

145 Early identification of obstructive sleep apnoea in patients with metabolic dysfunction, including

146 flex comprising bradycardia, hypotension and apnoea in rats anaesthetized with pentobarbitone.

147 the abdominal muscles during opioid-induced apnoea in the newborn rat.

148 spiratory chemosensitivity and central sleep apnoea in this disorder.

149 cause of central (and possibly obstructive) apnoeas in this population.

150 by administration of opioids (opioid-induced apnoea) in neonatal rats, abdominal muscles continue to

151 cantly reduced the severity of central sleep apnoea, including improvements in sleep metrics, and was

152 Three and six ventilator apnoeas induced phrenic and XII LTF with a magnitude sim

153 Both apnoea-induced and AIH-induced LTF were associated with

154 ep disruption (i.e. spontaneous arousals and apnoea-induced arousals) on this temporal relationship a

155 8 vs. 1.342 +/- 0.026 s); however, following apnoea-induced EEG perturbations, burst latencies were r

156 We conclude that apnoea-induced fluctuations in CFV were caused primarily

157 Hyperoxia also had no effect on the apnoea-induced increase in CFV (40 +/- 4 %).

158 played a smaller but significant role in the apnoea-induced increase in CFV; however, negative intrat

159 ockade, which abolished the increase in MAP, apnoea-induced increases in CFV were partially attenuate

160 de, a serotonin receptor antagonist, blocked apnoea-induced LTF but not changes in the CO(2)-recruitm

161 Similar to AIH-induced LTF, apnoea-induced LTF is serotonin dependent, and the relev

162 Apnoea-induced LTF may have implications for the mainten

163 Apnoea-induced LTF may preserve upper airway patency dur

164 It seems likely that post-swallowing apnoea inspiration is a non-specific concomitant of diso

165 orticobulbar involvement tended to have post-apnoea inspiration more often than those without.

166 Obstructive sleep apnoea is a common disease that is now more widely recog

167 Obstructive sleep apnoea is a disease of increasing importance because of

168 is convincing evidence to believe that sleep apnoea is a modifiable risk factor for stroke; however,

169 Central sleep apnoea is a serious breathing disorder associated with p

170 Obstructive sleep apnoea is an increasingly common disorder of repeated up

171 Obstructive sleep apnoea is associated with raised blood pressure.

172 A co-morbidity of sleep apnoea is hypertension associated with elevated sympathe

173 ypocapnia-induced apnoeic threshold, whereby apnoea is initiated by small transient reductions in art

174 rol and thus could explain why central sleep apnoea is less frequent in REM sleep.

175 analgesia, but maternal desaturation or even apnoea is more likely.

176 ry sleep disorders such as obstructive sleep apnoea may worsen epilepsy and treatment of these sleep

177 eceptor afferents terminate produced central apnoea, mimicking the effect of lung inflation.

178 In patients with most severe sleep apnoea, nCPAP reduces blood pressure, providing signific

179 pnoea (failure to trigger the ventilator) or apnoea (no breathing effort) occurred.

180 Mixed or obstructive apnoeas occurred with 9% of these seizures.

181 iratory depression are implicated, including apnoea of prematurity, sleep disordered breathing and co

182 ore than 4% SaO2 caused by obstructive sleep apnoea on overnight sleep study, were randomly assigned

183 3 months typically present with a history of apnoea or other breathing abnormalities, show axonal dam

184 Eaug and I neuronal activity coincident with apnoea or rapid shallow breathing.

185 Central apnoeas or hypopnoeas occurred with 50% of 100 seizures.

186 ut central adverse effects such as sedation, apnoea, or addiction.

187 Obstructive sleep apnoea (OSA) and type 2 diabetes frequently co-exist and

188 f elderly individuals with obstructive sleep apnoea (OSA) for comparison (n = 3, age 68 +/- 1 years,

189 A and vLTF are enhanced in obstructive sleep apnoea (OSA) participants compared to matched healthy co

190 AP) for moderate to severe obstructive sleep apnoea (OSA) syndrome have been established in middle-ag

191 saturation profiles during obstructive sleep apnoea (OSA), have been shown to exhibit a heightened ca

192 saturation profiles during obstructive sleep apnoea (OSA), have been shown to exhibit a heightened ca

193 (SF), a primary feature of obstructive sleep apnoea (OSA), impairs hippocampal long-term potentiation

194 Obstructive sleep apnoea (OSA), which is characterized by periodic inspira

195 gain (LG) in patients with obstructive sleep apnoea (OSA), yet its effects on the other traits respon

196 atively high prevalence of obstructive sleep apnoea (OSA).

197 to sleep in patients with obstructive sleep apnoea (OSA).

198 atively high prevalence of obstructive sleep apnoea (OSA).

199 acetazolamide may improve obstructive sleep apnoea (OSA).However, how acetazolamide affects the key

200 yed recovery of eupnoea from hypoxic-induced apnoea (P < 0.001).

201 crement in muscle activity is greater in the apnoea patient than in healthy controls.

202 sleep onset, and the decrement is greater in apnoea patients than in healthy controls.

203 monstrated spontaneous apnoeas during sleep, apnoea per se did not alter burst latency relative to sl

204 rogression of, obstructive and central sleep apnoea, possibly through the development of peripheral n

205 Further, we found that, during central apnoeas, post-inspiratory drive (adductor motor) to the

206 This apnoea prevented any effects of changes in respiration o

207 mental component summary (MCS) and the sleep apnoea quality-of-life index symptoms domain (sym).

208 teen elite apnoea-divers performed a maximal apnoea (range 3 min 36 s to 7 min 26 s) under dry labora

209 idative metabolism in man during a prolonged apnoea (ranging from 3 min 36 s to 7 min 26 s) that gene

210 In the post-apnoea recovery period, CFV returned to baseline in 45 +

211 Our aim was to see whether nCPAP for sleep apnoea reduces blood pressure compared with the most rob

212 he treatment of choice for obstructive sleep apnoea, reduces sleepiness and improves hypertension.

213 Apnoea responses of healthy subjects may result from cha

214 ring apnoea, and that autonomic responses to apnoea result from changes of chemoreceptor, barorecepto

215 at short-term exposure to repetitive hypoxic apnoeas (RHA) produces prolonged impairment in barorefle

216 more likely to have had recurrent infantile apnoeas (RR1.9; P < 0.005) than those with GLRA1 mutatio

217 Apnoea sets in motion a continuous and ever changing reo

218 ntation in 'tonic input.' Contrariwise, this apnoea should be permanent if the neuronal activities of

219 ography showed features of obstructive sleep apnoea, stridor, and abnormal sleep architecture (undiff

220 in the pathophysiology of obstructive sleep apnoea syndrome (OSA).

221 in the pathophysiology of obstructive sleep apnoea syndrome (OSA).

222 tion of genetic factors to obstructive sleep apnoea syndrome (OSAS) has led to a better understanding

223 healthy humans and three patients with sleep apnoea syndrome during NREM sleep.

224 holic fatty liver disease, obstructive sleep apnoea syndrome, erectile dysfunction, periodontitis, in

225 ant in the pathogenesis of obstructive sleep apnoea syndrome.

226 During central apnoea, T-peak frequencies in RVCN autospectra were simi

227 At apnoea termination when the airway opens, we observed (1

228 the absence of brainstem function, including apnoea testing, would suffice.

229 as larger in patients with more severe sleep apnoea than those who had less severe apnoea, but was in

230 Under conditions of hyperoxic, hypocapnic apnoea, the mean threshold for inducing phrenic nerve ac

231 Similarly to the apnoea, there was no change in the non-oxidative metabol

232 Clinically the apnoea threshold appears important only because of its a

233 tors were high gain and high mean CO(2); the apnoea threshold did not independently influence system

234 Increasing the apnoea threshold F(ETCO(2)) from 0.02 to 0.03 had no eff

235 Second, high apnoea threshold itself does not create instability.

236 0.0001), irrespective of chemoreflex gain or apnoea threshold.

237 de range of values of steady state CO(2) and apnoea thresholds.

238 two decades indicates that obstructive sleep apnoea, through the effects of intermittent hypoxaemia a

239 huttle mission with controlled breathing and apnoea, to identify autonomic changes that might contrib

240 tilated rats were exposed to a 30 min neural apnoea; upon resumption of respiratory neural activity,

241 , gastroesophageal reflux, obstructive sleep apnoea, vocal cord dysfunction, obesity, dysfunctional b

242 Apnoea was commonly preceded by hyperventilation.

243 decrease in P(ET,CO2) required to induce an apnoea was greater after treatment with leuprolide (2.56

244 and on landing day, but their control during apnoea was sharply altered: astronauts increased their b

245 The ED50 for apnoea was significantly greater than that for bradycard

246 Intrathecal TNFalpha without neural apnoea was sufficient to elicit long-lasting phrenic mot

247 ratures, whereas the duration of spontaneous apnoeas was longer in DNE pups than in controls at 33 de

248 racterized by pontocerebellar hypoplasia and apnoea, we discovered a missense mutation and an exonic

249 hogenesis and treatment of obstructive sleep apnoea, we have developed a novel application of magneti

250 Additionally, augmented breaths followed by apnoea were recorded and were not usually associated wit

251 late both burst areas and frequencies during apnoea were sharply diminished.

252 Hypotension and apnoea were subject to desensitization, and ATP was abou

253 Hypopnoeas and apnoeas were induced in all subjects during both normoxi

254 creased, breathing patterns were normalized, apnoeas were reduced, body weight was increased to near

255 The number and duration of apnoeas were similar between control and treatment perio

256 mechanical ventilation resulted in a central apnoea which demarcated the threshold of the ventilatory

257 reathing, and normally the great majority of apnoeas which accompany a swallow are followed by expira

258 patients with stroke have concomitant sleep apnoea, which can affect recovery potential.

259 o this region could account for the observed apnoea, which could in turn lead to hypoxic damage and b

260 BQX) prior to administering AMPA resulted in apnoea, which was not overcome by the agonist.

261 uch mechanisms (as in the patient with sleep apnoea) will be prone to collapse during sleep.

262 E-HF) showed that treatment of central sleep apnoea with adaptive servoventilation in patients with h

263 were exposed to three or six 25 s ventilator apnoeas with 5 min intervals, and compared to time contr

264 nsights and discoveries in obstructive sleep apnoea, with a focus on diagnostics and therapeutics.