ライフサイエンスコーパス: sleeping

1 infants devote the majority of their time to sleeping.

2 e time with screens than any activity except sleeping.

3 ng from playing sports, to driving, and even sleeping.

4 SPW-R was more pronounced during waking than sleeping.

5 r in the brain waves that occur while we are sleeping.

6 allowing (2.1, 1.1-3.9; p=0.017), difficulty sleeping (1.9, 1.3-2.8; p=0.001), arthralgias (2.0, 1.1-

7 expected left) in a small sample (n = 12) of sleeping 2-3 year olds with autism in contrast to typica

8 Telomeres were on average 6% shorter in men sleeping 5 hours or fewer compared with those sleeping m

9 On average, those who reported sleeping 6 or fewer hours per night had an increased ris

10 uring the day (when the animals are normally sleeping) accompanied by shorter periods of rest.

11 Waking and sleeping also affected lower- and higher-firing neurons

12 In the nighttime sleeping analysis, a clear U-shaped association with Par

13 illations were once thought to only occur in sleeping and anesthetized states.

14 Infants spend most of their time sleeping and are likely to be exposed to elevated concen

15 s with KCN should inquire about breathing or sleeping and, when appropriate, refer patients for evalu

16 tial (LFP) recordings on flies spontaneously sleeping, and compare their brain activity to flies indu

17 t consolidation occurs in both the awake and sleeping animal.

18 Sleeping animals do not move or feed and are less respon

19 the new design, especially the second-storey sleeping area because of the privacy and security of ups

20 choretic insect that hides within its host's sleeping area manages to travel long distances is not ye

21 t time, how leaving worn clothing exposed in sleeping areas when travelling can be exploited by bed b

22 intense physical labour and less comfortable sleeping arrangements.

23 Sleeping at least 9 hours per 24-hour period was reporte

24 Chronically eating and sleeping at unusual circadian times may create a health

25 incidence of botulism in shoreline birds at Sleeping Bear Dunes National Lakeshore (SLBE) in Lake Mi

26 ation operatorOPE) ranged from 93 pg/m(3) at Sleeping Bear Dunes to 1046 pg/m(3) at Chicago.

27 bling times of 5-10 years at Sturgeon Point, Sleeping Bear Dunes, and Eagle Harbor, but these concent

28 while remote areas, such as Eagle Harbor and Sleeping Bear Dunes, exhibited the lowest levels (0.050-

29 ased sequencing and bioinformatics pipeline, Sleeping Beauty (SB) capture hybridization sequencing (S

30 son mutagenesis strategy based on a two-step Sleeping Beauty (SB) forward genetic screen to identify

31 We have conducted a mutagenic screen using Sleeping Beauty (SB) in mice to identify new candidate c

32 A Sleeping Beauty (SB) in science refers to a paper whose

33 ystem actively suppresses tumorigenesis in a Sleeping Beauty (SB) mouse model of cancer.

34 e have advanced DNA vectors derived from the Sleeping Beauty (SB) system to avoid the expense and man

35 The Sleeping Beauty (SB) transposon mutagenesis screen is a

36 ectal cancer (CRC) progression, we performed Sleeping Beauty (SB) transposon mutagenesis screens in m

37 The Sleeping Beauty (SB) transposon mutagenesis system is a

38 We used Sleeping Beauty (SB) transposon mutagenesis to identify

39 driving leukemia, we targeted cre-dependent Sleeping Beauty (SB) transposon mutagenesis to the blood

40 Over the past decade, the Sleeping Beauty (SB) transposon system has been develope

41 The Sleeping Beauty (SB) transposon system has been used as

42 In this study we utilized the non-viral Sleeping Beauty (SB) transposon system using the SB100X

43 The Sleeping Beauty (SB) transposon system was used to eluci

44 n efficient non-viral approach combining the Sleeping Beauty (SB) Transposon System with selective pr

45 ed transgene expression in pigs by using the Sleeping Beauty (SB) transposon system.

46 transgene expression in rabbits by using the Sleeping Beauty (SB) transposon system.

47 The latest generation of Sleeping Beauty (SB) transposon vectors fulfills these r

48 a development and metastasis, we performed a Sleeping Beauty (SB) transposon-based forward genetic sc

49 ic drivers of MPNST development, we used the Sleeping Beauty (SB) transposon-based somatic mutagenesi

50 Here we use Sleeping Beauty (SB) transposon-mediated insertional mut

51 Here we show that Sleeping Beauty (SB) transposon-mediated mutagenesis dri

52 ying a mutant allele of Apc (Apc(Min)) using Sleeping Beauty (SB) transposon-mediated mutagenesis.

53 lls that were genetically modified using the Sleeping Beauty (SB) transposon/transposase system to ex

54 ite profiling of the piggyBac (PB), Tol2 and Sleeping Beauty (SB) transposons and the murine leukemia

55 IDO expression, through a human IDO-encoding Sleeping Beauty (SB)-based nonviral gene-integrating app

56 Forward genetic screens using Sleeping Beauty (SB)-mobilized T2/Onc transposons have b

57 eted copies in the IR/DR subgroup, including Sleeping Beauty (SB).

58 The germline transposition frequency for Sleeping Beauty and piggyBac was approximately 10% or ab

59 ON) and compare them with the preferences of Sleeping Beauty and piggyBac, showing that each superfam

60 were obtained by non-viral gene transfer of Sleeping Beauty DNA plasmids and selectively expanded ex

61 lated when delivered into the genome via the Sleeping Beauty DNA transposon, suggesting that the obse

62 tract cancer susceptibility gene in multiple Sleeping Beauty DNA transposon-based forward genetic scr

63 gene for colorectal cancer (CRC) in several Sleeping Beauty DNA transposon-based forward genetic scr

64 PiggyBac and Sleeping Beauty have different integration preferences.

65 ose loss accelerates tumorigenesis following Sleeping Beauty insertional mutagenesis in a mouse model

66 Sleeping Beauty insertional mutagenesis in this model le

67 A forward genetic screen utilizing Sleeping Beauty mutagenesis in mice previously identifie

68 ells with preserved TSCM potential using the Sleeping Beauty platform.

69 T cells genetically modified with the Sleeping Beauty system to express D-CAR stably were prop

70 We used electrotransfer of Sleeping Beauty system to introduce a CAR transposon and

71 ly modified T cells were generated using the Sleeping Beauty system to stably introduce the CD19-spec

72 PiggyBac or Sleeping Beauty transposase bigenic rats bred with wild-

73 d to ubiquitously express either piggyBac or Sleeping Beauty transposase were generated by standard z

74 locus to coexpress the Etv6-RUNX1 fusion and Sleeping Beauty transposase.

75 retrotransposition but were inactive against Sleeping Beauty transposition and long interspersed nucl

76 Sleeping Beauty transposon (SB-Tn) has emerged as an imp

77 5 (Stat5b-CA) with mice in which a mutagenic Sleeping Beauty transposon (T2/Onc) was mobilized only i

78 tercrossing these mice with those carrying a Sleeping Beauty transposon array.

79 Using the Sleeping Beauty transposon as a delivery system, we intr

80 For example, the Sleeping Beauty transposon has become highly instrumenta

81 Mobilizing the Sleeping Beauty transposon in cerebellar neural progenit

82 ectly tested this hypothesis by performing a Sleeping Beauty transposon mutagenesis screen in which c

83 We used it to perform a Sleeping Beauty transposon mutagenesis screen to identif

84 A new study uses Sleeping Beauty transposon mutagenesis to drive osteosar

85 An unbiased Sleeping Beauty transposon screen revealed MyoD as a put

86 ophic induced pluripotent stem cells using a Sleeping Beauty transposon system carrying the micro-utr

87 performed insertional mutagenesis using the Sleeping Beauty transposon system in mice carrying germl

88 an insertional mutagenesis screen using the Sleeping Beauty transposon system in mice with mammary-s

89 Recently in Nature, Sun et al. (2014) used a sleeping beauty transposon system to demonstrate that na

90 models, the mouse and the rat, by using the Sleeping Beauty transposon system.

91 were hydrodynamically codelivered using the Sleeping Beauty transposon to initiate liver tumorigenes

92 d mobilization of a single-copy inactivating Sleeping Beauty transposon to Pten disruption within the

93 in the biliary tract was accomplished by the Sleeping Beauty transposon transfection system with tran

94 Exploiting the local hopping activity of the Sleeping Beauty transposon, the lacZ reporter gene was d

95 We identified such mutations using a Sleeping Beauty transposon, which caused rapid-onset AML

96 A hybrid piggyBac/Sleeping Beauty transposon-based insertional mutagenesis

97 In this study, we conducted a Sleeping Beauty transposon-mediated insertional mutagene

98 Using a novel tyrosinase minigene-tagged Sleeping Beauty transposon-mediated mutagenesis, which a

99 formed genetic screen in Emu-TCL1 mice using Sleeping Beauty transposon-mediated mutagenesis.

100 in cultured human PAX7+ satellite cells with Sleeping Beauty transposon-mediated nonviral gene transf

101 y integrated throughout the genome using the Sleeping Beauty transposon.

102 Kras was expressed in p53fl/fl mice using a sleeping beauty transposon.

103 approach using ex vivo mutagenesis with the Sleeping Beauty transposon.

104 ession of hMet and mutant-beta-catenin using sleeping beauty transposon/transposase leads to hepatoce

105 essing mice and forward genetic screens with Sleeping Beauty transposons implicate additional signali

106 Mobilization of Sleeping Beauty transposons in NSCs induced the immortal

107 ion elements, which were further deployed by Sleeping Beauty transposons throughout the genome of hum

108 These results support the use of Sleeping Beauty vectors in carrying an insulated IHK-bet

109 ome-wide analysis of 23,417 piggyBac, 30,303 Sleeping Beauty, and 27,985 TcBuster integrations in HEK

110 le with two transposon systems, PiggyBac and Sleeping Beauty, and give guidance on the use of differe

111 alterations of human ICC, we electroporated Sleeping Beauty-based oncogenic transposon plasmids into

112 y hydrodynamic injection in combination with Sleeping Beauty-mediated somatic integration.

113 ve been associated with infants' feeding and sleeping behavior.

114 , attractiveness to mosquitoes, and modified sleeping behaviour.

115 rons to the presentation of song variants in sleeping birds, and by examining HVC activity in singing

116 There is a complex relation between the sleeping brain and its waking function.

117 The sleeping brain exhibits characteristic slow-wave activit

118 However, recent research has shown that the sleeping brain is not completely disconnected from its e

119 But how does the sleeping brain know which information to preserve and wh

120 This result shows that the sleeping brain's spontaneous activity heralds individual

121 a flexible and task-dependent manner by the sleeping brain, all the way up to the preparation of rel

122 hatic function is primarily a feature of the sleeping brain, rather than the waking brain, and is slo

123 The characteristic oscillations of the sleeping brain, spindles and slow waves, show trait-like

124 responses triggered by spoken stimuli in the sleeping brain.

125 an transiently "wake up" [8] in an otherwise sleeping brain.

126 their large-scale coherence in the awake and sleeping brain.

127 a common feature of both the waking and the sleeping brain.

128 s it continue to unfold automatically in the sleeping brain?

129 d by the number of individuals that shared a sleeping burrow.

130 aging in close-to-perfect conditions, these sleeping champagne bottles awoke to tell us a chapter of

131 adiposity measures is exacerbated by adverse sleeping characteristics.

132 in the primary auditory cortex of naturally sleeping common marmosets, we show that slow-wave sleep

133 f age, warm season, male gender, and crowded sleeping conditions.

134 homeostatic adjustment is disrupted in short-sleeping cv-c mutants.

135 ts and anxiety phenotype, without detectable sleeping disorders.

136 rther control for health status or nighttime sleeping duration attenuated the association for establi

137 n that daytime sleepiness, but not nighttime sleeping duration, is one of the early nonmotor symptoms

138 thors examined daytime napping and nighttime sleeping durations, reported in 1996-1997 by 220,934 US

139 ambers to measure changes in EE (EEchamber), sleeping EE (SEE), and RQ.

140 Twenty-four-hour EE (24EE) and sleeping EE (SleepEE) were measured on days 1, 14, and 5

141 expenditure (p = 2.7E-08) and in CHRNA3 for sleeping energy expenditure (p = 6.0E-08).

142 nt stimuli are larger in awake flies than in sleeping flies.

143 hereas regular physical activity and healthy sleeping habits help prevent it.

144 sed 2 additional contacts for guidance about sleeping habits.

145 rt system administered questions on life and sleeping habits; health; and sleep, mental, and organic

146 esting (P = 0.001), stressed (P = 0.037) and sleeping heart rate (P = 0.038) were increased compared

147 rt devices were fitted for 7 days to measure sleeping heart rate, activity levels, and resting, activ

148 eviant external stimuli detected by the less-sleeping hemisphere caused more arousals and faster beha

149 me in bed during weekdays, and later weekend sleeping hours correlate with smaller brain grey matter

150 Bed bugs are attracted to the odour of sleeping humans and we suggest that soiled clothing may

151 ative upper airway hydraulic diameter (D) in sleeping humans with narrowed upper airways.

152 n in vitro model and in the upper airways of sleeping humans.

153 se pharyngeal hypotonia pharmacologically in sleeping humans.

154 Sleeping in a 30 degrees head-up position leads to IOP l

155 le, which has similarities to flying west or sleeping in the daytime after night shifts.

156 It now appears that humans sleeping in unfamiliar environments do something quite s

157 in one hundred sixty-two 2- to 25-month-old sleeping infants (60 epsilon4 carriers and 102 noncarrie

158 s in a cohort of obese individuals reporting sleeping less than 6.5 hours per night.

159 uction of solid foods), and early childhood (sleeping <12 h/d, presence of a television set in the

160 egulation and control found in bihemispheric sleeping mammals and the harbor porpoise were present in

161 egulation and control found in bihemispheric sleeping mammals were present in the harbor porpoise, wi

162 igher than other large-brained bihemispheric sleeping mammals.

163 er than in other large-brained bihemispheric sleeping mammals.

164 roup reported less interference from pain in sleeping (mean difference -0.9 points, 95% CI -1.63 to -

165 rapid eye movement sleep (P < 0.001) and the sleeping metabolic rate (P = 0.02), increased glucose (P

166 nergy expenditure expressed as a multiple of sleeping metabolic rate (PALSMR) and resting metabolic r

167 stage for the whole night and separately for sleeping metabolic rate (SMR; ie, 3-h period during the

168 Local cortical activity of sleeping mice could be readily converted to the stereoty

169 cooling of lightly anesthetized or naturally sleeping mice disrupts thalamocortical slow oscillation

170 k for crash compared with those who reported sleeping more than 6 hours (relative risk [RR], 1.21; 95

171 leeping 5 hours or fewer compared with those sleeping more than 7 hours per night.

172 ns of intensified spindling in the naturally sleeping mouse.

173 as protein levels are up-regulated in short-sleeping mutants and also in wild type animals following

174 emically mutagenized flies to identify short-sleeping mutants and found one, redeye (rye) that shows

175 We found that chimpanzees left their sleeping nests earlier (often before sunrise when the fo

176 Moreover, the females positioned their sleeping nests more in the direction of the next day's b

177 Sleeping newborns rapidly learned the predictive relatio

178 or only 0.69 h d(-1) (7.4% of the time spent sleeping on land), indicating that ecological demands fo

179 l venous pressure or ocular compression from sleeping on the surgical side, followed by sudden decomp

180 ation sessions did not prevent patients from sleeping; on the contrary, they seem to aid sleep when c

181 ce an exogenous stressor, such as prone/side sleeping or soft bedding, during a critical developmenta

182 For instance, sleeping participants can create novel sensory associati

183 The unique sleeping pattern of fur seals allows us to distinguish n

184 roves after interventions restoring a normal sleeping pattern.

185 and ambient temperature on human resting or sleeping patterns using mobile phone data of a large num

186 Behavioral arousal in the sleeping period phase shifts the master clock in the sup

187 by sleep deprivation or caffeine during the sleeping period potentiates light resetting of the maste

188 nt number of occasions during the resting or sleeping period preceding the experience.

189 contribute to hippocampal plasticity during sleeping period.

190 induces NPC proliferation in both active and sleeping phases of the mice.

191 , a kinase partner of CycA, rescue the short-sleeping phenotype of tara and CycA mutants, while incre

192 brain injury when they are treated with the sleeping pill zolpidem.

193 idem (Ambien) is the most widely prescribed "sleeping pill." It makes the inhibitory neurotransmitter

194 This knowledge could help in the design of sleeping pills that induce a more natural sleep.

195 position), which mimics the natural resting/sleeping position of rodents.

196 es, addition of hydrocortisone reduced total sleeping problems and disorders of initiating and mainta

197 blems, quality of life, parenting stress and sleeping problems were compared between groups.

198 e SCORAD), symptoms (POEM, VAS pruritus, VAS sleeping problems) and previous treatment of AD were ass

199 e for previous AD severity and/or associated sleeping problems.

200 cillations in the spindle range in naturally sleeping rodents.

201 re time in screen activities (RR = 0.98) and sleeping (RR = 0.96) had the lowest compliance.

202 Human African sleeping sickness (HAT) is caused by the parasitic proto

203 Trypanosoma brucei, the causative agent of sleeping sickness (Human African Trypanosomiasis, HAT),

204 orcement of surveillance, for the control of sleeping sickness (human African trypanosomiasis, HAT).

205 e Trypanosoma brucei, the causative agent of sleeping sickness across sub-Saharan Africa, depends on

206 Chagas disease, leishmaniasis and sleeping sickness affect 20 million people worldwide and

207 oma brucei is the causative agent of African sleeping sickness and is known for its unique RNA proces

208 ors by parasitic protozoa that cause African sleeping sickness and malaria.

209 cei, the causative pathogen of human African sleeping sickness and nagana in domestic animals, myo-in

210 trends in the development of diagnostics for sleeping sickness are considered and progress towards a

211 soma brucei rhodesiense causes human African sleeping sickness because it has evolved an inhibitor of

212 very that may undermine efforts to eliminate sleeping sickness by 2020.

213 Trypanosoma brucei causes African sleeping sickness for which no vaccine exists and availa

214 cei causes African trypanosomiasis, known as sleeping sickness in humans and nagana in domestic anima

215 the diseases caused by African trypanosomes: sleeping sickness in humans and Nagana in livestock.

216 African trypanosomes cause sleeping sickness in humans, a disease that is typically

217 When they infect mammals, they cause African sleeping sickness in humans.

218 lated protozoan parasite that causes African sleeping sickness in humans.

219 Human African trypanosomiasis or sleeping sickness is a deadly disease endemic in sub-Sah

220 Human African trypanosomiasis (HAT) or sleeping sickness is caused by two subspecies of Trypano

221 African sleeping sickness or human African trypanosomiasis, caus

222 In the mammalian bloodstream, the sleeping sickness parasite Trypanosoma brucei is held po

223 Trypanosomatids, such as the sleeping sickness parasite Trypanosoma brucei, contain a

224 Motility of the sleeping sickness parasite, Trypanosoma brucei, impacts

225 The strategy that sleeping sickness parasites use to evade the mammalian i

226 ction of rare cell types in blood (including sleeping sickness parasites), and has the potential to e

227 Protozoan parasites such as the sleeping sickness pathogen Trypanosoma brucei adapt to d

228 s the only example of cross-resistance among sleeping sickness therapies.

229 rucei causes human African trypanosomiasis ("sleeping sickness") across sub-Saharan Africa and is a m

230 ambiense Human African Trypanosomiasis (HAT, sleeping sickness), a disease that has often been consid

231 en argued that the risk for trypanosomiasis (sleeping sickness), carried by tsetse flies in bushy env

232 copeia for human African trypanosomiasis (or sleeping sickness), orally dosed fexinidazole stands poi

233 tive agent of Human African Trypanosomiasis (sleeping sickness), yet little is known about which PKs

234 human African trypanosomiasis (HAT; African sleeping sickness).

235 oma brucei is the causative agent of African sleeping sickness, a devastating disease endemic to sub-

236 Trypanosoma brucei causes African sleeping sickness, a disease for which existing chemothe

237 ing target to develop new treatments against sleeping sickness, a fatal disease caused by this protoz

238 t and Southern Africa are foci for Rhodesian sleeping sickness, a fatal zoonotic disease caused by tr

239 animal trypanosomiases, including Rhodesian sleeping sickness, a zoonosis associated with wilderness

240 a brucei, causative agent of the fatal human sleeping sickness, are essential for the parasite.

241 ovide different levels of protection against sleeping sickness, but this comes with an increased risk

242 African sleeping sickness, caused by the protozoan parasite Tryp

243 anosoma brucei, a causative agent of African Sleeping Sickness, constantly changes its dense variant

244 osoma brucei, the etiologic agent of African Sleeping Sickness, deploys an RNA pol II that contains a

245 osoma brucei, the causative agent of African sleeping sickness, differs from its human host in severa

246 anosoma brucei, the causative agent of human sleeping sickness, has an intrinsic circadian clock that

247 Human African trypanosomiasis (HAT), or sleeping sickness, is a major threat to human health thr

248 Human African trypanosomiasis, or sleeping sickness, is caused by infection with parasites

249 osoma brucei, the causative agent of African sleeping sickness, is transmitted to its mammalian host

250 Trypanosoma brucei, the etiological agent of sleeping sickness, localized its replication origins to

251 he parasitic trypanosomes that cause African sleeping sickness, mating occurs during transmission by

252 oma brucei is the causative agent of African sleeping sickness, putting at risk up to 50 million peop

253 tance against Trypanosoma that cause African sleeping sickness, resulting in positive selection of th

254 ite Trypanosoma brucei, which causes African sleeping sickness, TbISWI down-regulates RNA polymerase

255 s typified by the causative agent of African sleeping sickness, Trypanosoma brucei In mitochondria of

256 energy metabolism in the causative agent of sleeping sickness, Trypanosoma brucei, with that of huma

257 can trypanosomes, parasites that cause human sleeping sickness, undergo a density-dependent different

258 n disease called African trypanosomiasis, or sleeping sickness.

259 asite that causes the deadly disease African sleeping sickness.

260 seases, including malaria, dengue fever, and sleeping sickness.

261 ucei rhodesiense, the cause of acute African sleeping sickness.

262 n trypanosomiasis (HAT), also called African sleeping sickness.

263 panosoma brucei, the causal agent of African sleeping sickness.

264 fforts to develop new treatments for African sleeping sickness.

265 ed by the tsetse fly and that causes African sleeping sickness.

266 the future therapeutic treatment of African sleeping sickness.

267 an African trypanosomiasis (HAT), or African sleeping sickness.

268 trypanosomiasis (HAT), also known as African sleeping sickness.

269 is a parasitic protozoan that causes African sleeping sickness.

270 osoma brucei, the causative agent of African sleeping sickness.

271 isease and human African trypanosomiasis, or sleeping sickness.

272 panosomal infection and protect from African sleeping sickness.

273 t for human African trypanosomiasis (HAT) or sleeping sickness.

274 cei is an extracellular parasite that causes sleeping sickness.

275 ally explain the weight loss associated with sleeping sickness.

276 osoma brucei, the causative agent of African sleeping sickness; and Plasmodium spp., the causative ag

277 ge attraction and repulsion from the troop's sleeping site, to relatively local influences including

278 k factors for infants include prone and side sleeping, soft bedding, bed sharing, inappropriate sleep

279 During resting and sleeping states, slow fluctuations (<1 Hz) of HFB activi

280 ing with her infant on the same bed or other sleeping surfaces for nighttime sleep or during the majo

281 cond (recovery) night of sleep revealed that sleeping the first half of the night, which is dominated

282 Conversely, sleeping the second half of the night, which is dominate

283 As newborns spend most of their time sleeping, the ability to learn about external stimuli in

284 glycemia associated with different levels of sleeping time (<11.0, 11.0-11.9, and >/=12.0 hours/day)

285 (SWS), rapid eye movement (REM)-sleep, total sleeping time (TST), sleep stage 2 (S2), and QS [(SWS +

286 based on arbitrary threshold parameters for sleeping time and number of citations, applied to small

287 rse association of either indoor activity or sleeping time with the risk of hyperglycemia among offsp

288 tion of physical activity, TV watching time, sleeping time with the risks of obesity and hyperglycemi

289 activity, outdoor activity, TV watching, and sleeping time.

290 e spontaneous cortical activity of naturally sleeping toddlers with autism, but not in toddlers with

291 of 1371; 1.10, 1.04-1.16; p=0.001), and baby sleeping under bednet for 8-56 days (4548 [79%] of 5756

292 ill at high altitude and whether training or sleeping under normobaric hypoxic conditions in the week

293 ion usually exceed the attention afforded by sleeping unihemispherically.

294 ng non-REM sleep in freely moving, naturally sleeping-waking rats.

295 cellular recording and labeling in naturally sleeping-waking, head-fixed rats, we investigated the di

296 Sometimes while sleeping we find ourselves thrown amidst an authentic, a

297 The symptoms of edema and trouble sleeping were variable among the countries and fell into

298 r orthokeratology (OR, undefined; P = 0.02), sleeping while wearing lenses (OR, 8.00; P = 0.04), stor

299 haring, defined as the mother lying down and sleeping with her infant on the same bed or other sleepi

300 nmental awareness and aerodynamic control by sleeping with only one eye closed and one cerebral hemis