ライフサイエンスコーパス: premature infant

1 ive pharmacological prevention of PVL in the premature infant.

2 hological substrate of cerebral palsy in the premature infant.

3 e the process of barrier acquisition for the premature infant.

4 nerability to PVL of the white matter in the premature infant.

5 tion of respiratory distress syndrome in the premature infant.

6 llectual deficits associated with PVL in the premature infant.

7 Cronobacter sakazakii and typically affects premature infants.

8 an inflammatory disease of the intestine in premature infants.

9 tegories identified in the fecal matter from premature infants.

10 natal morbidity and mortality, especially in premature infants.

11 markable finding is the undetectable MPOD in premature infants.

12 s, especially high-risk populations, such as premature infants.

13 importance in the delivery of healthcare for premature infants.

14 le blood, it can replace blood sampling from premature infants.

15 stinal injury with extensive inflammation in premature infants.

16 th) neurodevelopmental outcomes of extremely premature infants.

17 ption in production of interneurons in human premature infants.

18 t affects the gastrointestinal (GI) tract of premature infants.

19 impacts the health and future development of premature infants.

20 e pharmacokinetic study of oseltamivir in 12 premature infants.

21 neural cell death and white matter injury in premature infants.

22 poxia-a paradigm that mimics brain injury in premature infants.

23 ature rabbit pups and autopsy materials from premature infants.

24 d with neonatal necrotizing enterocolitis in premature infants.

25 duction and is a common complication seen in premature infants.

26 relevant to white matter injury observed in premature infants.

27 ntestinal disorder that affects 2%-5% of all premature infants.

28 ortant determinant of outcome, especially in premature infants.

29 ral route as the primary means of nourishing premature infants.

30 high doses of vitamin D in the management of premature infants.

31 a major cause of morbidity and mortality in premature infants.

32 h is selectively vulnerable to hemorrhage in premature infants.

33 morbidity from bronchopulmonary dysplasia in premature infants.

34 incidence of intraventricular hemorrhage in premature infants.

35 incidence and severity of GMH in susceptible premature infants.

36 creating a rationale for clinical studies in premature infants.

37 a higher PCO2 level may be well tolerated in premature infants.

38 he most common gastrointestinal emergency of premature infants.

39 n newborns, particularly in low-birth-weight premature infants.

40 h as freezing, may be warranted in high-risk premature infants.

41 al heart disease and is especially common in premature infants.

42 stating and unpredictable diseases affecting premature infants.

43 f many skin diseases and causes mortality in premature infants.

44 major disorder underlying cerebral palsy in premature infants.

45 c agent for respiratory distress syndrome in premature infants.

46 or small volume (5-15 mL/kg) transfusions in premature infants.

47 and is the leading cause of brain injury in premature infants.

48 ration of permeability barrier maturation in premature infants.

49 nduced IVH and analyzed autopsy samples from premature infants.

50 e frequency of bronchopulmonary dysplasia in premature infants.

51 icine, being especially prevalent among very premature infants.

52 can reduce longterm neurologic disability in premature infants.

53 studies had relatively small numbers of very premature infants.

54 ury and morbidity, particularly in extremely premature infants.

55 ood neurodevelopmental outcomes of extremely premature infants.

56 oduces diffuse white matter injury (DWMI) of premature infants.

57 ity (ROP) is a vision-threatening disease in premature infants.

58 edema, and atelectasis, were present in all premature infants.

59 n detecting early stages of NEC in suspected premature infants.

60 anization dedicated to improving the care of premature infants.

61 , overall mortality declined among extremely premature infants.

62 stinal microbiota preceding NEC diagnosis in premature infants.

63 a major cause of morbidity and mortality in premature infants.

64 rce of DNA for high-throughput sequencing in premature infants.

65 cting NSAIDs are preferred, with caution for premature infants.

66 axis appears to be well tolerated for use in premature infants.

67 ay also contribute to respiratory failure in premature infants.

68 lient implications for the care practices of premature infants.

69 ed a large increase in strabismus risk among premature infants.

70 Extended caffeine treatment decreases IH in premature infants.

71 , placebo-controlled trial of fluconazole in premature infants.

72 tion of invasive bacteria between and within premature infants.

73 h, and improve neurodevelopmental outcome of premature infants.

74 In premature infants, 10% of T cells were dividing; the pro

75 d 20-24 postconceptional weeks (PCW) and for premature infants (25-37 PCW), we found that radial glia

76 f retinal SDOCT images from 1 eye each of 22 premature infants, 30 term infants, 16 children, and 1 a

77 We included a total of 343 premature infants (401-1250 g birth weight [BW], from 19

78 nical observation of reduced ROP severity in premature infants after caffeine treatment for apnea sug

79 r evaluating subclinical macular findings in premature infants, although larger datasets are needed f

80 hi fermentation process, the microbiome of a premature infant and in microbial communities living on

81 e immunologic and functional immaturities of premature infants and ameliorating the risks of extrinsi

82 therapy have increased survival of extremely premature infants and changed the pathology of bronchopu

83 ocused on one homogenous diagnostic group of premature infants and children with complex congenital h

84 first-line treatment for MRSA bacteremia in premature infants and for PVL-positive isolates.

85 life-threatening lung-associated diseases in premature infants and immunocompromised children.

86 optical density (MPOD) and distributions in premature infants and in children.

87 With the increasing survival of premature infants and increased incidence of ROP, it is

88 asis (IC) is an important cause of sepsis in premature infants and is associated with a high risk of

89 al white matter injury seen most commonly in premature infants and is the major antecedent of cerebra

90 (ROP) remains a major cause of blindness in premature infants and the incidence is increasing with i

91 Premature infants and those with chronic lung disease or

92 e in reducing IC and Candida colonization in premature infants, and has no impact on resistance.

93 ulmonary insufficiency, as is encountered in premature infants, and in patients with acute respirator

94 use of gastrointestinal-related mortality in premature infants, and it develops under conditions of e

95 the cortex or white matter in human fetuses, premature infants, and premature rabbit pups.

96 a major cause of morbidity and mortality in premature infants, and the optimal treatment is uncertai

97 oduct transfusion in the fetus, neonate, and premature infant are often administered with poorly defi

98 emorrhage or periventricular leukomalacia in premature infants are associated with abnormal neurodeve

99 Premature infants are at an increased risk for infection

100 Premature infants are at risk for bronchopulmonary dyspl

101 Premature infants are at risk of developing encephalopat

102 Importance: Many premature infants are born without exposure to antenatal

103 in processing, it is still not known whether premature infants are capable of processing pain at a co

104 Premature infants are highly vulnerable to aberrant gast

105 Although premature infants are known to be deficient in pulmonary

106 er to administer intensive care to extremely premature infants are often based on gestational age alo

107 Ventilator-dependent premature infants are often treated with dexamethasone.

108 GF levels on the developing organ systems of premature infants are unknown, and there are limited lon

109 nal matrix angiogenesis in human fetuses and premature infants, as well as in premature rabbit pups,

110 icroorganisms that colonized co-hospitalized premature infants, assessed their metabolic potential, a

111 for the most vulnerable of children, namely premature infants at high risk for lung disease.

112 Participants were premature infants at risk for ROP with a known ROP outco

113 Participants included 7483 premature infants at risk for ROP with a known ROP outco

114 the potential for delivering timely care to premature infants at risk for serious ROP.

115 Retinopathy of prematurity adversely affects premature infants because of oxygen-induced damage of th

116 fects of human milk extend to the feeding of premature infants, because their nutrition support must

117 al cohort study, participants were extremely premature infants (birth weight range, 401-1000 g; gesta

118 tively collected high quality (1)H-MRS in 59 premature infants born </=32 weeks and 61 healthy full t

119 ma levels weekly and examined retinas in all premature infants born at gestational ages <32 weeks at

120 s one of the last organs to mature in utero, premature infants born before 34 weeks gestation are at

121 ilk may not meet the great nutrient needs of premature infants born weighing <1500 g.

122 intestinal emergency that primarily afflicts premature infants born weighing less than 1500 g.

123 ements in the care and survival of extremely premature infants, BPD remains a major clinical problem.

124 y reduce the risk of chronic lung disease in premature infants but can cause complications.

125 widely used to treat chronic lung disease in premature infants but their longer-term adverse effects

126 etinopathy of prematurity (ROP) affects only premature infants, but as premature births increase in m

127 original description of the disease in 1967, premature infants can develop chronic oxygen dependency

128 Invasive candidiasis in premature infants causes death and neurodevelopmental im

129 erocolitis (NEC) is a devastating disease of premature infants characterized by severe intestinal nec

130 life-threatening gastrointestinal disease of premature infants characterized by the sudden onset of i

131 ere disease of the gastrointestinal tract in premature infants, characterized by a disrupted intestin

132 In premature infants, clinical rickets and fractures are co

133 trials evaluating fluconazole prophylaxis in premature infants conducted in the United States.

134 In premature infants, danger signal-induced DC activation m

135 ges 6 to <11 mo, lost future earnings due to premature infant death, and the costs of purchasing infa

136 Significance statement: Approximately 12,000 premature infants develop IVH every year in the United S

137 leading cause of invasive fungal disease in premature infants, diabetics, and surgical patients and

138 leading cause of invasive fungal disease in premature infants, diabetics, and surgical patients, and

139 our understanding of intestinal defences in premature infants, dietary and bacterial factors, and ge

140 ned by initiating intensive care in the most premature infants does not justify doing so without pare

141 unities in 11 fecal samples collected from a premature infant during the first month of life.

142 the skin, mouth, and gut of two hospitalized premature infants during the first month of life.

143 A deficit in these proteins in premature infants, either because of immaturity or as a

144 Extremely premature infants exhibit high rates of proteolysis that

145 Premature infants exhibit neurodevelopmental delay and r

146 t clinical data suggest that a percentage of premature infants experience relative hyperoxia.

147 Nearly 90% of premature infants experience the stress of intermittent

148 nth neurodevelopmental outcomes of extremely premature infants exposed to no ANS or partial or comple

149 The axial length of the premature infant eye increases rapidly in a linear patte

150 fed unfortified human milk also are found in premature infants fed fortified human milk.

151 tizing enterocolitis, have been reported for premature infants fed their mothers' milk.

152 maternal-newborn skin-to-skin contact to 73 premature infants for 14 consecutive days compared with

153 anti-inflammatory agents are administered to premature infants for a variety of reasons.

154 ty DNA from buccal epithelial-cells (BEC) of premature infants for genomic analysis.

155 Impaired neurological development in premature infants frequently arises from periventricular

156 ides a rationale for protecting the severely premature infant from oxygen toxicity.

157 Data of 78 premature infants from diabetic mothers were compared wi

158 ad been of low birthweight (LBW) or had been premature infants, greater declines were seen among thos

159 Oseltamivir 3 mg/kg/dose once daily in premature infants >38 weeks postmenstrual age (born prem

160 Thus, we conclude that a component of premature infant gut colonization is the cycle of microb

161 Premature infants had Hib GMCs of 0.27 microg/mL, with 2

162 All premature infants had undetectable macular pigment, and

163 ing enterocolitis (NEC) affects up to 10% of premature infants, has a mortality of 30%, and can leave

164 (ROP), the most common cause of blindness in premature infants, has long been associated with inner r

165 tomegalovirus infections in low-birth-weight premature infants have been demonstrated to cause sympto

166 Premature infants have chronic hypoxia, resulting in cog

167 Very low birthweight premature infants have compromised skin barrier function

168 Some adults with iron-overload and some premature infants have potentially redox-active, bleomyc

169 Subclinical CME is seen in premature infants; however, CME does not appear to be co

170 s can lead to severe inflammatory disease in premature infants; however, investigating complex enviro

171 In the premature infant, hypoxic-ischemic damage to the cerebra

172 We report the case of a 27-week premature infant in whom magnetic resonance imaging (MRI

173 Premature infants in neonatal intensive care units (NICU

174 The hospital discharge of premature infants in neonatal intensive care units is of

175 Brain injury in the premature infant is associated with a high risk of neuro

176 Thus, the premature infant is at increased risk for the developmen

177 The premature infant is especially susceptible to ROS-induce

178 PVL in the premature infant is shown for the first time to be follo

179 Oxygen exposure in premature infants is a major risk factor for bronchopulm

180 Bronchopulmonary dysplasia in premature infants is associated with prolonged hospitali

181 articular, a pattern similar to that seen in premature infants is emerging, including learning disabi

182 We conclude that surfactant of newborn premature infants is markedly deficient in SPs, in parti

183 Brain injury in premature infants is of enormous public health importanc

184 opathological correlate of cerebral palsy in premature infants is periventricular leukomalacia (PVL),

185 ain abnormality underlying cerebral palsy in premature infants is periventricular leukomalacia (PVL),

186 of 3 g amino acids kg(-1)d(-1) to extremely premature infants is safe and effective.

187 The germinal matrix of premature infants is selectively vulnerable to hemorrhag

188 L), the dominant form of brain injury in the premature infant, is the major neuropathological substra

189 RDS), which is the leading cause of death in premature infants, is caused by surfactant deficiency.

190 ets are often deficient in omega-3-PUFA, and premature infants lack the important transfer from the m

191 Hypoxia-ischemia (H/I) in the premature infant leads to white matter injury termed per

192 cidence of chronic lung disease and death in premature infants (less than 34 weeks' gestation) who we

193 ch as glaucoma, brain edema, and swelling of premature infant lungs.

194 Tolerance induction of fetal and premature infant lymphocytes has become a paradigm for n

195 coordinated peristaltic responses develop as premature infants mature.

196 The epidermal permeability barrier of premature infants matures rapidly following birth.

197 the causes and timing of death in extremely premature infants may guide research efforts and inform

198 gastric mucosa, which is poorly developed in premature infants, may play a functional role in gastric

199 f strains across body sites implies that the premature infant microbiome can exhibit very low microbi

200 e risk of developing severe ROP in extremely premature infants might be reduced by improving nutritio

201 adverse neurodevelopmental outcomes in very premature infants, much of the variation in outcome rema

202 a major cause of morbidity and mortality in premature infants, occurs after the introduction of oral

203 Definition in the living premature infant of the anatomical and temporal characte

204 Premature infants often require oxygen supplementation a

205 s correlated with birth weight, and severely premature infants often require surgical repair.

206 eted ventilation have been developed for the premature infant or were adopted from those used in olde

207 might be linked to the increased survival of premature infants or to increased viability among births

208 ly because of the improved survival rates of premature infants over the past decade.

209 is a devastating gastrointestinal disease of premature infants partly caused by intestinal bacterial

210 These populations include premature infants, patients with long-term total parente

211 glutamatergic neurogenesis continues in the premature infants, preterm birth suppresses neurogenesis

212 o right to refuse resuscitation of extremely premature infants prior to birth because they cannot be

213 eurodevelopmental impairment among extremely premature infants randomly assigned to early CPAP or ear

214 re is persistence of inner retinal layers in premature infants regardless of maximal ROP stage.

215 Growth outcomes for extremely premature infants remain poor, and improving growth in t

216 erocolitis (NEC), a severe disease affecting premature infants, remain unknown.

217 Advances in nutrition of premature infants require the best practices and opinion

218 plasia is a chronic lung disease observed in premature infants requiring oxygen supplementation and v

219 from 58 subjects that the gut microbiota of premature infants residing in a tightly controlled micro

220 Hypoxic-ischemic brain injury in premature infants results in cerebral white matter lesio

221 Intraventricular hemorrhage (IVH) in premature infants results in inflammation, arrested olig

222 developing countries improve the survival of premature infants, retinopathy of prematurity is emergin

223 ne responses to intestinal microbiota by the premature infant's intestinal tract, leading to inflamma

224 ight partially restore neurogenesis in human premature infants.SIGNIFICANCE STATEMENT Prematurity res

225 with a better understanding of neonatal and premature infant skin.

226 a devastating inflammatory bowel disease of premature infants speculatively associated with infectio

227 An observational study of premature infants starting at 32 weeks' postmenstrual ag

228 s not a prominent feature of brain injury in premature infants, the possibility of a deleterious effe

229 t, and, despite an increase in the number of premature infants, the surgical mortality rate has impro

230 To determine the immune response of premature infants to meningococcal serogroup C capsular

231 ew will examine the unique susceptibility of premature infants to oxidative stress, the role of react

232 tributing to the increased susceptibility of premature infants to pulmonary infections.

233 ngs may explain the unique susceptibility of premature infants to the development of NEC and offer th

234 composition of certain high-risk groups, eg, premature infants, travelers, and children receiving ant

235 Premature infants treated with inhaled nitric oxide have

236 Premature infants undergoing intensive care are highly v

237 is is the first analysis of ON parameters in premature infants using SD-OCT.

238 The decreased P-selectin in premature infants was associated with decreased numbers

239 P vaccine used in this study, the Hib GMC of premature infants was extremely low.

240 se of inhaled nitric oxide in critically ill premature infants weighing less than 1500 g does not dec

241 those weighing 1500 to 2500 g, 66% to 80% of premature infants weighing more than 2500 g, and 65% to

242 A total of 11580 low-birth-weight and premature infants were enrolled from birth to age 2 mont

243 A total of 207 premature infants were enrolled.

244 Premature infants were excluded.

245 enteric venules and umbilical veins of human premature infants when compared with term human infants.

246 e therapy improves the pulmonary outcome for premature infants who are at risk for bronchopulmonary d

247 ion, and the optimal discharge management of premature infants who are at risk of low bone mass.

248 Because these ROP patients are vulnerable premature infants who are still in a fragile state of in

249 Serial ROP examinations of premature infants who had 2 or more ROP examinations.

250 prospective, longitudinal follow-up study of premature infants who had received inhaled nitric oxide

251 results indicating that endothelial cells of premature infants who later develop BPD or die have impa

252 ues to be an important cause of morbidity in premature infants who require mechanical ventilation.

253 amounts may present additional risk to those premature infants who require prolonged periods of venti

254 te phase II) that can be life-threatening in premature infants who suffer from frequent apnoeas and r

255 This is particularly important for premature infants who, born with inadequate copper store

256 n is warranted, however, in low-birth-weight premature infants, who are at increased risk of cytomega

257 This is especially evident in premature infants whose prolonged stays in hospital and

258 Participants in the e-ROP Study were premature infants with a birth weight less than 1251 g a

259 ith the development of ROP and type 1 ROP in premature infants with a birth weight of 1500 g or more.

260 Given the high number of premature infants with alveolar dysgenesis and lung dysp

261 g was performed on DNAs obtained from BEC on premature infants with and without necrotizing enterocol

262 le-blind, randomized controlled trial in 377 premature infants with birth weights less than 1250 g ad

263 om May 1, 2011, to October 31, 2013, in 1257 premature infants with birth weights less than 1251 g in

264 udy of the effects of light reduction on 409 premature infants with birth weights of less than 1251 g

265 Among premature infants with BW of less than 2000 g, a GA of 3

266 reatment of respiratory distress syndrome in premature infants with continuous positive airway pressu

267 Treatment of ventilator-dependent premature infants with dexamethasone at two weeks of age

268 The mean HCDR3 length distribution in 10 premature infants with documented bacterial sepsis was t

269 d to measure brain tissue volumes at term in premature infants with earlier ultrasonographic and magn

270 DNAs from BEC were obtained from premature infants with gestational age </= 36 weeks.

271 tive strategy for minimizing brain damage in premature infants with intraventricular haemorrhage.

272 antly elevated in both rabbit pups and human premature infants with IVH compared with controls.

273 ition might enhance neurological recovery in premature infants with IVH.

274 es might improve the neurological outcome of premature infants with IVH.

275 h might improve the neurological outcome for premature infants with IVH.

276 reatment might enhance neurologic outcome in premature infants with IVH.

277 ans about the need for careful monitoring of premature infants with low BW for strabismus.

278 ge at birth, 28.7 +/- 2.0 weeks; n = 10), in premature infants with normal imaging studies (mean gest

279 that may influence the treatment of severely premature infants with PDA and lead to improvement of th

280 Premature infants with PVL had a marked reduction in cer

281 ceptor was not detected in lung and liver of premature infants with respiratory distress syndrome.

282 cysteine for glutathione synthesis is low in premature infants with respiratory distress.

283 were successfully obtained in 3 consecutive premature infants with retinopathy of prematurity at the

284 ra-wide-field oral fluorescein angiograms in premature infants with retinopathy of prematurity.

285 od for evaluating the retinal vasculature in premature infants with retinopathy of prematurity.

286 We report the outcome of 6 eyes of 4 premature infants with ROP stage 3 plus disease treated

287 examined prospectively collected stools from premature infants with sepsis to find pathogens that sub

288 itric oxide is a controversial treatment for premature infants with severe respiratory failure.

289 nic lung disease of infancy affecting mostly premature infants with significant morbidity and mortali

290 ndomized, controlled, single-center trial of premature infants with the respiratory distress syndrome

291 The use of inhaled nitric oxide in premature infants with the respiratory distress syndrome

292 cidence of chronic lung disease and death in premature infants with the respiratory distress syndrome

293 Six eyes of 4 premature infants with threshold ROP 3 plus disease in z

294 Premature infants with type 1 ROP (subdivided into stage

295 Between May 2015 and September 2016, 61 premature infants with type 1 ROP in 1 or both eyes were

296 dysplasia (BPD) is a common lung disease of premature infants, with devastating short- and long-term

297 t common serious complication experienced by premature infants, with more than 8,000 newly diagnosed

298 l-term infants (7.3 +/- 8.2%; P = 0.020) and premature infants without BPD (8.2 +/- 6.4%; P = 0.026).

299 e severe than the lung injury that occurs in premature infants without NEC, the mechanisms leading to

300 cal gray matter at term compared with either premature infants without PVL or normal term infants (me