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 tted, disseminated adenovirus infection in a premature infant.

6 D risk assessment, particularly in extremely premature infants.

7 on standards and the Fenton growth chart for premature infants.

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

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

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

11 anization dedicated to improving the care of premature infants.

12 , overall mortality declined among extremely premature infants.

13 stinal microbiota preceding NEC diagnosis in premature infants.

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

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

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

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

18 ay also contribute to respiratory failure in premature infants.

19 lient implications for the care practices of premature infants.

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

21 Extended caffeine treatment decreases IH in premature infants.

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

23 tion of invasive bacteria between and within premature infants.

24 h, and improve neurodevelopmental outcome of premature infants.

25 tood pathophysiology predominantly affecting premature infants.

26 an inflammatory disease of the intestine in premature infants.

27 tegories identified in the fecal matter from premature infants.

28 natal morbidity and mortality, especially in premature infants.

29 f visual impairment in diabetic patients and premature infants.

30 markable finding is the undetectable MPOD in premature infants.

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

32 importance in the delivery of healthcare for premature infants.

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

34 stinal injury with extensive inflammation in premature infants.

35 th) neurodevelopmental outcomes of extremely premature infants.

36 ly 2 months premature to affecting extremely premature infants.

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

38 e pharmacokinetic study of oseltamivir in 12 premature infants.

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

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

41 ature rabbit pups and autopsy materials from premature infants.

42 d with neonatal necrotizing enterocolitis in premature infants.

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

44 relevant to white matter injury observed in premature infants.

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

46 ortant determinant of outcome, especially in premature infants.

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

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

49 h is selectively vulnerable to hemorrhage in premature infants.

50 morbidity from bronchopulmonary dysplasia in premature infants.

51 incidence of intraventricular hemorrhage in premature infants.

52 incidence and severity of GMH in susceptible premature infants.

53 creating a rationale for clinical studies in premature infants.

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

55 he most common gastrointestinal emergency of premature infants.

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

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

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

59 stating and unpredictable diseases affecting premature infants.

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

61 major disorder underlying cerebral palsy in premature infants.

62 nism of diffuse white matter injury (WMI) in premature infants.

63 c agent for respiratory distress syndrome in premature infants.

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

65 iferative disorder that can affect extremely premature infants.

66 uation of current transfusion guidelines for premature infants.

67 of commensal microbes from the intestines of premature infants.

68 zation schedule may disproportionally affect premature infants.

69 n idiopathic, inflammatory bowel necrosis of premature infants.

70 d to be considered when clinicians deal with premature infants.

71 ins a major respiratory illness in extremely premature infants.

72 Cronobacter sakazakii and typically affects premature infants.

73 ption in production of interneurons in human premature infants.

74 impacts the health and future development of premature infants.

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

76 nduced IVH and analyzed autopsy samples from premature infants.

77 acia, a major form of brain injury affecting premature infants.

78 ury and morbidity, particularly in extremely premature infants.

79 ood neurodevelopmental outcomes of extremely premature infants.

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

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

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

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

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

85 ctor for bronchopulmonary dysplasia (BPD) in premature infants, a disease characterized by dysregulat

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

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

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

89 rting neural and vascular development of the premature infant and retina.

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

91 s (NEC) is an inflammatory bowel necrosis of premature infants and an orphan disease with no specific

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

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

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

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

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

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

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

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

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

101 Premature infants and those with chronic lung disease or

102 e 51-5 was isolated from stool of a healthy, premature infant, and found to contain the genotoxin isl

103 by $10 164 (95% CI, $8835-$11 493) for late premature infants, and by $5404 (95% CI, $5110-$5698) fo

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

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

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

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

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

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

110 d patterns of IgA binding to gut bacteria in premature infants are associated with necrotizing entero

111 Premature infants are at an increased risk for infection

112 Premature infants are at risk for bronchopulmonary dyspl

113 Premature infants are at risk of developing encephalopat

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

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

116 Premature infants are highly vulnerable to aberrant gast

117 Although premature infants are known to be deficient in pulmonary

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

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

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

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

122 1,259 premature infants at risk for ROP were evaluated.

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

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

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

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

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

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

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

130 from a voxel placed in the cerebellum of 53 premature infants born at a median gestational age of 27

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

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

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

134 stion simulating the digestive conditions of premature infant, bovine BCMs still occurred in fortifie

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

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

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

138 nts, by $14 034 (95% CI, $5095- $22 973) for premature infants, by $10 164 (95% CI, $8835-$11 493) fo

139 nce interval [CI], -$5800-$42 543) for early premature infants, by $14 034 (95% CI, $5095- $22 973) f

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

141 Invasive candidiasis in premature infants causes death and neurodevelopmental im

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

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

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

145 In premature infants, clinical rickets and fractures are co

146 ippocampal maturation.SIGNIFICANCE STATEMENT Premature infants commonly sustain hypoxia-ischemia, whi

147 risk of IPD remains significantly higher in premature infants compared to infants born at term, for

148 V13-type, non-PCV13-type, and overall IPD in premature infants compared to term infants during a 4-ye

149 Incidence was significantly higher in premature infants compared with those born at term (49/1

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

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

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

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

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

155 Premature infants did not have a higher CFR than term in

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

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

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

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

160 Extremely premature infants exhibit high rates of proteolysis that

161 Premature infants exhibit neurodevelopmental delay and r

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

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

164 utic target for prevention of diffuse WMI in premature infants experiencing chronic IH stress.

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

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

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

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

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

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

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

172 Impaired neurological development in premature infants frequently arises from periventricular

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

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

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

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

177 We find that 23% of microbial genomes from premature infant guts have siderophore-like BGCs, but on

178 All premature infants had undetectable macular pigment, and

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

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

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

182 Premature infants have chronic hypoxia, resulting in cog

183 Very low birthweight premature infants have compromised skin barrier function

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

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

186 is required to promote survival of severely premature infants, hyperoxia is simultaneously harmful t

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

188 Premature infants in neonatal intensive care units (NICU

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

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

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

192 The premature infant is especially susceptible to ROS-induce

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

194 Bronchopulmonary dysplasia in premature infants is associated with prolonged hospitali

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

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

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

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

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

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

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

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

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

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

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

206 This is a longitudinal cohort of premature infants (<=32 weeks PMA, n = 188; Washington D

207 ted in an independent longitudinal cohort of premature infants (<=36 weeks PMA, n = 130; Bogota).

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

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

210 dian of 3 more days than infants 5-8 weeks), premature infants (median of 4 more days than term infan

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

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

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

214 Premature infants often require oxygen supplementation a

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

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

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

218 nce interval [CI], 41.7-118.2) for 213 early premature infants (P < .001), 18.2 hospitalizations/100

219 ient-years (95% CI, 29.1-39.2) for 4446 late premature infants (P < .001), and 16.1 hospitalizations/

220 /100 patient-years (95% CI, .8-35.7) for 397 premature infants (P = .04), 34.2 hospitalizations/100 p

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

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

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

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

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

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

227 underlying associated gray-matter defects in premature infants remain unknown.

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

229 ective for prevention of allergic disease in premature infants remains lacking; adequately powered ra

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

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

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

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

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

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

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

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

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

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

240 Premature infants subjected to mechanical ventilation (M

241 networks previously shown to be decreased in premature infants: the salience network with the superio

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

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

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

245 Premature infants treated with inhaled nitric oxide have

246 Premature infants undergoing intensive care are highly v

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

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

249 In total, 296 premature infants were enrolled and compared with a cont

250 A total of 207 premature infants were enrolled.

251 Premature infants were excluded.

252 Risk factors for RF and death in premature infants were investigated.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

267 Serial fecal samples were collected from premature infants with birth weight (BW) <= 1800 g, esti

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

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

270 Premature infants with bronchopulmonary dysplasia, chara

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

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

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

274 erocolitis (NEC) is a devastating disease of premature infants with high mortality rate, indicating t

275 tis (NEC) is a devastating disease affecting premature infants with intestinal inflammation and necro

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

295 Premature infants with type 1 ROP (subdivided into stage

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

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

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

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

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