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1 fants with established chronic lung disease (bronchopulmonary dysplasia).
2 irus, airway hyperresponsiveness, and severe bronchopulmonary dysplasia.
3 atory syncytial virus infection, asthma, and bronchopulmonary dysplasia.
4 ed lung injury in a murine neonatal model of bronchopulmonary dysplasia.
5 weeks of postmenstrual age or survival with bronchopulmonary dysplasia.
6 ponsible for neonatal lung injury leading to bronchopulmonary dysplasia.
7 ficant difference in the outcome of death or bronchopulmonary dysplasia.
8 bility to postnatal normoxia, reminiscent of bronchopulmonary dysplasia.
9 2 is also increased in neonates that develop bronchopulmonary dysplasia.
10 00 g does not decrease the rates of death or bronchopulmonary dysplasia.
11 ncidence of pneumonia and the development of bronchopulmonary dysplasia.
12 have been implicated in the pathogenesis of bronchopulmonary dysplasia.
13 ed lung injury using a fetal baboon model of bronchopulmonary dysplasia.
14 nstitutes of Health Collaborative Project on Bronchopulmonary Dysplasia.
15 hma stimulated its use in infants to prevent bronchopulmonary dysplasia.
16 respiratory illness in preterm children with bronchopulmonary dysplasia.
17 eucomalacia, retinopathy of prematurity, and bronchopulmonary dysplasia.
18 ns with PPHN, congenital heart diseases, and bronchopulmonary dysplasia.
19 arance of phenotypical changes suggestive of bronchopulmonary dysplasia.
20 TGF-beta signaling, ultimately resulting in bronchopulmonary dysplasia.
21 nistration did not alter the early course of bronchopulmonary dysplasia.
22 A composite of death or bronchopulmonary dysplasia.
23 how to prevent fetal lung injury leading to bronchopulmonary dysplasia.
24 ng hypotheses about the molecular origins of bronchopulmonary dysplasia.
25 atory syncytial virus infection, asthma, and bronchopulmonary dysplasia.
26 itric oxide therapy reduced the incidence of bronchopulmonary dysplasia (29.8 percent vs. 59.6 percen
27 ta were available, 191 died or survived with bronchopulmonary dysplasia (38.4%), as compared with 180
28 risk difference, -3.3 to 4.5; P = .70), and bronchopulmonary dysplasia (4.4% vs 5.1%; 95% CI of risk
29 itis (48.1%, 37.1%, and 32.5%), and death or bronchopulmonary dysplasia (74.9%, 68.9%, and 65.5%).
30 posure to inflammation increases the risk of bronchopulmonary dysplasia, a chronic, developmental lun
32 ciated with a lower likelihood of developing bronchopulmonary dysplasia, a sequelae of RDS (p<0.03).
33 ased odds of a composite outcome of death or bronchopulmonary dysplasia (adjusted odds ratio [AOR], 0
34 nd immunogenic and may protect children with bronchopulmonary dysplasia against serious RSV disease o
35 achypnea of the newborn, surfactant use, and bronchopulmonary dysplasia also occurred significantly l
36 emic glucocorticoids reduce the incidence of bronchopulmonary dysplasia among extremely preterm infan
37 tive lung vascular development can result in bronchopulmonary dysplasia and alveolar capillary dyspla
38 premature infants is a major risk factor for bronchopulmonary dysplasia and can impair the host respo
39 orn and developmental lung diseases, such as bronchopulmonary dysplasia and congenital diaphragmatic
41 2 were decreased in airways of neonates with bronchopulmonary dysplasia and in mice after airway inju
42 crease oxygen demands in these infants, like bronchopulmonary dysplasia and increased oxygen consumpt
43 iciously, weighing up the competing risks of bronchopulmonary dysplasia and neurodevelopmental harm.
44 ed with a reduction in the rates of death or bronchopulmonary dysplasia and patent ductus arteriosus.
46 Evidence suggests that preterm neonates with bronchopulmonary dysplasia and prolonged mechanical vent
47 may explain the complex relationship between bronchopulmonary dysplasia and retinopathy of prematurit
48 on groups were low-risk VLBW infants without bronchopulmonary dysplasia and term infants (>36 weeks,
49 ns of systemic dexamethasone used to prevent bronchopulmonary dysplasia and thus more restricted use,
51 h-risk VLBW infants were diagnosed as having bronchopulmonary dysplasia, and comparison groups were l
52 th respiratory distress syndromes, including bronchopulmonary dysplasia, and differential gene expres
53 y hypertension in pediatric diseases such as bronchopulmonary dysplasia, and increasingly expanding d
54 g enterocolitis, retinopathy of prematurity, bronchopulmonary dysplasia, and intraventricular hemorrh
55 pulmonary disease, asthma, cystic fibrosis, bronchopulmonary dysplasia, and muscular dystrophies.
56 idities such as intraventricular hemorrhage, bronchopulmonary dysplasia, and necrotizing enterocoliti
57 m, briefly explore pulmonary hypertension in bronchopulmonary dysplasia, and provide updates on the d
58 ing arrested alveolar growth in experimental bronchopulmonary dysplasia, and that exogenous ECFCs res
59 atory syncytial virus infection, asthma, and bronchopulmonary dysplasia; and genotyped and analyzed i
62 hoc analyses suggest that rates of death and bronchopulmonary dysplasia are reduced for infants with
63 ion) were classified as having physiological bronchopulmonary dysplasia, as compared with 269 (43.9%)
64 tional involvement of pulmonary apoptosis in bronchopulmonary dysplasia- associated alveolar disrupti
68 efficacy outcome was a composite of death or bronchopulmonary dysplasia at 36 weeks of postmenstrual
72 ated no difference in death or survival with bronchopulmonary dysplasia between nasal intermittent po
73 cant difference in the incidence of death or bronchopulmonary dysplasia between patients receiving in
75 remature labor and, among VLBW infants, with bronchopulmonary dysplasia (BPD) and chronic lung diseas
76 tion damage resulting in a high incidence of bronchopulmonary dysplasia (BPD) and chronic respiratory
77 decreased capillary density in infants with bronchopulmonary dysplasia (BPD) and in BPD-like animal
78 th of life are independently associated with bronchopulmonary dysplasia (BPD) and long-term respirato
79 k factors associated with increased risk for bronchopulmonary dysplasia (BPD) and respiratory disease
81 neonatologists on the role of Ureaplasma in bronchopulmonary dysplasia (BPD) development, the use of
82 emature infants and changed the pathology of bronchopulmonary dysplasia (BPD) from one of acute lung
83 cigarette smoke increases the risk of AA and bronchopulmonary dysplasia (BPD) in children and animal
84 is a key contributor to the pathogenesis of bronchopulmonary dysplasia (BPD) in neonates, for which
98 ith Ureaplasma parvum is causally related to bronchopulmonary dysplasia (BPD) or adverse respiratory
101 redict which premature infants would develop bronchopulmonary dysplasia (BPD) than single measurement
102 s a major contributor to the pathogenesis of bronchopulmonary dysplasia (BPD), a chronic lung disease
103 levels are elevated in newborns that develop bronchopulmonary dysplasia (BPD), a chronic lung disease
106 vents normal lung morphogenesis and leads to bronchopulmonary dysplasia (BPD), a common complication
108 e and chronic pulmonary disorders, including bronchopulmonary dysplasia (BPD), a respiratory conditio
109 significantly to morbidity and mortality in bronchopulmonary dysplasia (BPD), but little is known ab
110 ith poor outcomes among preterm infants with bronchopulmonary dysplasia (BPD), but whether early sign
111 evelop a chronic form of lung disease called bronchopulmonary dysplasia (BPD), characterized by decre
112 and worsened respiratory outcomes, including bronchopulmonary dysplasia (BPD), in preterm infants.
113 Outcomes included 28-day survival/death, bronchopulmonary dysplasia (BPD), periventricular/intrav
114 lung disease of early infancy, often called bronchopulmonary dysplasia (BPD), remains unclear, partl
116 re during gestation may increase the risk of bronchopulmonary dysplasia (BPD)-a developmental lung co
129 mon aspects in the genetic predisposition to bronchopulmonary dysplasia, bronchiolitis, and childhood
130 no significant difference in the outcome of bronchopulmonary dysplasia but a potential reduction in
131 as been reported to improve survival without bronchopulmonary dysplasia but its safety with regard to
132 Early beclomethasone therapy did not prevent bronchopulmonary dysplasia but was associated with lower
133 turated fatty acid, might reduce the risk of bronchopulmonary dysplasia, but appropriately designed t
134 m 50% to 16% (p = 0.002) among children with bronchopulmonary dysplasia, but it increased from 14% to
135 ted ventilation and reduces the incidence of bronchopulmonary dysplasia, but its effects on respirato
137 al lung macrophage activation contributes to bronchopulmonary dysplasia by generating a localized inf
139 segregated from those infants who developed bronchopulmonary dysplasia by the magnitude of the epith
142 olar enlargement, which is characteristic of bronchopulmonary dysplasia, congenital matrix disorders,
144 evere, acute respiratory distress; this "new bronchopulmonary dysplasia" could be the result of impai
145 function and morphology in animal models of bronchopulmonary dysplasia, creating a rationale for cli
150 val to 36 weeks of postmenstrual age without bronchopulmonary dysplasia did not differ significantly
151 present in the lungs of patients developing bronchopulmonary dysplasia disrupt expression of multipl
152 xide did not reduce the overall incidence of bronchopulmonary dysplasia, except among infants with a
154 1P in the pathobiological characteristics of bronchopulmonary dysplasia has not been investigated.
155 Infants with a history of prematurity and bronchopulmonary dysplasia have a high risk of asthma an
156 g mesenchymal stromal cell (MSC) therapy for bronchopulmonary dysplasia have been initiated; however,
157 ted to the respiratory distress syndrome and bronchopulmonary dysplasia in 2008-2011 than in 2000-200
158 e Hydrocortisone to Improve Survival without Bronchopulmonary Dysplasia in Extremely Preterm Infants)
159 e were seen from birth to the development of bronchopulmonary dysplasia in extremely preterm infants.
167 Rates of other morbidities declined, but bronchopulmonary dysplasia increased between 2009 and 20
169 lations of respiratory distress syndrome and bronchopulmonary dysplasia infants could be differentiat
170 bidities such as retinopathy of prematurity, bronchopulmonary dysplasia, injury to the developing bra
177 ed, there is an increased risk of developing bronchopulmonary dysplasia, leading to significant respi
178 hyperoxic exposure, a predisposing factor to bronchopulmonary dysplasia, modulates the innate immune
179 sease (n=6), bronchiolitis obliterans (n=2), bronchopulmonary dysplasia (n=1), graft failure due to v
180 , neurodevelopmental outcomes, hearing loss, bronchopulmonary dysplasia, necrotizing enterocolitis, a
181 s were the individual composites of death or bronchopulmonary dysplasia, necrotizing enterocolitis, r
182 ric), a composite of death, brain injury, or bronchopulmonary dysplasia (neonatal), and a standardise
184 on is relevant to clinical disorders such as bronchopulmonary dysplasia of premature babies and lung
188 rrhage, surgery for abdominal complications, bronchopulmonary dysplasia, or retinopathy of prematurit
189 n rates of necrotizing enterocolitis, severe bronchopulmonary dysplasia, or severe cerebral lesions w
190 erences in necrotizing enterocolitis, severe bronchopulmonary dysplasia, or severe cerebral lesions.
191 ate-onset sepsis, necrotizing enterocolitis, bronchopulmonary dysplasia, periventricular leucomalacia
192 alveolar growth-arrested rat lungs mimicking bronchopulmonary dysplasia proliferated less, showed dec
193 or in an array of pulmonary diseases such as bronchopulmonary dysplasia, pulmonary hypertension, and
194 nsplantation include pulmonary hypertension, bronchopulmonary dysplasia, pulmonary vein stenosis, and
195 ate data were available (46.3%), died or had bronchopulmonary dysplasia (relative risk, stratified ac
196 cystic periventricular leukomalacia, severe bronchopulmonary dysplasia, retinopathy of prematurity (
197 ROS-induced diseases of the newborn, such as bronchopulmonary dysplasia, retinopathy of prematurity,
198 erences in death or disability at 24 months, bronchopulmonary dysplasia, retinopathy of prematurity,
199 utcomes, which included perinatal mortality, bronchopulmonary dysplasia, sepsis, intraventricular hae
200 al morbidities (pulmonary hemorrhage, severe bronchopulmonary dysplasia, severe cerebral lesions, and
201 severe necrotizing enterocolitis, infection, bronchopulmonary dysplasia, severe intracranial hemorrha
202 luding severe respiratory distress syndrome, bronchopulmonary dysplasia, severe intraventricular hemo
203 or apnea of prematurity reduces the rates of bronchopulmonary dysplasia, severe retinopathy, and neur
204 not result in a lower risk of physiological bronchopulmonary dysplasia than a control emulsion among
207 such as bronchiolitis, cystic fibrosis, and bronchopulmonary dysplasia, their use is controversial a
210 rval, 0.86 to 1.06; P=0.52), and the rate of bronchopulmonary dysplasia was 60 percent versus 68 perc
213 extremely preterm infants, the incidence of bronchopulmonary dysplasia was lower among those who rec
215 those characteristics of infants developing bronchopulmonary dysplasia were evaluated by masked comp
216 cal cord blood, and blood from newborns with bronchopulmonary dysplasia, were conducted both with and
218 me for premature infants who are at risk for bronchopulmonary dysplasia when it is started between 7
220 chanical ventilation and reduced severity of bronchopulmonary dysplasia without an increase in advers
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