ライフサイエンスコーパス: bronchopulmonary

1 or detailed morphologies available for human bronchopulmonary afferent nerves.

2 ient mice were subjected to a mouse model of bronchopulmonary allergy to assess the impact of C5 on p

3 in systemic vessels and the possible role of bronchopulmonary anastomoses in the development of plexo

4 ers are the key to the diagnosis of allergic bronchopulmonary aspergillosis (ABPA) and fungal sensiti

5 ent of atopic lung diseases such as allergic bronchopulmonary aspergillosis (ABPA) and severe asthma

6 onance (MR) imaging to discriminate allergic bronchopulmonary aspergillosis (ABPA) in cystic fibrosis

7 pulmonary aspergillosis (CCPA) and allergic bronchopulmonary aspergillosis (ABPA) in overtly immunoc

8 Allergic bronchopulmonary aspergillosis (ABPA) is caused by a dom

9 Allergic bronchopulmonary aspergillosis (ABPA) is caused by A fum

10 Allergic bronchopulmonary aspergillosis (ABPA) is characterized b

11 Although allergic bronchopulmonary aspergillosis (ABPA) leads to deteriora

12 Allergic bronchopulmonary aspergillosis (ABPA) results from the i

13 se A fumigatus sensitization and/or allergic bronchopulmonary aspergillosis (ABPA), which affects pul

14 cystic fibrosis (CF) patients with allergic bronchopulmonary aspergillosis (ABPA).

15 Bronchopulmonary aspergillosis (n = 16), severe asthma w

16 Allergic bronchopulmonary aspergillosis (odds ratio [OR], 2.66; P

17 ; only 388 patients were tested for allergic bronchopulmonary aspergillosis and 82 patients had been

18 The best understood conditions are allergic bronchopulmonary aspergillosis and severe asthma with fu

19 ions of inhaled Aspergillus include allergic bronchopulmonary aspergillosis and severe asthma with fu

20 mised individuals but also triggers allergic bronchopulmonary aspergillosis in a subset of otherwise

21 migatus is commonly associated with allergic bronchopulmonary aspergillosis in patients with severe a

22 Allergic bronchopulmonary aspergillosis is often difficult to tre

23 Allergic bronchopulmonary aspergillosis is one of the most severe

24 Allergic bronchopulmonary aspergillosis occurs almost exclusively

25 methylprednisolone in patients with allergic bronchopulmonary aspergillosis or cystic fibrosis are am

26 The diagnosis of allergic bronchopulmonary aspergillosis relies on criteria first

27 IgE/IgG, and positive GM (serologic allergic bronchopulmonary aspergillosis); class 3 (n = 19, 14.6%)

28 to A. fumigatus spores also causes allergic bronchopulmonary aspergillosis, a Th2 CD4+-T-cell-mediat

29 s triggering factors (e.g., asthma, allergic bronchopulmonary aspergillosis, and chronic obstructive

30 in the treatment of asthma, croup, allergic bronchopulmonary aspergillosis, and subglottic hemangiom

31 Aspergillus fumigatus may result in allergic bronchopulmonary aspergillosis, chronic necrotizing pulm

32 reviously reported that in a murine model of bronchopulmonary aspergillosis, maternal exposure to mai

33 ty responses to Aspergillus, beyond allergic bronchopulmonary aspergillosis, which require classifica

34 rgillosis, fungal colonization, and allergic bronchopulmonary aspergillosis.

35 update and improve the diagnosis of allergic bronchopulmonary aspergillosis.

36 ory tract and cause fungal rhinosinusitis or bronchopulmonary aspergillosis.

37 Four patients had allergic bronchopulmonary aspergillosis.

38 fungal allergic asthma that mimics allergic bronchopulmonary aspergillosis.

39 cellular recording preparation of individual bronchopulmonary C fibers in the mouse.

40 t an increase in temperature activates vagal bronchopulmonary C-fiber sensory nerves, which upon acti

41 Prolongation of bronchopulmonary C-fiber-mediated apnea by prenatal nico

42 cotinic exposure (PNE) reportedly sensitizes bronchopulmonary C-fibers (PCFs) and prolongs PCF-mediat

43 triction, resulting from activation of vagal bronchopulmonary C-fibers and Adelta afferents.

44 tial firing from the terminals of individual bronchopulmonary C-fibers using a mouse ex vivo lung-vag

45 ted TRPA1-expressing "nociceptor-like" mouse bronchopulmonary C-fibers.

46 The activation of mouse bronchopulmonary C-fibre terminals by 4ONE (10-100 micro

47 tential discharge or tachykinin release from bronchopulmonary C-fibre terminals.

48 ential discharge and tachykinin release from bronchopulmonary C-fibre terminals.

49 red a pronounced stimulatory effect on vagal bronchopulmonary C-fibres in anaesthetized rats.

50 Single-unit activities of bronchopulmonary C-fibres in response to inhalation chal

51 ronchoconstriction, and stimulation of vagal bronchopulmonary C-fibres is primarily responsible.

52 t the stimulatory effect of inhaled SO(2) on bronchopulmonary C-fibres was generated by acidification

53 g capsaicin-sensitive TRPV1-expressing vagal bronchopulmonary C-fibres, and are activated by electrop

54 T2 responses characteristic of the allergic bronchopulmonary C. neoformans infection.

55 itric oxide therapy reduced the incidence of bronchopulmonary dysplasia (29.8 percent vs. 59.6 percen

56 ta were available, 191 died or survived with bronchopulmonary dysplasia (38.4%), as compared with 180

57 risk difference, -3.3 to 4.5; P = .70), and bronchopulmonary dysplasia (4.4% vs 5.1%; 95% CI of risk

58 itis (48.1%, 37.1%, and 32.5%), and death or bronchopulmonary dysplasia (74.9%, 68.9%, and 65.5%).

59 61.6%) in the placebo group survived without bronchopulmonary dysplasia (absolute difference, -5.0% [

60 ased odds of a composite outcome of death or bronchopulmonary dysplasia (adjusted odds ratio [AOR], 0

61 The primary outcome was bronchopulmonary dysplasia (BPD) among survivors.

62 tion damage resulting in a high incidence of bronchopulmonary dysplasia (BPD) and chronic respiratory

63 decreased capillary density in infants with bronchopulmonary dysplasia (BPD) and in BPD-like animal

64 Preterm infants with bronchopulmonary dysplasia (BPD) and pulmonary hypertens

65 y, are associated with an increased risk for bronchopulmonary dysplasia (BPD) and pulmonary hypertens

66 k factors associated with increased risk for bronchopulmonary dysplasia (BPD) and respiratory disease

67 Bronchopulmonary dysplasia (BPD) and retinopathy of prem

68 o associate two key antecedent risk factors, bronchopulmonary dysplasia (BPD) and retinopathy of prem

69 st week of life reduces the rate of death or bronchopulmonary dysplasia (BPD) but may cause long-term

70 Autopsied lungs of infants with bronchopulmonary dysplasia (BPD) demonstrate impaired al

71 neonatologists on the role of Ureaplasma in bronchopulmonary dysplasia (BPD) development, the use of

72 emature infants and changed the pathology of bronchopulmonary dysplasia (BPD) from one of acute lung

73 cigarette smoke increases the risk of AA and bronchopulmonary dysplasia (BPD) in children and animal

74 is a key contributor to the pathogenesis of bronchopulmonary dysplasia (BPD) in neonates, for which

75 Systemic sepsis is a known risk factor for bronchopulmonary dysplasia (BPD) in premature infants, a

76 Bronchopulmonary dysplasia (BPD) is a chronic disease of

77 Bronchopulmonary dysplasia (BPD) is a chronic lung disea

78 Bronchopulmonary dysplasia (BPD) is a chronic respirator

79 Bronchopulmonary dysplasia (BPD) is a common lung diseas

80 Bronchopulmonary dysplasia (BPD) is a disease prevalent

81 Bronchopulmonary dysplasia (BPD) is a frequent complicat

82 Rationale: Bronchopulmonary dysplasia (BPD) is a leading complicati

83 Bronchopulmonary dysplasia (BPD) is a major complication

84 Bronchopulmonary dysplasia (BPD) is a prevalent yet poor

85 Bronchopulmonary dysplasia (BPD) is characterized by lif

86 Bronchopulmonary dysplasia (BPD) occurs in approximately

87 ith Ureaplasma parvum is causally related to bronchopulmonary dysplasia (BPD) or adverse respiratory

88 Bronchopulmonary dysplasia (BPD) remains a major respira

89 Bronchopulmonary dysplasia (BPD) remains a serious morbi

90 Bronchopulmonary dysplasia (BPD) remains the most common

91 dysfunction is strongly associated with high bronchopulmonary dysplasia (BPD) risk in preterm infants

92 r example, we have shown in a mouse model of bronchopulmonary dysplasia (BPD) that mesenchymal stem c

93 levels are elevated in newborns that develop bronchopulmonary dysplasia (BPD), a chronic lung disease

94 Bronchopulmonary dysplasia (BPD), a chronic lung disease

95 s a major contributor to the pathogenesis of bronchopulmonary dysplasia (BPD), a chronic lung disease

96 vents normal lung morphogenesis and leads to bronchopulmonary dysplasia (BPD), a common complication

97 The pathogenesis of bronchopulmonary dysplasia (BPD), a devastating lung dis

98 ck of Pdgfra arrested alveologenesis akin to bronchopulmonary dysplasia (BPD), a neonatal chronic lun

99 e and chronic pulmonary disorders, including bronchopulmonary dysplasia (BPD), a respiratory conditio

100 s associated with a high risk for developing bronchopulmonary dysplasia (BPD), but its relationship w

101 ith poor outcomes among preterm infants with bronchopulmonary dysplasia (BPD), but whether early sign

102 term complications of prematurity, including bronchopulmonary dysplasia (BPD), cause mortality and mo

103 evelop a chronic form of lung disease called bronchopulmonary dysplasia (BPD), characterized by decre

104 and worsened respiratory outcomes, including bronchopulmonary dysplasia (BPD), in preterm infants.

105 Bronchopulmonary dysplasia (BPD), the main consequence o

106 re during gestation may increase the risk of bronchopulmonary dysplasia (BPD)-a developmental lung co

107 Bronchopulmonary dysplasia (BPD)-associated pulmonary hy

108 Rationale: Patients with bronchopulmonary dysplasia (BPD)-associated pulmonary hy

109 ematurity suffering the most severe forms of bronchopulmonary dysplasia (BPD).

110 ality of chronic lung disease of infancy, or bronchopulmonary dysplasia (BPD).

111 ogenesis, leading to chronic lung disease or Bronchopulmonary dysplasia (BPD).

112 cells in inflammatory lung diseases, such as bronchopulmonary dysplasia (BPD).

113 -ALRI in children less than 5 years old with bronchopulmonary dysplasia (BPD).

114 s have long sought preventive treatments for bronchopulmonary dysplasia (BPD).

115 inhibition of lung growth that characterizes bronchopulmonary dysplasia (BPD).

116 h severe pediatric lung disorders, including bronchopulmonary dysplasia (BPD).

117 ies associated with preterm birth, including bronchopulmonary dysplasia (BPD).

118 athways in three pulmonary diseases (asthma; bronchopulmonary dysplasia (BPD); and chronic obstructiv

119 Length of stay increased with bronchopulmonary dysplasia (BPD; 1.77), whereas total co

120 ften develop chronic lung dysfunction termed bronchopulmonary dysplasia (BPD; also known as chronic l

121 ric), a composite of death, brain injury, or bronchopulmonary dysplasia (neonatal), and a standardise

122 ate data were available (46.3%), died or had bronchopulmonary dysplasia (relative risk, stratified ac

123 neutrophil-driven disease of ECM remodeling (bronchopulmonary dysplasia [BPD]).

124 ria that best predicted this outcome defined bronchopulmonary dysplasia according to treatment with t

125 achypnea of the newborn, surfactant use, and bronchopulmonary dysplasia also occurred significantly l

126 emic glucocorticoids reduce the incidence of bronchopulmonary dysplasia among extremely preterm infan

127 tive lung vascular development can result in bronchopulmonary dysplasia and alveolar capillary dyspla

128 premature infants is a major risk factor for bronchopulmonary dysplasia and can impair the host respo

129 orn and developmental lung diseases, such as bronchopulmonary dysplasia and congenital diaphragmatic

130 Bronchopulmonary dysplasia and emphysema are life-threat

131 iciously, weighing up the competing risks of bronchopulmonary dysplasia and neurodevelopmental harm.

132 ed with a reduction in the rates of death or bronchopulmonary dysplasia and patent ductus arteriosus.

133 cted), independent of degree of prematurity, bronchopulmonary dysplasia and postnatal sepsis.

134 may explain the complex relationship between bronchopulmonary dysplasia and retinopathy of prematurit

135 d from EP subjects with and without neonatal bronchopulmonary dysplasia and term-born control subject

136 ns of systemic dexamethasone used to prevent bronchopulmonary dysplasia and thus more restricted use,

137 Several definitions of bronchopulmonary dysplasia are clinically used; however,

138 Measures to reduce bronchopulmonary dysplasia are not always effective or h

139 The primary outcome was survival without bronchopulmonary dysplasia at 36 weeks of postmenstrual

140 The rate of survival without bronchopulmonary dysplasia at 36 weeks of postmenstrual

141 efficacy outcome was a composite of death or bronchopulmonary dysplasia at 36 weeks of postmenstrual

142 The combined outcome of death or bronchopulmonary dysplasia at 36 weeks' postmenstrual ag

143 Bronchopulmonary dysplasia based on a clinical definitio

144 ated no difference in death or survival with bronchopulmonary dysplasia between nasal intermittent po

145 cant difference in the incidence of death or bronchopulmonary dysplasia between patients receiving in

146 no significant difference in the outcome of bronchopulmonary dysplasia but a potential reduction in

147 as been reported to improve survival without bronchopulmonary dysplasia but its safety with regard to

148 al lung macrophage activation contributes to bronchopulmonary dysplasia by generating a localized inf

149 Defining bronchopulmonary dysplasia by the use of oxygen alone is

150 Bronchopulmonary dysplasia continues to be an important

151 Various traditional bronchopulmonary dysplasia criteria based on respiratory

152 val to 36 weeks of postmenstrual age without bronchopulmonary dysplasia did not differ significantly

153 present in the lungs of patients developing bronchopulmonary dysplasia disrupt expression of multipl

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 ary dysplasia.Conclusions: Most infants with bronchopulmonary dysplasia have impaired oxygenation qua

158 ted to the respiratory distress syndrome and bronchopulmonary dysplasia in 2008-2011 than in 2000-200

159 e Hydrocortisone to Improve Survival without Bronchopulmonary Dysplasia in Extremely Preterm Infants)

160 e were seen from birth to the development of bronchopulmonary dysplasia in extremely preterm infants.

161 To reduce the risk of bronchopulmonary dysplasia in extremely-low-birth-weight

162 ith the alveolar simplification phenotype of bronchopulmonary dysplasia in premature human infants an

163 Bronchopulmonary dysplasia in premature infants is assoc

164 nagement strategy to decrease morbidity from bronchopulmonary dysplasia in premature infants.

165 and blunted lung development associated with bronchopulmonary dysplasia in preterm infants.

166 Dexamethasone to prevent bronchopulmonary dysplasia in very preterm neonates was

167 Rates of other morbidities declined, but bronchopulmonary dysplasia increased between 2009 and 20

168 several morbidities were observed, although bronchopulmonary dysplasia increased.

169 eased and V . a/Q . decreased as severity of bronchopulmonary dysplasia increased.

170 Bronchopulmonary dysplasia is a chronic lung disease obs

171 Bronchopulmonary dysplasia is a chronic lung disease of

172 Bronchopulmonary dysplasia is a chronic lung disease tha

173 Bronchopulmonary dysplasia is a common pulmonary complic

174 Rationale: Bronchopulmonary dysplasia is a heterogeneous lung disea

175 Although bronchopulmonary dysplasia is characterized histological

176 e use of this therapy in infants at risk for bronchopulmonary dysplasia is controversial.

177 occurred in 20/492 (4.1%) vs 28/518 (5.4%); bronchopulmonary dysplasia occurred in 130/458 (28.4%) v

178 Bronchopulmonary dysplasia occurred in 41.7% of survivin

179 on is relevant to clinical disorders such as bronchopulmonary dysplasia of premature babies and lung

180 Bronchopulmonary dysplasia of the premature newborn is c

181 The composite outcome of physiological bronchopulmonary dysplasia or death before 36 weeks of p

182 Bronchopulmonary dysplasia or death prior to 36 weeks' p

183 es are seen in airway samples and blood from bronchopulmonary dysplasia patients, the innate immune r

184 alveolar growth-arrested rat lungs mimicking bronchopulmonary dysplasia proliferated less, showed dec

185 Rationale: Current diagnostic criteria for bronchopulmonary dysplasia rely heavily on the level and

186 not result in a lower risk of physiological bronchopulmonary dysplasia than a control emulsion among

187 al impairment.Conclusions: The definition of bronchopulmonary dysplasia that best predicted early chi

188 To identify the optimal definition of bronchopulmonary dysplasia that best predicts respirator

189 h of 18 prespecified, revised definitions of bronchopulmonary dysplasia that variably define disease

190 ased stepwise from 10% among infants without bronchopulmonary dysplasia to 77% among those with grade

191 exchange in preterm infants with and without bronchopulmonary dysplasia to grade disease severity and

192 The incidence of bronchopulmonary dysplasia was 27.8% in the budesonide g

193 rval, 0.86 to 1.06; P=0.52), and the rate of bronchopulmonary dysplasia was 60 percent versus 68 perc

194 The rate of death or bronchopulmonary dysplasia was 80 percent in the nitric

195 Bronchopulmonary dysplasia was defined as continuous sup

196 extremely preterm infants, the incidence of bronchopulmonary dysplasia was lower among those who rec

197 izing enterocolitis, systemic infections and bronchopulmonary dysplasia were associated with altered

198 sedated, quiet-breathing infants with severe bronchopulmonary dysplasia were reconstructed into end-i

199 ther species between infants with or without bronchopulmonary dysplasia when isolated alone.

200 me for premature infants who are at risk for bronchopulmonary dysplasia when it is started between 7

201 chanical ventilation and reduced severity of bronchopulmonary dysplasia without an increase in advers

202 A sensitive outcome measure for infants with bronchopulmonary dysplasia would facilitate clinical ben

203 evere, acute respiratory distress; this "new bronchopulmonary dysplasia" could be the result of impai

204 selected cohorts (eg, only participants with bronchopulmonary dysplasia) or in which few participants

205 fants with established chronic lung disease (bronchopulmonary dysplasia).

206 inopathy of prematurity stage 3-5, or severe bronchopulmonary dysplasia).

207 cumulate in the lungs of infants with severe bronchopulmonary dysplasia, a chronic lung disease assoc

208 posure to inflammation increases the risk of bronchopulmonary dysplasia, a chronic, developmental lun

209 Premature infants are at risk for bronchopulmonary dysplasia, a complex condition characte

210 nsufficient generation of alveoli results in bronchopulmonary dysplasia, a disease of prematurity.

211 ciated with a lower likelihood of developing bronchopulmonary dysplasia, a sequelae of RDS (p<0.03).

212 rtality, enlarged alveolar spaces resembling bronchopulmonary dysplasia, and altered expression of ge

213 th respiratory distress syndromes, including bronchopulmonary dysplasia, and differential gene expres

214 y hypertension in pediatric diseases such as bronchopulmonary dysplasia, and increasingly expanding d

215 g enterocolitis, retinopathy of prematurity, bronchopulmonary dysplasia, and intraventricular hemorrh

216 pulmonary disease, asthma, cystic fibrosis, bronchopulmonary dysplasia, and muscular dystrophies.

217 idities such as intraventricular hemorrhage, bronchopulmonary dysplasia, and necrotizing enterocoliti

218 m, briefly explore pulmonary hypertension in bronchopulmonary dysplasia, and provide updates on the d

219 iratory parameters were worse after neonatal bronchopulmonary dysplasia, and respiratory function dif

220 ing arrested alveolar growth in experimental bronchopulmonary dysplasia, and that exogenous ECFCs res

221 ion) were classified as having physiological bronchopulmonary dysplasia, as compared with 269 (43.9%)

222 mon aspects in the genetic predisposition to bronchopulmonary dysplasia, bronchiolitis, and childhood

223 turated fatty acid, might reduce the risk of bronchopulmonary dysplasia, but appropriately designed t

224 enoic acid (DHA) supplementation may prevent bronchopulmonary dysplasia, but evidence remains inconcl

225 ted ventilation and reduces the incidence of bronchopulmonary dysplasia, but its effects on respirato

226 Arrested lung development leads to bronchopulmonary dysplasia, but the molecular pathways t

227 Premature infants with bronchopulmonary dysplasia, characterized by interrupted

228 The primary outcome was death or bronchopulmonary dysplasia, confirmed by means of standa

229 olar enlargement, which is characteristic of bronchopulmonary dysplasia, congenital matrix disorders,

230 function and morphology in animal models of bronchopulmonary dysplasia, creating a rationale for cli

231 The primary outcome was bronchopulmonary dysplasia, defined on a physiological b

232 xide did not reduce the overall incidence of bronchopulmonary dysplasia, except among infants with a

233 bidities such as retinopathy of prematurity, bronchopulmonary dysplasia, injury to the developing bra

234 ed, there is an increased risk of developing bronchopulmonary dysplasia, leading to significant respi

235 hyperoxic exposure, a predisposing factor to bronchopulmonary dysplasia, modulates the innate immune

236 , neurodevelopmental outcomes, hearing loss, bronchopulmonary dysplasia, necrotizing enterocolitis, a

237 s were the individual composites of death or bronchopulmonary dysplasia, necrotizing enterocolitis, r

238 The rates of bronchopulmonary dysplasia, neurodevelopmental outcomes,

239 dless of prior or current oxygen therapy: no bronchopulmonary dysplasia, no support (n = 773); grade

240 morrhage, sepsis, necrotizing enterocolitis, bronchopulmonary dysplasia, or death or in the frequency

241 rrhage, surgery for abdominal complications, bronchopulmonary dysplasia, or retinopathy of prematurit

242 n rates of necrotizing enterocolitis, severe bronchopulmonary dysplasia, or severe cerebral lesions w

243 erences in necrotizing enterocolitis, severe bronchopulmonary dysplasia, or severe cerebral lesions.

244 ate-onset sepsis, necrotizing enterocolitis, bronchopulmonary dysplasia, periventricular leucomalacia

245 or in an array of pulmonary diseases such as bronchopulmonary dysplasia, pulmonary hypertension, and

246 cystic periventricular leukomalacia, severe bronchopulmonary dysplasia, retinopathy of prematurity (

247 erences in death or disability at 24 months, bronchopulmonary dysplasia, retinopathy of prematurity,

248 ROS-induced diseases of the newborn, such as bronchopulmonary dysplasia, retinopathy of prematurity,

249 utcomes, which included perinatal mortality, bronchopulmonary dysplasia, sepsis, intraventricular hae

250 al morbidities (pulmonary hemorrhage, severe bronchopulmonary dysplasia, severe cerebral lesions, and

251 severe necrotizing enterocolitis, infection, bronchopulmonary dysplasia, severe intracranial hemorrha

252 or apnea of prematurity reduces the rates of bronchopulmonary dysplasia, severe retinopathy, and neur

253 When adjusted for bronchopulmonary dysplasia, the difference in flow rates

254 such as bronchiolitis, cystic fibrosis, and bronchopulmonary dysplasia, their use is controversial a

255 cal cord blood, and blood from newborns with bronchopulmonary dysplasia, were conducted both with and

256 tional involvement of pulmonary apoptosis in bronchopulmonary dysplasia- associated alveolar disrupti

257 eonatal period did not significantly improve bronchopulmonary dysplasia-free survival at 36 weeks' po

258 The primary outcome was bronchopulmonary dysplasia-free survival in infants at 3

259 arance of phenotypical changes suggestive of bronchopulmonary dysplasia.

260 TGF-beta signaling, ultimately resulting in bronchopulmonary dysplasia.

261 nistration did not alter the early course of bronchopulmonary dysplasia.

262 A composite of death or bronchopulmonary dysplasia.

263 how to prevent fetal lung injury leading to bronchopulmonary dysplasia.

264 ng hypotheses about the molecular origins of bronchopulmonary dysplasia.

265 atory syncytial virus infection, asthma, and bronchopulmonary dysplasia.

266 irus, airway hyperresponsiveness, and severe bronchopulmonary dysplasia.

267 atory syncytial virus infection, asthma, and bronchopulmonary dysplasia.

268 ed lung injury in a murine neonatal model of bronchopulmonary dysplasia.

269 ctly contribute to disrupted angiogenesis in bronchopulmonary dysplasia.

270 weeks of postmenstrual age or survival with bronchopulmonary dysplasia.

271 ponsible for neonatal lung injury leading to bronchopulmonary dysplasia.

272 ficant difference in the outcome of death or bronchopulmonary dysplasia.

273 bility to postnatal normoxia, reminiscent of bronchopulmonary dysplasia.

274 2 is also increased in neonates that develop bronchopulmonary dysplasia.

275 secondary outcomes, including mortality and bronchopulmonary dysplasia.

276 ng factor in neonatal lung injury leading to bronchopulmonary dysplasia.

277 are prone to lung injury that may result in bronchopulmonary dysplasia.

278 a/Q . , and shunt to preterm infants without bronchopulmonary dysplasia.

279 sitive and specific index of the severity of bronchopulmonary dysplasia.Conclusions: Most infants wit

280 Severe bronchopulmonary dysplasia/death rates at 36 weeks' post

281 atory syncytial virus infection, asthma, and bronchopulmonary dysplasia; and genotyped and analyzed i

282 glycaemia, and one (3%) patient with grade 2 bronchopulmonary haemorrhage.

283 , and vascular cell adhesion molecule in the bronchopulmonary LNs and large airways of asthmatic pati

284 adhesion molecule 1 in the large airways and bronchopulmonary LNs of 11 nonsmokers who died from an a

285 osition of different cell populations in the bronchopulmonary LNs of asthmatic patients.

286 ease in the expression of these cells in the bronchopulmonary LNs.

287 tamibi and immunohistochemical expression of bronchopulmonary multidrug resistance protein 1 (MRP1) a

288 Allergic bronchopulmonary mycosis (ABPM) is a hypersensitivity lu

289 t infection with characteristics of allergic bronchopulmonary mycosis (ABPM).

290 ABPA is the most common form of allergic bronchopulmonary mycosis (ABPM); other fungi, including

291 C57BL/6 mice develop an allergic bronchopulmonary mycosis following intratracheal inocula

292 stological analysis revealed severe allergic bronchopulmonary mycosis pathology in H99-infected mice

293 mice is an established model of an allergic bronchopulmonary mycosis that has also been used to test

294 mice is an established model of an allergic bronchopulmonary mycosis.

295 the infection, i.e., a model of an allergic bronchopulmonary mycosis.

296 tential discharge in a subset of nociceptive bronchopulmonary nerves, namely slow conducting C-fibres

297 G-CSFR(-/-) mice are markedly susceptible to bronchopulmonary P aeruginosa infection, exhibiting decr

298 Individual bronchopulmonary segments were labeled voxel by voxel fr

299 obtained from studies in isolated rat vagal bronchopulmonary sensory neurones and also in the cough

300 lated events affecting the cardiovascular or bronchopulmonary system, and chemotherapy or immunosuppr