ライフサイエンスコーパス: bronchopulmonary

1 s C) nerve-lung preparation for the study of bronchopulmonary afferent nerve activity in the mouse.

2 or detailed morphologies available for human bronchopulmonary afferent nerves.

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

4 c immunoglobulin (IgE) binding with allergic bronchopulmonary aspergillosis (ABPA) and cystic fibrosi

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

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

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

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

9 Allergic bronchopulmonary aspergillosis (ABPA) is a hypersensitiv

10 Allergic bronchopulmonary aspergillosis (ABPA) is a syndrome seen

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

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

13 Allergic bronchopulmonary aspergillosis (ABPA) is characterized b

14 Although allergic bronchopulmonary aspergillosis (ABPA) leads to deteriora

15 Allergic bronchopulmonary aspergillosis (ABPA) results from the i

16 s observed and those likely to have allergic bronchopulmonary aspergillosis (ABPA) were identified.

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

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

19 irway responses during experimental allergic bronchopulmonary aspergillosis (ABPA).

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

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

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

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

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

25 Allergic bronchopulmonary aspergillosis is a hypersensitivity dis

26 Allergic bronchopulmonary aspergillosis is often difficult to tre

27 Allergic bronchopulmonary aspergillosis is one of the most severe

28 Allergic bronchopulmonary aspergillosis occurs almost exclusively

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

30 The diagnosis of allergic bronchopulmonary aspergillosis relies on criteria first

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

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

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

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

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

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

37 ients with corticosteroid-dependent allergic bronchopulmonary aspergillosis, the addition of itracona

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

39 Four patients had allergic bronchopulmonary aspergillosis.

40 fungal allergic asthma that mimics allergic bronchopulmonary aspergillosis.

41 iteria for corticosteroid-dependent allergic bronchopulmonary aspergillosis.

42 llus fumigatus allergen involved in allergic bronchopulmonary aspergillosis.

43 update and improve the diagnosis of allergic bronchopulmonary aspergillosis.

44 ory tract and cause fungal rhinosinusitis or bronchopulmonary aspergillosis.

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

46 hyper-responsiveness, and an involvement of bronchopulmonary C fibre activation has been suggested.

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

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

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

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

51 Thus, the sensitization of the bronchopulmonary C-fibre endings by chronic exposure to

52 l tobacco smoke increases the sensitivity of bronchopulmonary C-fibre endings, but the physiological

53 sult, in part, from stimulation of the vagal bronchopulmonary C-fibre reflex.

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

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

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

57 e of a defined subtype of the vagal afferent bronchopulmonary C-fibres (conduction velocity < 0.7 ms(

58 in the TRPV1+/+ mice, but failed to activate bronchopulmonary C-fibres in TRPV1-/- animals (n = 10).

59 The sensitivity of the bronchopulmonary C-fibres to the vanilloid receptor 1 (V

60 A total of 83 bronchopulmonary C-fibres were studied.

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

62 in bradykinin and acid-induced activation of bronchopulmonary C-fibres, it is not required for action

63 nient in vitro method for the study of mouse bronchopulmonary C-fibres.

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

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

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

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

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

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

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

71 remature labor and, among VLBW infants, with bronchopulmonary dysplasia (BPD) and chronic lung diseas

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

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

74 th of life are independently associated with bronchopulmonary dysplasia (BPD) and long-term respirato

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

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

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

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

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

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

81 The clinical syndrome of bronchopulmonary dysplasia (BPD) in preterm infants resu

82 Bronchopulmonary dysplasia (BPD) is a chronic lung disea

83 Bronchopulmonary dysplasia (BPD) is a chronic lung disea

84 Bronchopulmonary dysplasia (BPD) is a chronic lung disea

85 Bronchopulmonary dysplasia (BPD) is a chronic respirator

86 Bronchopulmonary dysplasia (BPD) is a common lung diseas

87 Bronchopulmonary dysplasia (BPD) is a frequent complicat

88 Bronchopulmonary dysplasia (BPD) is a major complication

89 Bronchopulmonary dysplasia (BPD) is a prevalent yet poor

90 Bronchopulmonary dysplasia (BPD) is characterized by lif

91 School-age children who survive bronchopulmonary dysplasia (BPD) may have a permanent re

92 Bronchopulmonary dysplasia (BPD) occurs in approximately

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

94 Bronchopulmonary dysplasia (BPD) remains a serious morbi

95 Bronchopulmonary dysplasia (BPD) remains the most common

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

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

98 Bronchopulmonary dysplasia (BPD), a chronic lung disease

99 The etiology of bronchopulmonary dysplasia (BPD), a chronic lung disease

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

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

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

103 significantly to morbidity and mortality in bronchopulmonary dysplasia (BPD), but little is known ab

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

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

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

107 Outcomes included 28-day survival/death, bronchopulmonary dysplasia (BPD), periventricular/intrav

108 lung disease of early infancy, often called bronchopulmonary dysplasia (BPD), remains unclear, partl

109 Bronchopulmonary dysplasia (BPD), the main consequence o

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

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

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

113 cells in inflammatory lung diseases, such as 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 ) are elevated in newborns who later develop bronchopulmonary dysplasia (BPD).

117 vasculature may be an important component of bronchopulmonary dysplasia (BPD).

118 n tracheal aspirates of newborns who develop bronchopulmonary dysplasia (BPD).

119 onged pulmonary inflammation and fibrosis in bronchopulmonary dysplasia (BPD).

120 A borderline viability model of bronchopulmonary dysplasia (BPD)/chronic lung disease of

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

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

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

124 nd immunogenic and may protect children with bronchopulmonary dysplasia against serious RSV disease o

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 2 were decreased in airways of neonates with bronchopulmonary dysplasia and in mice after airway inju

132 crease oxygen demands in these infants, like bronchopulmonary dysplasia and increased oxygen consumpt

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

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

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

136 Evidence suggests that preterm neonates with bronchopulmonary dysplasia and prolonged mechanical vent

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

138 on groups were low-risk VLBW infants without bronchopulmonary dysplasia and term infants (>36 weeks,

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

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

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

142 hoc analyses suggest that rates of death and bronchopulmonary dysplasia are reduced for infants with

143 The primary outcome measure was bronchopulmonary dysplasia at 28 days of age.

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

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

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

147 Secondary outcomes included bronchopulmonary dysplasia at 36 weeks of postmenstrual

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

149 Bronchopulmonary dysplasia based on a clinical definitio

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

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

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

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

154 Early beclomethasone therapy did not prevent bronchopulmonary dysplasia but was associated with lower

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

156 Defining bronchopulmonary dysplasia by the use of oxygen alone is

157 Bronchopulmonary dysplasia continues to be an important

158 Various traditional bronchopulmonary dysplasia criteria based on respiratory

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

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

161 1P in the pathobiological characteristics of bronchopulmonary dysplasia has not been investigated.

162 Infants with a history of prematurity and bronchopulmonary dysplasia have a high risk of asthma an

163 g mesenchymal stromal cell (MSC) therapy for bronchopulmonary dysplasia have been initiated; however,

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

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

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

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

168 Bronchopulmonary dysplasia in premature infants is assoc

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

170 cocorticoids would decrease the frequency of bronchopulmonary dysplasia in premature infants.

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

172 ed nitric oxide reduced the rate of death or bronchopulmonary dysplasia in such infants.

173 Dexamethasone to prevent bronchopulmonary dysplasia in very preterm neonates was

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

175 several morbidities were observed, although bronchopulmonary dysplasia increased.

176 Bronchopulmonary dysplasia is a chronic lung disease obs

177 Bronchopulmonary dysplasia is a chronic lung disease of

178 Bronchopulmonary dysplasia is a chronic lung disease tha

179 Bronchopulmonary dysplasia is a common pulmonary complic

180 Although bronchopulmonary dysplasia is characterized histological

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

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

183 Bronchopulmonary dysplasia of the premature newborn is c

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

185 Bronchopulmonary dysplasia or death prior to 36 weeks' p

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

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

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

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

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

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

192 Bronchopulmonary dysplasia was defined as continuous sup

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

194 The frequency of bronchopulmonary dysplasia was similar in the two groups

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

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

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

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

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

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

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

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

203 One child died of a thoracic tumor and bronchopulmonary dysplasia, and another died of acute my

204 h-risk VLBW infants were diagnosed as having bronchopulmonary dysplasia, and comparison groups were l

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

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

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

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

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

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

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

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

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

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

215 m 50% to 16% (p = 0.002) among children with bronchopulmonary dysplasia, but it increased from 14% to

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

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

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

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

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

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

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

223 Bronchopulmonary dysplasia, family history of asthma, sm

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

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

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

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

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

229 The rates of bronchopulmonary dysplasia, neurodevelopmental outcomes,

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

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

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

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

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

235 nsplantation include pulmonary hypertension, bronchopulmonary dysplasia, pulmonary vein stenosis, and

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

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

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

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

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

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

242 luding severe respiratory distress syndrome, bronchopulmonary dysplasia, severe intraventricular hemo

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

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

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

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

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

248 ng hypotheses about the molecular origins of bronchopulmonary dysplasia.

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

250 irus, airway hyperresponsiveness, and severe bronchopulmonary dysplasia.

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

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

253 weeks of postmenstrual age or survival with bronchopulmonary dysplasia.

254 ponsible for neonatal lung injury leading to bronchopulmonary dysplasia.

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

256 bility to postnatal normoxia, reminiscent of bronchopulmonary dysplasia.

257 2 is also increased in neonates that develop bronchopulmonary dysplasia.

258 00 g does not decrease the rates of death or bronchopulmonary dysplasia.

259 ncidence of pneumonia and the development of bronchopulmonary dysplasia.

260 have been implicated in the pathogenesis of bronchopulmonary dysplasia.

261 ed lung injury using a fetal baboon model of bronchopulmonary dysplasia.

262 nstitutes of Health Collaborative Project on Bronchopulmonary Dysplasia.

263 hma stimulated its use in infants to prevent bronchopulmonary dysplasia.

264 respiratory illness in preterm children with bronchopulmonary dysplasia.

265 eucomalacia, retinopathy of prematurity, and bronchopulmonary dysplasia.

266 arance of phenotypical changes suggestive of bronchopulmonary dysplasia.

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

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

269 A composite of death or bronchopulmonary dysplasia.

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

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

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

273 We examined the effects of bronchopulmonary infection on mice homozygous for the S4

274 Because animal models of chronic bronchopulmonary infection with P. aeruginosa used to st

275 ntimicrobial peptides in the pathogenesis of bronchopulmonary infections in cystic fibrosis appeared.

276 oted in the incidence of bacterial or fungal bronchopulmonary infections.

277 lopathies, Goodpasture's syndrome, and acute bronchopulmonary infections.

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

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

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

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

282 These data demonstrate that in the mouse bronchopulmonary model, adaptive immunity to S. flexneri

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

284 Allergic bronchopulmonary mycosis (ABPM) is a hypersensitivity lu

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

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

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

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

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

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

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

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

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

294 ss the safety and tolerability of sequential bronchopulmonary segmental lavage with a dilute syntheti

295 Bronchopulmonary segmental lavage with Surfaxin (KL(4)-s

296 Individual bronchopulmonary segments were labeled voxel by voxel fr

297 via a wedged bronchoscope to each of the 19 bronchopulmonary segments.

298 cystic adenomatoid malformation [CCAM], two bronchopulmonary sequestration [BPS]).

299 hways and immune responses in BALT and other bronchopulmonary tissues.

300 estines, lungs, and lymph nodes draining the bronchopulmonary tree and oral cavity.