ライフサイエンスコーパス: bronchial

1 e expression signature of IL-17A response in bronchial airway epithelial brushings from smokers with

2 ) overlap (ACO) represents the confluence of bronchial airway hyperreactivity and chronic airflow lim

3 creased invasion of, and persistence within, bronchial alveolar epithelial cells.

4 Rhinoceros bronchial alveolar lavage fluid (BALF) was found to have

5 ription factors Stat1 and Rorc Additionally, bronchial alveolar lavage fluid from infected IL-8R2-def

6 Bronchial alveolar lavage, blood, and lung samples were

7 The provocation test was positive in 95% of bronchial and 90% of conjunctival challenges in cases, a

8 To conclude, we show increased bronchial and alveolar ACE2 protein expression in patien

9 6.6% +/- 5.5% reduction in invasion of human bronchial and alveolar epithelial cells at 1, 3, and 6 h

10 n Results: DSP is expressed predominantly in bronchial and alveolar epithelial cells, with reduced ex

11 d response on physiologically relevant human bronchial and alveolar lung mucosa models cultured at ai

12 ve higher ROS concentrations compared to the bronchial and alveolar regions.

13 Airway epithelial cells were obtained from bronchial and bronchiolar brushing performed under radio

14 tance at the cell surface of patient-derived bronchial and nasal epithelial cultures.

15 es 5 (16%) and 6 (14%): high level of nasal, bronchial and ocular symptoms with nasal impairment (non

16 ed using either the BACS approach, where the bronchial and pulmonary arteries were synchronously perf

17 COPD patients compared to controls in nasal, bronchial and small airways brushings.

18 Both systemic (tracheal and bronchial) and pulmonary circulations perfuse the lung.

19 avated mucus production, peri-vascular, peri-bronchial, and allergic inflammation that was unresponsi

20 Viral RNA was detectable in pharyngeal, bronchial, and colonic mucosa but not bile.

21 ed microvasculature resulting from disrupted bronchial arterial circulation appears to trigger chroni

22 We recently developed a bronchial-arterial-circulation-sparing (BACS) lung prese

23 included Rasmussen aneurysms (4%), enlarged bronchial arteries (3%), and systemic bronchial collater

24 s of the vasa vasorum, which are branches of bronchial arteries, is seen in the walls of large pulmon

25 f feasible, must always be considered before bronchial artery embolisation because it precisely ident

26 circumvents chances of re-bleed if standard bronchial artery embolisation is done without CTBA.

27 differences in surgical technique, including bronchial artery revascularization, for incorporation in

28 COVID-19 correlated with lower viral load in bronchial aspirates and faster viral clearance and a hig

29 idly formed highly organized and distinctive Bronchial Associated Lymphoid Tissue (BALT) not induced

30 Evidences have shown that bronchial asthma (BA) enhances the risk of pulmonary thr

31 Atopic dermatitis and bronchial asthma are common diseases in children.

32 The diagnosis was bronchial asthma associated with bronchiolitis.

33 In intractable bronchial asthma cases, it is necessary to consider the

34 Any mother with a child diagnosed with bronchial asthma for more than 3 months, and who attende

35 ase of a 17-year-old woman with a history of bronchial asthma since two years of age.

36 idered to reflect VCD, and the treatment for bronchial asthma was stepped down without any recurrence

37 ds are used for a long time in patients with bronchial asthma, a decrease in adrenal cortex function

38 e has been suffering from atopic dermatitis, bronchial asthma, and food allergies since childhood.

39 dermatitis, diagnosed at 1 year of age, and bronchial asthma, diagnosed at 4 years of age.

40 Hereby, Asm(-/-) animals are protected from bronchial asthma, which possibly offers novel therapeuti

41 FM) was evaluated in pediatric patients with bronchial asthma.

42 noted in management of atopic dermatitis and bronchial asthma.

43 les are considered as an emerging target for bronchial asthma.

44 the role of ASM in T(H) 2-regulated allergic bronchial asthma.

45 rm and extend our previous report of reduced bronchial bacterial burden and compositional complexity

46 al efficiency was analyzed in infected human bronchial BEAS-2B cells and ex vivo-cultured human sinon

47 To study IL-17-related cytokines in nasal/bronchial biopsies from controls and mild asthmatics (MA

48 We analyzed the transcriptomic data from bronchial biopsies of 81 patients with moderate-to-sever

49 sed p53 mediated apoptosis was replicated in bronchial biopsies of COPD patients.

50 IL33 levels are elevated in sputum and bronchial biopsies of patients with asthma.

51 Asthmatic bronchial biopsies were immunostained for CD48.

52 Human bronchial biopsies were stained for cholinergic marker v

53 IL-33 and receptor ST2 were investigated in bronchial biopsies.

54 was performed by using epithelial brushings, bronchial biopsy specimens (91 asthmatic patients and 46

55 5, and retinoic acid-inducible protein I in bronchial biopsy specimens from 10 atopic asthmatic pati

56 anced mesenchymal signatures are observed in bronchial biopsy specimens from patients with allergic a

57 nalysis, and immunohistochemical analysis of bronchial biopsy specimens.

58 uivalence of VFA levels within the mixed and bronchial breath of cancer patients suggests that their

59 including analysis of mixed breath, isolated bronchial breath, and gastric-endoluminal air.

60 Compared with mixed- and bronchial-breath samples, all examined VFAs were found i

61 In bronchial brush isolated AECs, 849 differentially methyl

62 of any difference in the mutational load of bronchial brush samples between former smoking COPD case

63 signals are expression quantitative loci in bronchial brushes and cultured HBECs, but not in lung ti

64 IL1RL1 gene expression in bronchial brushes was not different between health and d

65 nd between SNPs and expression (lung tissue, bronchial brushes, HBECs) was done using regression mode

66 ) and associates with viral load measured in bronchial brushes.

67 digestion (9 non-asthmatic, 8 asthmatic) and bronchial brushings (7 non-asthmatic and 9 asthmatic).

68 d primary bronchial epithelial cells and the bronchial brushings from human subjects express canonica

69 cal characteristics and gene expression from bronchial brushings in COPD and asthma.

70 In bronchial brushings Toll-like receptor pathway genes wer

71 We ran linear regression analysis of the bronchial brushings transcriptional signal versus blood

72 In addition, bronchial brushings were also obtained from healthy cont

73 alyses revealed an elevated risk of lung and bronchial cancer (n = 808 deaths; for >12.1 ppm-year vs.

74 set, cohort predominates for female lung and bronchial cancer and period predominates for male prosta

75 and End Results data (1975-2014) on lung and bronchial cancer mortality in females and prostate and c

76 We report that H727 human bronchial carcinoid cells are inherently resistant to Cf

77 criptomic datasets of hypercapnia in a human bronchial cell line, flies and nematodes.

78 -activating protease of IAV in primary human bronchial cells and of both IAV and IBV in primary human

79 olves a dynamic co-evolution of pre-invasive bronchial cells and the immune response.

80 mented(6-10), but equivalent data for normal bronchial cells are lacking.

81 ut were followed up clinically with repeated bronchial challenge tests over 1 year.

82 We identified bronchial ciliated cells and type II alveolar cells as a

83 breakdown, increased anastomosis within the bronchial circulation, and perivascular inflammation.

84 ysis, TAE of the BAA and of the pathological bronchial circulation, in association with the treatment

85 ion (TAE) of the BAA and of the pathological bronchial circulation.

86 larged bronchial arteries (3%), and systemic bronchial collaterals in 1% of our patients.

87 probable IA (n = 2), possible IA (n = 1), or bronchial colonization (n = 6).

88 Bronchial computed tomography angiography (CTBA), if fea

89 The Proliferative subtype is enriched with bronchial dysplasia and exhibits up-regulation of metabo

90 sue culture to build an organotypic model of bronchial dysplasia.

91 ia co-expressed p120-3 and p120-1, including bronchial epithelia and mammary luminal epithelial cells

92 colocalization with CFTR in CF human primary bronchial epithelia by proximity ligation assay, immunop

93 while deleterious effects were observed when bronchial epithelia were exposed to cysteamine plus the

94 e epithelium is disrupted (e.g. wounded skin/bronchial epithelia) and where T cells frequently are pr

95 ithelial cells in the renal tubules), lungs (bronchial epithelia), thymus (epithelial cells inside th

96 lergens induce the release of ATP from human bronchial epithelial (HBE) cells by activating a conduct

97 Human bronchial epithelial (HBE) cells exposed to allergens de

98 ectively blocks aberrant splicing in primary bronchial epithelial (hBE) cells from CF patients with t

99 hannel activity and anion secretion in human bronchial epithelial (HBE) cells from patients with CF w

100 airways in vivo and in differentiated human bronchial epithelial (HBE) cells grown at air-liquid int

101 -1alpha and IL-1beta stimulated non-CF human bronchial epithelial (HBE) cells to upregulate and secre

102 (PM), promoting Cl(-) secretion across human bronchial epithelial (HBE) cells.

103 onses in primary, well-differentiated, human bronchial epithelial (HBE) cultures.

104 Differentiated normal bronchial epithelial (NHBE) cells and tracheal cells fro

105 ally expressed genes in primary normal human bronchial epithelial (NHBE) cells that were exposed to d

106 e time evolution of response of Normal Human Bronchial Epithelial (NHBE) cells to aerosols is essenti

107 mes, and pro-inflammatory chemokine in human bronchial epithelial and endothelial cells.

108 In contrast, killing of bronchial epithelial and renal cortical cells with low F

109 typing based on a transcriptomic analysis of bronchial epithelial and sputum cells has identified a T

110 r (ROCKi), and low oxygen (2%), normal human bronchial epithelial basal progenitor cells (HBECs) divi

111 ipts heavily enriched in oxidations in human bronchial epithelial BEAS-2B cell cultures exposed to 1

112 with increased expression of MUC5AC mRNA in bronchial epithelial brush samples via proxy SNP rs11602

113 mimicked using a novel differentiated bovine bronchial epithelial cell (BBEC) infection model.

114 ican production, we studied an ex vivo human bronchial epithelial cell (BEC)/human lung fibroblast (H

115 effect of increased IL33 expression on human bronchial epithelial cell (HBEC) function.

116 ator efficacy was confirmed in primary human bronchial epithelial cell cultures generated from a N130

117 2 cytokines in WT mice and in primary human bronchial epithelial cell cultures.

118 Immortalized primary bronchial epithelial cell line (BEAS-2B cells), human pr

119 The ASL pH of human bronchial epithelial cell lines and primary respiratory

120 atory variants in the FAM13A region in human bronchial epithelial cell lines.

121 icant mitochondrial superoxide production in bronchial epithelial cells (16-HBE).

122 ecombination in alveolar macrophages (AMFs), bronchial epithelial cells (BECs), and alveolar epitheli

123 Human bronchial epithelial cells (HBE) obtained from normal, n

124 sion was evaluated by real-time PCR in human bronchial epithelial cells (HBEC) and blood neutrophils

125 n airway cell culture systems: primary human bronchial epithelial cells (HBEC), primary type II alveo

126 obal proteome analysis of immortalized human bronchial epithelial cells (HBEC3-KT) at day 7 post expo

127 tures of control and asthmatic primary human bronchial epithelial cells (HBECs) by means of analysis

128 eved 30%-50% allelic correction in UABCs and bronchial epithelial cells (HBECs) from 10 CF patients a

129 culum stress (ERS) and cytotoxicity in human bronchial epithelial cells (HBECs) treated with pneumoto

130 rily by innate cells in the lungs, including bronchial epithelial cells (known producers of IL-25), a

131 ntent of EV secreted by primary normal human bronchial epithelial cells (NHBE) is altered upon asthma

132 Primary normal human bronchial epithelial cells (NHBE) represent a good lung

133 hBE33 cells and normal human bronchial epithelial cells (NHBE) were pretreated with 1

134 nisms and clinical relevance in normal human bronchial epithelial cells (NHBEs) and nasal polyp tissu

135 nses were quantified in biopsies and primary bronchial epithelial cells (PBECs) in response to RSV, p

136 es (MDMs), alveolar macrophages, and primary bronchial epithelial cells (PBECs) were isolated from he

137 ial cell line (BEAS-2B cells), human primary bronchial epithelial cells (PBECs), and PBECs derived po

138 reaction to NiV in primary porcine and human bronchial epithelial cells (PBEpC and HBEpC, respectivel

139 that was tested in BEAS-2B and primary human bronchial epithelial cells (pHBECs) using formoterol and

140 SLC26A9 immunofluorescence in primary human bronchial epithelial cells (pHBEs) homozygous for F508de

141 genomes of 632 colonies derived from single bronchial epithelial cells across 16 subjects.

142 ntiinflammatory therapy in CF using CF human bronchial epithelial cells and an ovine model of CF-like

143 om bleomycin-induced apoptosis using primary bronchial epithelial cells and BEAS-2B cells.

144 hingosine is present in nasal, tracheal, and bronchial epithelial cells and constitutes a central ele

145 anilloid-3 (TRPV3) agonists can affect human bronchial epithelial cells and highlight novel physiolog

146 ucociliary parameters were measured in human bronchial epithelial cells and in sheep.

147 ed increased expression of MMP-10 and MET in bronchial epithelial cells and in subepithelial inflamma

148 Mucin 1-CT expression was downregulated in bronchial epithelial cells and peripheral blood neutroph

149 ted allergen-induced PGE2 secretion in human bronchial epithelial cells and prostanoid-dependent bron

150 ypes, and pathway analysis were performed in bronchial epithelial cells and replicated.

151 recently shown that ex-vivo cultured primary bronchial epithelial cells and the bronchial brushings f

152 R pathways by Tet1 was also present in human bronchial epithelial cells at base line and following HD

153 Primary human bronchial epithelial cells cultured in air-liquid interf

154 r-liquid interface cultures of primary human bronchial epithelial cells derived from non-asthmatic do

155 In contrast, NuLi-1 immortalized human bronchial epithelial cells did express STING, which was

156 In vitro primary bronchial epithelial cells expressed ST2 and IL-33 stimu

157 t, only a few viral antigens are detected in bronchial epithelial cells from autopsied lung sections.

158 Here we report that the transfer of human bronchial epithelial cells from stiff to soft substrates

159 ation and increased mucus viscosity of human bronchial epithelial cells in a nicotine-dependent manne

160 as expressed by interstitial macrophages and bronchial epithelial cells in the inflamed lung, suggest

161 on was negatively regulated by PP2A in human bronchial epithelial cells isolated from healthy nonsmok

162 mucociliary function in differentiated human bronchial epithelial cells isolated from never-smokers a

163 PTCH1 mRNA expression was measured in bronchial epithelial cells obtained from individuals wit

164 ntracytoplasmic inclusion bodies in ciliated bronchial epithelial cells of fatal cases.

165 Human bronchial epithelial cells play a key role in airway imm

166 In human primary bronchial epithelial cells ST2 mRNA and protein expressi

167 from air-liquid interface cultures of human bronchial epithelial cells stimulated with IL-6 and sIL-

168 -genome sequence and RNA sequence from human bronchial epithelial cells to dissect functional genes/S

169 Correspondingly, human lung fibroblasts and bronchial epithelial cells were found to express DR3 and

170 tures induced in vitro by IL-17 and IL-13 in bronchial epithelial cells were used to identify patient

171 gene and protein levels, in peptide-treated bronchial epithelial cells with a functional or mutated

172 ded with drugs in vitro (normal and CF human bronchial epithelial cells) and in vivo (homozygote/homo

173 lating DSP (desmoplakin) expression in human bronchial epithelial cells, and DSP regulates extracellu

174 USPs 1, 4, and 10) were expressed in primary bronchial epithelial cells, and one of them, DUSP10, was

175 uses were also characterized in normal human bronchial epithelial cells, and the results were consist

176 In human bronchial epithelial cells, formoterol, a long-acting be

177 basal levels of PINK-1-mediated mitophagy in bronchial epithelial cells, mitochondrial trafficking of

178 ure on genome-wide DNA methylation of target bronchial epithelial cells, using 17 volunteers, each ra

179 sly established for culture of primary human bronchial epithelial cells.

180 miRNA-200b in TGF-beta1-induced EMT in human bronchial epithelial cells.

181 increase mucin expressions in primary human bronchial epithelial cells.

182 e chloride channel activity in primary human bronchial epithelial cells.

183 omolecular complexes at the surface of human bronchial epithelial cells.

184 target gene expression in mice and in human bronchial epithelial cells.

185 rneal epithelial cells and insulin-sensitive bronchial epithelial cells.

186 cells, such as interstitial macrophages and bronchial epithelial cells.

187 replicated selected findings in normal human bronchial epithelial cells.

188 l cell culture of fully differentiated human bronchial epithelial cells.

189 induced goblet cell differentiation of human bronchial epithelial cells.

190 pEMT) or UJT in differentiated primary human bronchial epithelial cells.

191 naria extract-induced IL-33 release by human bronchial epithelial cells.

192 hese CREs from the endogenous locus in human bronchial epithelial cells.

193 red by diesel particles or allergen in human bronchial epithelial cells.

194 L-17-high asthma phenotype, characterized by bronchial epithelial dysfunction and upregulated antimic

195 Bronchial epithelial IFN-alpha/beta expression and numbe

196 ription factors specifying most alveolar and bronchial epithelial lineages.

197 rotective function for the IL-33-ST2 axis in bronchial epithelial repair, and implicate ST2 in myeloi

198 0 x 10(-5)) and MUC5AC mRNA was increased in bronchial epithelial samples from patients with severe a

199 Bronchial epithelial ST2 protein expression was signific

200 The regulation of bronchial epithelial TJs by TH2 cells and their cytokine

201 sed ability for intracellular survival in CF bronchial epithelial-F508del cells compared to ancestral

202 We observed IFN-alpha/beta deficiency in the bronchial epithelium at 3 time points in asthmatic patie

203 However, deletion of GR in the bronchial epithelium blocked rhythmic CXCL5 production,

204 subjects with asthma and healthy controls in bronchial epithelium from biopsies (n = 27 versus n = 9)

205 , but quitting promotes replenishment of the bronchial epithelium from mitotically quiescent cells th

206 , the anti-viral and repair responses of the bronchial epithelium in children with severe therapy-res

207 kin (IL)-33 genes in asthma, but its role in bronchial epithelium is unclear.

208 cantly increased in both alveolar tissue and bronchial epithelium of patients with diabetes compared

209 In asthma, bronchial epithelium protein expression of ST2 is decrea

210 rotein expressed in airway smooth muscle and bronchial epithelium that regulates the activity of G-pr

211 Bronchospasm compresses the bronchial epithelium, and this compressive stress has be

212 ry cells sparsely distributed throughout the bronchial epithelium, many in innervated clusters of 20-

213 enotypes and with IL33 expression in lung or bronchial epithelium.

214 converting enzyme-2 (ACE2) expression within bronchial epithelium.

215 tory syndrome coronavirus 2 receptor ACE2 in bronchial epithelium.

216 issue samples and quantified in alveolar and bronchial epithelium.

217 Participants in classes 5 and 6 had more bronchial exacerbations and unscheduled medical visits (

218 m bacterial burden inversely associated with bronchial expression of type 2 (T2)-related genes.

219 inophilia, reduced type 2 cytokine levels in bronchial fluid, and improved airway hyperresponsiveness

220 was measured, and alveolar concentration and bronchial flux were calculated.

221 oking status on AGER (encodes RAGE) and TLR4 bronchial gene expression in patients with and without C

222 noglobulin synthesis, airway remodeling, and bronchial hyperreactivity were measured.

223 of pneumonia, bronchiolitis, bronchitis, or bronchial hyperreactivity.

224 have allergic airway inflammation and had no bronchial hyperreactivity.

225 e airway eosinophilia, mucus overproduction, bronchial hyperresponsiveness (BHR), and immunogloubulin

226 atory disease characterized by inflammation, bronchial hyperresponsiveness and narrowing of the airwa

227 corticosteroid-unresponsive inflammation and bronchial hyperresponsiveness driven by IL-13.

228 ronin 60.1 inhibits leucocyte diapedesis and bronchial hyperresponsiveness in a murine model of aller

229 e were ventilated with a flexiVent setup and bronchial hyperresponsiveness was determined using acety

230 d inflammation and, if appropriate, negative bronchial hyperresponsiveness.

231 showed better lung mechanics, but unaltered bronchial hyperresponsiveness.

232 der characterized by airway inflammation and bronchial hyperresponsiveness.

233 relationship between the presence of chronic bronchial infection (CBI), reduced number of circulating

234 uction in these patients was associated with bronchial inflammation and airway structural changes.

235 /anti-inflammatory therapies could attenuate bronchial inflammation and ameliorate virus-induced COPD

236 TT were placed into 12 categories, including bronchial insertion and distance from the carina at 1.0-

237 downstream miR-200b targets were studied in bronchial lung epithelial cells using a SMAD luciferase

238 dy was to examine the response of the host's bronchial lymph node transcriptome to Bovine Respiratory

239 ted in the lung from two of five monkeys, in bronchial lymph nodes from one of the five monkeys, and

240 racted and sequenced (75 bp paired-end) from bronchial lymph nodes.

241 els with pulmonary function and responses to bronchial methacholine challenge from childhood up to ag

242 ild steroid-naive asthma, differences in the bronchial microbiome are associated with immunologic and

243 l subtypes of lung cancer and non-neoplastic bronchial mucosa as in vitro models representing individ

244 We previously reported increased bronchial mucosa eosinophil and neutrophil inflammation

245 iral IgA-response, possibly triggered in the bronchial mucosa, induces systemic autoimmunity.

246 noids maintain cellular components of normal bronchial mucosa.

247 Experimental RV infection induces bronchial mucosal eosinophilia and neutrophilia only in

248 RV infection increased the numbers of bronchial mucosal eosinophils and neutrophils only in CO

249 sought to determine the extent and nature of bronchial mucosal inflammation following experimental rh

250 t it is unclear whether virus per se induces bronchial mucosal inflammation, nor whether this relates

251 Bronchial mucosal inflammatory cell phenotypes were dete

252 th COPD and smokers had increased numbers of bronchial mucosal monocytes/macrophages and CD8(+) T lym

253 We sought to compare bronchial mucosal type I interferon and PRR expression a

254 patients with SA from the national Cohort of Bronchial Obstruction and Asthma cohort were enrolled fo

255 vors, nicotine content, and/ or lung models (bronchial or alveolar).

256 regime, and the region of respiratory tree (bronchial or alveolar).

257 ss 1 (25%): nonallergic participants without bronchial or ocular symptoms.

258 , we report lung cancer organoids and normal bronchial organoids established from patient tissues com

259 The normal bronchial organoids maintain cellular components of norm

260 ronchial severity differed among groups, but bronchial pathology was comparable among all cohorts.

261 Bronchial premalignant lesions (PMLs) are precursors of

262 ore (Visit 1) and 24 hours after (Visit 3) a bronchial provocation test with Dermatophagoides pterony

263 Conjunctival and bronchial provocation tests were performed with purified

264 Ms to ST2-deficient mice completely restores bronchial re-epithelialization.

265 Bronchial reactivity (>=35% change in mean crude values

266 ng episode were more often likely to develop bronchial reactivity (odds ratio 8.8, P = 0.03) than the

267 an important early risk factor for increased bronchial reactivity at preschool age.

268 However, determinants of childhood bronchial reactivity, a key feature of asthma, are large

269 om inflammatory and immunological processes, bronchial remodeling, or by the aspiration of pathogenic

270 feasibility, safety, and initial outcomes of bronchial rheoplasty in patients with CB.Methods: Pooled

271 Bronchial rheoplasty uses an endobronchial catheter to a

272 s enrolling 30 patients undergoing bilateral bronchial rheoplasty was conducted.

273 nnaire (SGRQ).Measurements and Main Results: Bronchial rheoplasty was performed in all 30 patients (6

274 ts for this study from those enrolled in the Bronchial Sample Collection for a Novel Genomic Test (BR

275 cal examination revealed eosinophilia in the bronchial secretions and mild nonspecific inflammatory c

276 cosity and mostly decrease the elasticity of bronchial secretions by reducing disulfide bonds in prot

277 nvestigated DCs and monocytes from blood and bronchial secretions of patients with varying COVID-19 s

278 asure mediators of asthmatic inflammation in bronchial secretions.

279 Bronchial severity differed among groups, but bronchial

280 Bronchial soluble mediators were measured using quantita

281 f cases in which the bleeding was from a non-bronchial source were archived and details of imaging an

282 Haemoptysis can be from non-bronchial sources, which may be either from systemic or

283 n = 24) patients having haemoptysis from non-bronchial sources.

284 Sputum, induced sputum, or bronchial specimens are all suitable specimens for detec

285 vement was noted as bronchiectasis (77%) and bronchial stenosis (4%) but none with broncholithiasis.

286 Thickening of the bronchial subepithelial layer is a contributing factor t

287 We found lower frequencies of bronchial subepithelial monocytes/macrophages expressing

288 onship between the allergen exposure and the bronchial symptoms has not been studied.

289 R, 18 AR, and 19 NAR patients self-reporting bronchial symptoms suggestive of asthma and 8 healthy co

290 allergic rhinitis (LAR) patients self-report bronchial symptoms suggestive of asthma, but the relatio

291 ants with co-occurrence of ocular, nasal and bronchial symptoms, and exacerbation-prone were identifi

292 The bronchial termini had robust neutrophil infiltration, an

293 nale: Adverse events have limited the use of bronchial thermoplasty (BT) in severe asthma.Objectives:

294 Bronchial thermoplasty is not recommended as part of sta

295 oxide, CCL26 and SERPINB2 mRNA expression in bronchial tissues also reduced.

296 nd reduced key pharmacodynamic biomarkers in bronchial tissues.

297 ith inflammatory pathways and modulate human bronchial tone.

298 High density consolidations in the bronchial tree and in the pulmonary parenchyma have been

299 Bronchial wall thickening at CT histologically correspon

300 ere evaluated for CT morphometric indices of bronchial wall thickness (BWT) and wall area percentage