ライフサイエンスコーパス: bronchial

1 nfection of A549, BEAS-2B, and primary human bronchial airway cells were assessed by means of quantit

2 eptor phosphorylation-dependent signaling in bronchial airway contraction and lung function regulated

3 f MT in influenza virus replication in human bronchial airway epithelial cells.

4 aled highest expression of miR-218-5p in the bronchial airway epithelium.

5 to meet the indications of the diagnosis of bronchial airway hyperreactivity in subjects who do not

6 n with safety and useful in the diagnosis of bronchial airway hyperresponsiveness.

7 The diversity and composition of the bronchial airway microbiome of asthmatic patients is dis

8 ure, followed by saline-controlled segmental bronchial allergen challenge.

9 Bronchial allergen provocations (BAP) were repeated at w

10 onger in the LLT group, but the incidence of bronchial anastomotic complications was higher in the PD

11 The levels of both bronchial and alveolar iNOS are increased in uncontrolle

12 eral airways and compare it with the exhaled bronchial and alveolar NO levels in patients with asthma

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

14 prevalence of less than 1% of all selective bronchial arterial angiograms.

15 ther CT findings included hypertrophy of the bronchial arteries along the mediastinal course, diffuse

16 Ablation of the bronchial artery after the initiation of tumor growth re

17 Bronchial artery aneurysm (BAA) is a rare condition with

18 An incidental finding of a bronchial artery aneurysm necessitates prompt treatment.

19 CT angiography revealed a single bronchial artery aneurysm of 9 mm in diameter, abutting

20 Results show that bronchial artery perfusion, quantified by fluorescent mi

21 egies to improve airway oxygenation, such as bronchial artery re-anastomosis and hyperbaric oxygen th

22 and contraction both in murine and in human bronchial aSMCs, through its association with phospholip

23 Diagnosis of bronchial asthma and atopic dermatitis was made, but she

24 All patients had a diagnosis of bronchial asthma inadequately controlled by at least a m

25 Differentiation from bronchial asthma is also important.

26 the blood of adult and elderly patients with bronchial asthma to establish potential association of C

27 mask in two young children with acute severe bronchial asthma.

28 Left-right bronchial asymmetry, as seen in Vegavis, is only known i

29 e 2-high asthma harbored significantly lower bronchial bacterial burden.

30 Compositional differences in the bronchial bacterial microbiota have been associated with

31 We sought to compare the bronchial bacterial microbiota in adults with steroid-na

32 ratified epithelia derived from normal human bronchial basal cells.

33 A with regard to pulmonary function indices, bronchial basement membrane thickness, and BAL fluid neu

34 t variation analysis signatures expressed in bronchial biopsies and airway epithelial brushings disti

35 The transcriptome derived from bronchial biopsies and epithelial brushings of 107 subje

36 edict the subtypes of gene expression within bronchial biopsies and epithelial cells with good sensit

37 IL-17A(+), IL-17F(+), and IL-21(+) cells in bronchial biopsies and higher numbers (P < .01) of IL-17

38 ile in asthma and control subjects utilizing bronchial biopsies and serum, and to relate uPAR express

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

40 MAIT cells were reduced in bronchial biopsies from subjects with COPD treated with

41 tory and structural pathological features in bronchial biopsies of severe asthmatics that could be re

42 ed in control (n = 9) and asthmatic (n = 27) bronchial biopsies using immunohistochemistry, with a se

43 CEACAM6 protein expression in bronchial biopsies was increased in airway epithelial ce

44 Asthmatic bronchial biopsies were immunostained for CD48.

45 In asthmatic bronchial biopsies, mCD48 was expressed predominantly by

46 Bronchial biopsy sections from control subjects, patient

47 Bronchial biopsy specimens (n = 300) were collected from

48 Bronchial biopsy specimens were processed for immunohist

49 ion of CEACAM6 using immunohistochemistry on bronchial biopsy tissue obtained from patients with mild

50 diffuse thickening of the walls of numerous bronchial branches and a "ground glass" opacity in the a

51 rom BAL (2.3% of live cells), BW (32.5%) and bronchial brushing samples (88.9%) correlated significan

52 y stage NSCLC tissue samples and noninvasive bronchial brushing specimens.

53 Gene and miRNA expression in bronchial brushings and lung inflammatory markers were m

54 Bacterial communities in protected bronchial brushings from 42 atopic asthmatic subjects, 2

55 NLRP3 or enrichment of IL-1R family genes in bronchial brushings or biopsy specimens in patients with

56 Bronchial Cdc42 loss destroys contact inhibition potenti

57 y human and mouse sinonasal cells, and human bronchial cells at air-liquid interface and examined the

58 that their mRNA expression in primary human bronchial cells is stimulated by IAV infection.

59 The bronchial cells were obtained from a cystic fibrosis pat

60 face cultures of primary human sinonasal and bronchial cells, we imaged ciliary beat frequency (CBF),

61 Dyspnea scores during adenosine bronchial challenge and incremental exercise testing wer

62 f sensitization was demonstrated by specific bronchial challenge test (SBCT) with peach leaf extract.

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

64 d symptom monitoring, spirometry, and serial bronchial challenge tests, and those participants using

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

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

67 circulations, the pulmonary and the systemic bronchial circulation.

68 utic approaches that target specifically the bronchial circulation.

69 common pathological end point: irreversible bronchial dilatation arrived at through diverse etiologi

70 airway and the potential role of IgE in the bronchial disease will be also reviewed.

71 We recapitulated human bronchial dysplasia in vitro.

72 (1) To develop an in vitro model of bronchial dysplasia that recapitulates key molecular and

73 l context, acute deregulation of SOX2 drives bronchial dysplasia.

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

75 is a key early event in the pathogenesis of bronchial dysplasia; and (3) to use the model for studie

76 L-15, OVA-challenged mice exhibited enhanced bronchial eosinophilic inflammation, elevated IL-13 prod

77 ance tRNA that is particularly rare in human bronchial epithelia, but not in other human tissues, sug

78 dulate TGF beta-induced IL-8 secretion in CF bronchial epithelia.

79 onal expression at the apical PM in human CF bronchial epithelia.

80 nel in primary CFTRDeltaF508/DeltaF508 human bronchial epithelia.

81 K293T cells and in well-differentiated human bronchial epithelia.

82 Our results showed that treatment of human bronchial epithelial (BEAS-2B) cells with arsenic induce

83 ermine the functions of EHF in primary human bronchial epithelial (HBE) cells and relevant airway cel

84 agy in primary homozygous F508del-CFTR human bronchial epithelial (hBE) cells at submicromolar concen

85 e the transcriptomes of differentiated human bronchial epithelial (HBE) cells exposed to air, MSS fro

86 We show that primary human bronchial epithelial (HBE) cells secrete lactate into AS

87 Primary human bronchial epithelial (NHBE) cells differentiated at air-

88 Whereas, normal human bronchial epithelial (NHBE) cells with poor integrin alp

89 ry cells in the lamina propria (P = 0.0019), bronchial epithelial (P = 0.0002) and airway smooth musc

90 thelial cells (A549 and primary normal human bronchial epithelial [NHBE]) cells and macrophages (J774

91 eron (IFN)-alpha, IFN-beta and IFN-lambda in bronchial epithelial and bronchial lavage cells in atopi

92 data demonstrated that syndecan-1 suppresses bronchial epithelial apoptosis during influenza infectio

93 ive signals through c-Met signaling to limit bronchial epithelial apoptosis, thereby attenuating lung

94 the levels of histone modifications in human bronchial epithelial BEAS-2B cells and human nasal RPMI2

95 Time course analysis of human bronchial epithelial BEAS-2B cells infected with HMPV re

96 implicated in EGFR signaling, we transduced bronchial epithelial BEAS-2B cells with retroviral vecto

97 onally analysed expression of these genes in bronchial epithelial brushings from healthy, steroid-nai

98 fter lung transplantation (LTx) results from bronchial epithelial cell (BECs) damages, thought to be

99 compared signaling changes across six human bronchial epithelial cell (HBEC) strains that were syste

100 ysLTr1(-/-) mice also demonstrated prolonged bronchial epithelial cell apoptosis following Cl2 WT mic

101 ARG2 overexpression in a human bronchial epithelial cell line accelerated oxidative bio

102 To test this hypothesis, we used human bronchial epithelial cell line Nuli-1 and C57BL/6 mice.

103 nce the cell viability of human immortalized bronchial epithelial cell line of Beas-2B.

104 C transcript and protein levels in the human bronchial epithelial cell line, 16HBE, Lyn overexpressio

105 nucleotide exchange factors (GEFs) in human bronchial epithelial cell monolayers, we identified GEFs

106 Bronchial epithelial cell proliferation was evaluated by

107 sis of HMPV replication and transcription in bronchial epithelial cell-derived immortal cells was per

108 o determine whether ex vivo RSV infection of bronchial epithelial cells (BECs) from children with ast

109 plasma from 48 CF patients and in primary CF bronchial epithelial cells (CF-HBEC).

110 Here, data from human bronchial epithelial cells (HBEC) confirm that cigarette

111 ts within the lower airways to examine human bronchial epithelial cells (HBEC) is essential for under

112 lignant lung cancer wherein we treated human bronchial epithelial cells (HBEC) with low doses of toba

113 we modeled malignant transformation in human bronchial epithelial cells (HBECs) and determined that E

114 d that LZTFL1 is expressed in ciliated human bronchial epithelial cells (HBECs) and its expression co

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

116 We used primary human bronchial epithelial cells (HBECs) from asthmatics and h

117 ust-mite (HDM) induced AAI and primary human bronchial epithelial cells (NHBE) cultured at the air-li

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

119 rent cell lines, well-differentiated primary bronchial epithelial cells (WD-PBECs), and RSV isolates

120 h levels and higher, are toxic for the human bronchial epithelial cells after 4-day exposure.

121 se activity and strong ability in protecting bronchial epithelial cells against elastase-induced anti

122 A damage potential of aeroallergens on human bronchial epithelial cells and elucidated the mechanisms

123 . aureus to the intracellular niche in human bronchial epithelial cells and in a murine pneumonia mod

124 A biculture of human bronchial epithelial cells and lung microvascular endoth

125 nd 3O-C12-HSL induce barrier derangements in bronchial epithelial cells by lowering the expression of

126 duced by insulin deprivation in normal human bronchial epithelial cells cultured in organotypic condi

127 l mucosal production of IL-17A which acts on bronchial epithelial cells directly and in concert with

128 t epigenetic alterations can sensitize human bronchial epithelial cells for transformation by a singl

129 Primary human bronchial epithelial cells from asthma patients and cont

130 SCD1 expression was suppressed in bronchial epithelial cells from asthma patients.

131 internalization by SPX-101 in primary human bronchial epithelial cells from healthy and CF donors wa

132 Gene expression studies of bronchial epithelial cells in individuals with asthma ha

133 ce and absence of bacterial LPS was shown in bronchial epithelial cells lines (16HBE14o-, CFBE41o-) a

134 ased; these alterations were not observed in bronchial epithelial cells recovered after treatment wit

135 In bronchial epithelial cells recovered from asthmatic vs h

136 erleukin-8 mRNA in BEAS-2B and primary human bronchial epithelial cells through activation of both TR

137 Our results show that direct exposure of bronchial epithelial cells to HDM leads to the productio

138 the response of well-differentiated cultured bronchial epithelial cells to interleukin-13 (IL-13).

139 ndividual granules in differentiated primary bronchial epithelial cells using fluorescence lifetime i

140 adherence to pharynx, type II alveolar, and bronchial epithelial cells was mainly attributed to fibr

141 hylation studies in saliva, PBMCs, and human bronchial epithelial cells were done to support our find

142 Primary bronchial epithelial cells were stimulated with IL-17A a

143 Human bronchial epithelial cells were used to investigate cyto

144 However, NY/108 virus replicated in human bronchial epithelial cells with an increased efficiency

145 Stimulation of cultured human bronchial epithelial cells with IL-13, a key mediator in

146 Stimulation of primary bronchial epithelial cells with IL-17A enhanced mRNA exp

147 Transfecting human bronchial epithelial cells with miR-629-3p mimic induced

148 ull)), TLR4(Hi), and TCM(Hi) cells and human bronchial epithelial cells with small interfering RNA-in

149 expression by dexamethasone in primary human bronchial epithelial cells, and in A549 cells IL1B-induc

150 ne expression, Nrf2 nuclear translocation in bronchial epithelial cells, and increased reduced glutat

151 tent in inducing mdig protein and/or mRNA in bronchial epithelial cells, B cells and MM cell lines.

152 Human bronchial epithelial cells, BEAS-2B, directly exposed to

153 In normal human bronchial epithelial cells, IL-8 secretion in response t

154 diate MNGC formation of vein endothelial and bronchial epithelial cells, indicating that the T6SS-5 i

155 three-dimensional cultures of primary human bronchial epithelial cells, we demonstrated that loss of

156 e direct DNA-damaging effect of HDM on human bronchial epithelial cells, we exposed BEAS-2B cells to

157 In primary bronchial epithelial cells, we found that basolateral, b

158 ma-specific miRNA profiles were reported for bronchial epithelial cells, whereas sncRNA expression in

159 trap beta1-integrins on the luminal pole of bronchial epithelial cells.

160 n cigarette smoke-exposed mice, and in human bronchial epithelial cells.

161 ible activation of oncogenes in immortalized bronchial epithelial cells.

162 as well as malignant transformation of human bronchial epithelial cells.

163 3O-C12-HSL attenuate PPARgamma expression in bronchial epithelial cells.

164 ecreted exosomes, which were internalized by bronchial epithelial cells.

165 as biofilms on the Cystic Fibrosis genotype bronchial epithelial cells.

166 sulting in malignant transformation of human bronchial epithelial cells.

167 ced miR-132-3p may contribute to shedding of bronchial epithelial cells.

168 suppression rescues F508del-CFTR function in bronchial epithelial cells.

169 in vitro transfecting miRNA mimics in human bronchial epithelial cells.

170 induced goblet cell differentiation of human bronchial epithelial cells.

171 mouse embryonic fibroblasts and normal human bronchial epithelial cells.

172 vivo murine model of COPD, and primary human bronchial epithelial cells.

173 e (CpG) resolution global DNA methylation in bronchial epithelial cells.

174 opy videos of in vitro samples of live human bronchial epithelial ciliated cells.

175 We exposed human bronchial epithelial cultures (HBECs) to air or whole to

176 erally from healthy, but not asthmatic human bronchial epithelial cultures (HBECs), where it suppress

177 t of allergen and diesel exhaust exposure on bronchial epithelial DNA methylation.

178 Bronchial epithelial goblet cell metaplasia (GCM) with h

179 (RELMalpha and beta), previously considered bronchial epithelial growth factors.

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

181 BEAS2B (bronchial epithelial) cells were treated with IL-4 follo

182 ew HIF2alpha-dependent mechanism involved in bronchial epithelium adaptation to oxygen fluctuations.

183 ed DNA damage and cytokine production in the bronchial epithelium and apoptosis in the allergic airwa

184 enzymes were significantly increased in the bronchial epithelium and inflammatory immune cells infil

185 ons, immunomodulatory cross-talk between the bronchial epithelium and tissue-resident immune cells co

186 nergic receptor agonist (LABA) on GCM in the bronchial epithelium are unknown.

187 or trigger of asthma exacerbations, with the bronchial epithelium being the major site of HRV infecti

188 ified that GSDMB is highly expressed in lung bronchial epithelium in human asthma.

189 Overexpression of GSDMB in primary human bronchial epithelium increased expression of genes impor

190 The bronchial epithelium is continuously exposed to a multit

191 Ormdl3 transcript levels specifically in the bronchial epithelium resulted in reinstatement of suscep

192 The ability of the bronchial epithelium to control the balance of inhibitor

193 ould be important for early responses of the bronchial epithelium to Th2-stimuli.

194 hma where their numbers are increased in the bronchial epithelium with increasing disease severity.

195 way contributing to IL-8 secretion in the CF bronchial epithelium with KL functioning as an endocrine

196 and increased localization to the asthmatic bronchial epithelium, we investigated whether HRV infect

197 xpression of miR-629-3p was localized in the bronchial epithelium, whereas miR-223-3p and miR-142-3p

198 ly involved in protection and maintenance of bronchial epithelium.

199 ch GSDMB induces 5-LO to induce TGF-beta1 in bronchial epithelium.

200 DSB marker gamma Histone 2AX (H2AX) foci in bronchial epithelium.

201 Whether this imbalance also occurs in bronchial epitheliumof asthmatics is unknown.

202 were obtained from culture media of primary bronchial fibroblasts and characterized using Western bl

203 ns were tested as chemoattractants for human bronchial fibroblasts in the xCELLigence cell migration

204 To evaluate the role of exosomes released by bronchial fibroblasts on epithelial cell proliferation i

205 Bronchial fibroblasts play a key role in airway remodell

206 We showed that bronchial fibroblasts secreted exosomes, which were inte

207 al stricture (grade 2), and 1 (2%) a grade 4 bronchial fistula.

208 tissue did not relate to alveolar NO, nor to bronchial flux of NO.

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

210 is was performed on 150 children with MPP or bronchial foreign body (FB) admitted in our hospital.

211 c signaling mechanism, we tested retinal and bronchial human epithelial cells and fibroblasts.

212 atal variables and the prevalence of asthma, bronchial hyperreactivity (BHR), flexural eczema (FE), a

213 ic bronchial inflammation, post-AAI mice had bronchial hyperreactivity and increased inflammatory cel

214 ssed by using multicolor flow cytometry, and bronchial hyperreactivity was studied.

215 Likewise, T-cell cytokine content and bronchial hyperreactivity were reduced.

216 Bronchial hyperreactivity, airway inflammation, and sens

217 IL-33 and eotaxin production, eosinophilia, bronchial hyperreactivity, and goblet cell hyperplasia i

218 The severity of bronchial hyperresponsiveness (BHR) is a fundamental fea

219 Bronchial hyperresponsiveness (BHR) is a phenotypic hall

220 The bronchial hyperresponsiveness (BHR) test is useful to di

221 inophil counts in relation to lung function, bronchial hyperresponsiveness (BHR), and asthma control

222 he associations of parental asthma severity, bronchial hyperresponsiveness (BHR), and total and speci

223 asthma through the assessment of nonspecific bronchial hyperresponsiveness (NSBH) is a key step in th

224 as significantly associated with more severe bronchial hyperresponsiveness (P < .0001) and with curre

225 symptoms, reversible airflow obstruction, or bronchial hyperresponsiveness after having all asthma me

226 y of the Genetics and Environment of Asthma, bronchial hyperresponsiveness and atopy) (170 with and 1

227 assumed coughing occurs as a consequence of bronchial hyperresponsiveness and inflammation, but the

228 In patients with moderate to severe bronchial hyperresponsiveness and nasal polyposis, the c

229 regression analysis, only moderate to severe bronchial hyperresponsiveness and nasal polyps were inde

230 mplementary roles of FENO and FOT to predict bronchial hyperresponsiveness in adult stable asthmatic

231 R5 or R20 and FENO can predict the level of bronchial hyperresponsiveness in adult stable asthmatics

232 cle growth, MMP-1 levels are associated with bronchial hyperresponsiveness, and MMP-1 activation are

233 was >37.8ppb, 29 of 43 subjects (67.4%) had bronchial hyperresponsiveness.

234 liferation and MMP-1 protein associated with bronchial hyperresponsiveness.

235 eral blood eosinophilia, high level of FENO, bronchial hyperresponsiveness.

236 mediated inflammation, tissue remodeling and bronchial hyperresponsiveness.

237 was >37.8ppb, 25 of 38 subjects (65.7%) had bronchial hyperresponsiveness.

238 Nasal IL-17F(+) cells correlated with bronchial IL-17F (r = 0.35), exacerbation rate (r = 0.47

239 ff values of bronchial neutrophils and nasal/bronchial IL-17F for discriminating between asthmatics a

240 Bronchial IL-17F(+) cells correlated with bronchial neut

241 of specific miRNAs and genes associated with bronchial immune responses were significantly modulated

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

243 Airway hyperresponsiveness (AHR) and bronchial inflammation were analyzed after intranasal ch

244 zed mice displayed a more pronounced AHR and bronchial inflammation when challenged with allergen com

245 After clearing the allergic bronchial inflammation, post-AAI mice had bronchial hype

246 cialization, which, through interaction with bronchial labia, contributes to different acoustic featu

247 a and IFN-lambda in bronchial epithelial and bronchial lavage cells in atopic asthmatics.

248 and lung lesions and in the lymphoid tissues bronchial lymph node, retropharyngeal lymph node, nasoph

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

250 The bronchial microbiome differed significantly among the 3

251 bjects and to determine relationships of the bronchial microbiota to phenotypic features of asthma.

252 il numbers was significantly elevated in the bronchial mucosa of the asthmatic smokers compared to th

253 Neutrophil density in the bronchial mucosa was similar across health and the spect

254 eosinophil peroxidase by eosinophils in the bronchial mucosa, was maintained after mepolizumab.

255 lia, and eosinophil peroxidase deposition in bronchial mucosa.

256 side of neighboring epithelial cells in the bronchial mucosa.

257 ddress the hypothesis that smoking increases bronchial mucosal production of IL-17A which acts on bro

258 e of scales, from arterial blood vessels and bronchial mucus transport in humans to bacterial flow th

259 immunohistochemistry in cryostat sections of bronchial/nasal biopsies obtained from 33 SAs (21 freque

260 trophils/eosinophils/CD4(+)/CD8(+) cells and bronchial/nasal IL-17F(+) cells.

261 IL-17F protein was also measured by ELISA in bronchial/nasal lysates and by immunohistochemistry in b

262 IL-17F protein increased in bronchial/nasal lysates of SAs and FEs and in bronchial

263 elated cytokines expression was amplified in bronchial/nasal mucosa of neutrophilic asthma prone to e

264 ly ASM, neuroendocrine epithelial cells, and bronchial nerve endings.

265 Bronchial IL-17F(+) cells correlated with bronchial neutrophils (r = 0.54), exacerbation rate (r =

266 alysis evidenced predictive cutoff values of bronchial neutrophils and nasal/bronchial IL-17F for dis

267 FEs showed increased number of bronchial neutrophils/eosinophils/CD4(+)/CD8(+) cells an

268 t [Cohorte Obstruction Bronchique et Asthme; Bronchial Obstruction and Asthma Cohort; sponsored by th

269 Classical postulated mechanisms for bronchial obstruction in this population include the osm

270 ing: dry powder mannitol for inhalation as a bronchial provocation test is FDA approved however not c

271 of Rac1 in aSMC, ex and in vitro analyses of bronchial reactivity were performed on bronchi from smoo

272 normalities involved in airway narrowing and bronchial reactivity, particularly ASM, neuroendocrine e

273 terol, alone or combined, to the reversal of bronchial remodelling and inflammation.

274 6.02 are the most efficient predictors of a bronchial response to NRL.

275 95% CI, -0.21 to -0.02; P = .02), decreased bronchial responsiveness (abeta coefficient, 0.53 log-mu

276 al (CI), 1.11-14.43]; P = 0.0337), increased bronchial responsiveness to methacholine (adjusted beta-

277 associated with asthma, airway obstruction, bronchial responsiveness, and aeroallergen sensitization

278 ars along with assessments of lung function, bronchial responsiveness, fraction of exhaled nitric oxi

279 oms of gastroesophageal reflux and rhinitis, bronchial reversibility, and exhaled nitric oxide values

280 or previous evidence of airflow limitation, bronchial reversibility, or airway hyperresponsiveness (

281 Administration of chymase to human bronchial rings abrogated IL-13-enhanced contraction, an

282 ells, whereas sncRNA expression in asthmatic bronchial smooth muscle (BSM) cells is almost completely

283 Increase of bronchial smooth muscle (BSM) mass is a crucial feature

284 Increased bronchial smooth muscle (BSM) mass is a key feature of a

285 expressed in vascular endothelial cells and bronchial smooth muscle cells, leading to lethal vascula

286 e, of a role for M3-mAChR phosphorylation in bronchial smooth muscle contraction in health and in a d

287 e and phosphorylated myosin light chain 2 in bronchial smooth muscles.

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

289 Two (3%) patients developed a bronchial stricture (grade 2), and 1 (2%) a grade 4 bron

290 We sought to examine the effect of BT on bronchial structures and to explore the association with

291 h severe asthma, yet its effect on different bronchial structures remains unknown.

292 e respiratory epithelium and goblet cells of bronchial structures.

293 The effectiveness of bronchial thermoplasty (BT) has been reported in patient

294 Bronchial thermoplasty, a new technique to reduce airway

295 s, including newer biological treatments and bronchial thermoplasty.

296 nasal lysates and by immunohistochemistry in bronchial tissue obtained from subjects who died because

297 ronchial/nasal lysates of SAs and FEs and in bronchial tissue of fatal asthma.

298 In bronchial tissue, uPAR was elevated in inflammatory cell

299 itative CT-derived metrics for emphysema and bronchial wall thickness were calculated.

300 s, sampling the proximal and distal airways (bronchial wash and bronchoalveolar lavage, respectively)