ライフサイエンスコーパス: airway

1 sues or facial skeleton to enlarge the upper airway.

2 uld lead to a more relaxed and thereby wider airway.

3 deletion of both Trp53 and Rb1 in the adult airway.

4 ecognize and reluctance to manage the failed airway.

5 14% around small vessels, and 7% around the airways.

6 t improve clearance of mucus strands from CF airways.

7 , SIX3) and tracheobronchial (SCGB1A1, TFF3) airways.

8 elial cell types of the normal and IPF human airways.

9 e infected with Klebsiellapneumoniae via the airways.

10 errets rather than from trachea or the lower airways.

11 EDA-KO pigs lacked SMGs throughout the airways.

12 ation and pneumococcal presence in the lower airways.

13 mouse displayed histopathologic alveolar and airway abnormalities.

14 types (H1N1, H3N2, and B) can be achieved by airway administration of a single combination of relativ

15 utes a central element of the defense of the airways against bacterial pathogens.

16 BS for 4 consecutive days to evaluate innate airway allergic inflammation.

17 ions in the structure and composition of the airway and alveolar epithelium in regions of fibrosis.

18 together with lineage tracing revealed that airway and alveolar stem cells converge on a unique Krt8

19 typically reside adjacent to the conducting airway and assume a mucosal phenotype (MC(T)).

20 An urbanized structure of the airway and gut microbiotas was associated with an increa

21 m experiments with murine models of allergic airway and skin inflammation and offer an overview of st

22 zing/effector function-positive bNAb via the airway and systemic routes showed increased effectivenes

23 In contrast, Th2 Trm cells proliferated near airways and induced mucus metaplasia, airway hyperrespon

24 tinct immune defence programmes in the upper airways and intestine to limit K. pneumoniae colonizatio

25 cellular immune response affecting the small airways and lung parenchyma.

26 e whether upregulation of ACE2 expression in airways and lungs has consequences on infectivity and cl

27 al ganglia supply sensory innervation to the airways and lungs.

28 piratory system, which includes the trachea, airways, and distal alveoli, is a complex multi-cellular

29 a greater amount of lymphoid tissue, smaller airways, and smaller lower facial skeletons from measure

30 -6), IL-8, and myeloperoxidase levels in the airway are indicative of severe infection.

31 med to quantitatively characterize the upper airway as well as craniofacial abnormalities in Dp(16)1Y

32 ides a promising genetic strategy to prevent airway bacterial infections in farm animals by bacteria-

33 well as its consequence on the regulation of airway barrier integrity and S. pneumoniae disease.

34 directed differentiation of human iPSCs into airway basal cells ("iBCs"), a population resembling the

35 er T2 markers in sputum (paucigranulocytic), airway biopsies or in blood.

36 CPR, sequence for starting CPR (compressions-airway-breaths versus airway-breaths-compressions), CPR

37 ting CPR (compressions-airway-breaths versus airway-breaths-compressions), CPR before calling for hel

38 ed to controls in nasal, bronchial and small airways brushings.

39 irus disease 2019 (COVID-19) is infection of airway cells by severe acute respiratory syndrome corona

40 the epithelial tissue barrier by generating airway cells instead of olfactory cells.

41 sin-converting enzyme 2 receptor in lung and airway cells.

42 nd impedes Nm adhesion and invasion of human airway cells.

43 ponses were assessed before upper- and lower-airway challenge with SARS-CoV-2.

44 Col6a1(-/-) mice also displayed multiple airway changes, including increased branching (59%; P <

45 e keratinocytes, olfactory epithelial cells, airway club cells and respiratory ciliated cells as pote

46 ermates, showing the potential risk of upper airway collapse.

47 amine the pathophysiology of increased upper airway collapsibility of DS and to evaluate the efficacy

48 NETs were found in the airway compartment and neutrophil-rich inflammatory area

49 ssue is demonstrated by 3D bioprinting human airways composed of regionally specified primary human a

50 including aspiration pneumonia, fistula and airway compression.

51 bited allergen-induced histamine release and airway contraction in guinea pig PCLS.

52 in particular Aspergillus fumigatus, in the airway correlated with asthma severity and control.

53 Airway dendritic cells (DCs) are recognized as important

54 Furthermore, airway diameter is reduced in the mutant, counter to the

55 The presence of Aspergillus within the airway did not relate to serum IgE positivity for Asperg

56 Together, this work sheds light on human airway differentiation in vitro and provides a single-ce

57 e in the pathogenesis of asthma and allergic airway disease (AAD).

58 wer alpha-1 antitrypsin and functional small airway disease (P = 0.007).Conclusions: In this integrat

59 were recruited into a COPD (emphysema versus airway disease [EvA]) or asthma cohort (Unbiased BIOmark

60 nted IFN-gamma responses in the HDM allergic airway disease model were accompanied by increased disru

61 ic progress in treating cystic fibrosis (CF) airway disease, airway inflammation with associated muco

62 therapeutic effects, on established allergic airway disease, and prevented the development of ovalbum

63 tulate cystic fibrosis-like mucoinflammatory airway disease, deficient in innate lymphoid (Il2rg knoc

64 ent of eosinophilic inflammation in allergic airway disease, including asthma.

65 ctor phase in the ovalbumin-induced allergic airway disease.

66 ions in the pathogenesis of mucoinflammatory airway disease.

67 thma is a widespread, multifactorial chronic airway disease.

68 Abnormal mPRM measurements of small airways disease (normal CT, not ventilated) and mild emp

69 crucial role in the pathogenesis of allergic airways disease by increasing IL-1beta-induced proinflam

70 centrally involved in the pathophysiology of airway diseases such as asthma and chronic obstructive p

71 ion of SOCS3 within EVs serves as a brake on airway EC responses during allergic inflammation, but is

72 restrain allergic inflammatory responses in airway ECs.

73 ion is a non-invasive method to evaluate the airway environment, particularly for asthma.

74 metaplasia, airway hyperresponsiveness, and airway eosinophil activation.

75 A response to HDM, reducing IL-13 levels and airway eosinophilia without affecting IgE levels or airw

76 at may inhibit recruitment and activation of airway eosinophils, reducing airway inflammation.

77 P(Cl) /P(Na) of airway epithelia was unaltered by pH 7.4 vs.

78 response to P. aeruginosa by cystic fibrosis airway epithelia.

79 res of human cystic fibrosis (CF) and non-CF airway epithelia.

80 l genomic RNA were clearly observed in human airway epithelial (HAE) culture.

81 led SARS-CoV-2 infection using primary human airway epithelial (pHAE) cultures, which are maintained

82 PAG1 deficiency increased airway epithelial activation, ILC2 expansion, and T(H) 2

83 pulmonary ACE2 expression in vitro in human airway epithelial cell cultures and in vivo in mouse mod

84 r work in IL-13 biology to determine whether airway epithelial cell expression of 2 key mediators cri

85 erferon-stimulated gene (ISG) in vitro using airway epithelial cells and extend our findings to in vi

86 sulatum-infected canine and feline lungs and airway epithelial cells could serve as higher animal mod

87 ntaining gene expression data from nasal and airway epithelial cells from children and adults with as

88 E2 and TMPRSS2 expression ex vivo in primary airway epithelial cells from participants with and witho

89 ce of AC6, we demonstrated that AC6 knockout airway epithelial cells have longer cilia compared with

90 bits SARS-CoV-2 replication in primary human airway epithelial cells in vitro-both prophylactic and t

91 hat hRV infection of polarized primary human airway epithelial cells resulted in increased adherence

92 ects on asthma pathophysiology, including on airway epithelial cells, mucus hypersecretion, and airwa

93 if19a into autophagosomes for degradation in airway epithelial cells.

94 plified itself and ST2 protein expression in airway epithelial cells.

95 Il33, and muc5ac mRNA expression in cultured airway epithelial cells.

96 ng SARS-CoV-2 and influenza A virus in human airway epithelial cultures, we observe the absence of IF

97 evaluated in human cell and animal models of airway epithelial function and mucus transport.Measureme

98 drug concentrations measured in plasma, lung/airway epithelial lining fluid, and alveolar cells.

99 mposed of regionally specified primary human airway epithelial progenitor and smooth muscle cells.

100 um, supporting the notion that events at the airway epithelial surface are critical for the developme

101 gin of asthma is orchestrated by a disrupted airway epithelium and further perpetuated by a predispos

102 ambda responses to dsRNA in the human infant airway epithelium are regulated by p38-MAPK and NF-kB si

103 The physical barrier function of the airway epithelium is tightly interwoven with its immunom

104 ace (ALI) usually provide a pseudostratified airway epithelium with similar abnormalities than origin

105 bility genes for asthma are expressed in the airway epithelium, supporting the notion that events at

106 were accompanied by increased disruption of airway epithelium, which was reversed by therapeutic blo

107 re also observed at the protein level in the airway epithelium.

108 a population resembling the stem cell of the airway epithelium.

109 igration of neutrophils, using primary human airway epithelium.

110 ogical process by which mammalian conducting airways expel pathogens and unwanted surface materials f

111 At baseline, the groups had similar airway experience (p = 0.34) and skill scores (p = 0.97)

112 ces with videolaryngoscope, independently of airway expertise with direct laryngoscopies) and 87% in

113 r tracheal intubation, presence of difficult airway features, more experienced provider level, and tr

114 HFEV(1) asthmatics had larger airways (FEV(1) z-scores 1.12 vs -2.37; P < .05), greate

115 ed regeneration of lung tissue, and reverted airway fibrosis and systemic muscle wasting.

116 Airway fluid was analyzed for the release of NETs by mye

117 al sensory motor reflex circuit protects our airways from aspirated foods or liquids.

118 It is suggested that airway fungi, in particular Aspergillus may impinge on c

119 ding the tracheal architecture and promoting airway growth.

120 In the airways, highly activated unconventional T cells were de

121 y in the ICZ of aged mice and contributed to airway homeostasis and repair.

122 or chronic disease modeling of IL-13-induced airway hyper-responsiveness.

123 then challenged with IL-33 and assessed for airway hyperreactivity and lung inflammation.

124 evented the development of ovalbumin-induced airway hyperreactivity, eosinophilia, and goblet cell me

125 esis and ORMDL3 overexpression are linked to airway hyperreactivity.

126 2 cytokine production, serum IgE levels, and airway hyperreactivity.

127 tors correlates with airway neutrophilia and airway hyperresponsiveness (AHR) in COPD patients.

128 In ST2 knockout mice, IL-33 and OVA induced airway hyperresponsiveness and eosinophilic airway infla

129 lung, and bronchoalveolar lavage as well as airway hyperresponsiveness and goblet cell metaplasia we

130 sistent observation has been the increase in airway hyperresponsiveness, a characteristic of asthma,

131 d near airways and induced mucus metaplasia, airway hyperresponsiveness, and airway eosinophil activa

132 Profoundly enhanced airway hyperresponsiveness, inflammation, and fibrosis w

133 sPLA(2)-X gene (Pla2g10) display attenuated airway hyperresponsiveness, innate and adaptive immune r

134 ILC2s; and exaggerated mucus metaplasia and airway hyperresponsiveness.

135 eosinophilia without affecting IgE levels or airway hyperresponsiveness.

136 iratory distress in response to allergen and airway hyperresponsiveness.

137 rophin associated with airway remodeling and airway hyperresponsiveness.

138 lung inflammation, cellular infiltrate, and airway hyperresponsiveness.

139 hroughout the airways, the so-called unified airway hypothesis, but the evidence to support this is p

140 Studies involving MRI of the upper airway illustrated that OSAS populations tend to have a

141 o define the transcriptional profile of this airway immune dysfunction, we performed the first single

142 Airway immune mediator levels were modestly affected by

143 Lower airway immune profiles show considerable heterogeneity o

144 relative involvement of the large and small airways in asthma is not clear.

145 nia pestis replicates to high numbers in the airways in the absence of disease symptoms or notable in

146 omized to treatment of the six most involved airways in the first session (guided group) or a standar

147 effector-memory T cells transferred into the airways indicated that the environment was necessary to

148 Eosinophilia is a hallmark of allergic airway inflammation (AAI).

149 We measured airway inflammation and AHR in wild-type, RAGE(-/-) , TL

150 ronic inflammatory disorder characterized by airway inflammation and bronchial hyperresponsiveness.

151 the mechanisms by which Rab27 contributes to airway inflammation and cytokine release remain ambiguou

152 ident innate effector cells that can mediate airway inflammation and hyperresponsiveness through prod

153 The constellation of findings includes airway inflammation and rapid development of pulmonary e

154 revented house dust mite-driven eosinophilic airway inflammation and significantly reduced Th2 cytoki

155 f epithelial expression of versican promotes airway inflammation during RSV infection further demonst

156 grass pollen exposure and lung function and airway inflammation in a community-based sample, and whe

157 ST2 is required for the exacerbated allergic airway inflammation in Bcl6(fl/fl) Foxp3-Cre mice.

158 ma is a chronic respiratory disease in which airway inflammation is a key feature, even in the milder

159 mechanistic analysis of TSLP-mediated type 2 airway inflammation METHODS: To dissect the mechanisms o

160 airway hyperresponsiveness and eosinophilic airway inflammation were both completely diminished, and

161 reating cystic fibrosis (CF) airway disease, airway inflammation with associated mucociliary dysfunct

162 , usually with a severe course, eosinophilic airway inflammation, and increased production of pro-inf

163 e recombinant Asp t 36 was able to stimulate airway inflammation, as demonstrated by an influx of eos

164 r to the forefront of the pathophysiology of airway inflammation, different approaches to diagnose an

165 treatment targets, such as control of type-2 airway inflammation, that can be achieved with currently

166 ngs such as house dust mite-induced allergic airway inflammation, the lack of IRF4 expression in the

167 -induced allergic sensitization and allergic airway inflammation.

168 ophil trafficking in the setting of allergic airway inflammation.

169 ng increased IL-33 release and ILC2-mediated airway inflammation.

170 ollowing RSV infection and may contribute to airway inflammation.

171 33 signaling in myeloid cells is crucial for airway inflammation.

172 ne the role of endothelial miR-1 in allergic airway inflammation.

173 d activation of airway eosinophils, reducing airway inflammation.

174 pment of acute T(H)2-cell-dependent allergic airway inflammation.

175 IL-33 release, ILC2 cytokine production, and airway inflammation.

176 ated FeNO, suggesting increased eosinophilic airway inflammation.

177 luding Tfr cells, in the context of allergic airway inflammation.

178 rons initiate defensive reflexes that ensure airway integrity.

179 whether ciliary ACE2 expression in the upper airway is influenced by patient demographics, clinical c

180 COVID-19 affects primarily the respiratory airways leading to dry cough, fever, myalgia, headache,

181 RSV infection showed the highest IFN-lambda airway levels; and (c) individuals with the highest viru

182 tually all in vitro regenerative activity of airway lineages.

183 Ventilation with a cuffless laryngeal mask airway (LMA) has potential advantages over face-mask ven

184 r receptor B1 (SR-B1) as an EsxA receptor on airway M cells.

185 The ontogeny of airway macrophages (AMs) in human lung and their contrib

186 Congenital pulmonary airway malformation volume ratio (CVR) measurements were

187 and cardiovascular collapse during emergency airway management.

188 ges associated with neutrophil counts in the airway.Measurements and Main Results: Six microRNA modul

189 n in tongue fat volume was the primary upper airway mediator of the relationship between weight loss

190 Our results suggest that upper airway microbial composition in infancy contributes to t

191 who were carefully characterized (including airway microbiology) and followed for a median of 84 mon

192 To characterize the upper airway microbiome, we used 16S ribosomal RNA and shotgun

193 We studied upper airway microbiota at 1 week, 1 month, and 3 months of li

194 lation and gene expression profiles in upper airway mucosal cells and assessed AR at age 6 years in c

195 ated differentially methylated CpGs in upper airway mucosal cells at age 6 years, 792 of which formed

196 gh altered DNA methylation patterns in upper airway mucosal cells.

197 between fungal pneumonia and FOXA2-regulated airway mucus homeostasis.

198 these data indicate that, in the context of airway mucus obstruction, the adaptive immune system sup

199 anied by MCM, elevated MUC5B expression, and airway mucus obstruction.

200 re OSA severity, arousal threshold and upper airway muscle responsiveness.

201 nge during sleep, related to transient upper airway narrowing disrupting ventilation, and causing oxy

202 Neuronal VAChT staining and airway narrowing in response to electrical field stimula

203 ntact mucociliary barrier function and early airway neutrophil responses are critical for clearing fu

204 xpression of these receptors correlates with airway neutrophilia and AHR in COPD patients.

205 but not TLR4 signalling may protect against airway neutrophilia and AHR in COPD.

206 xpression of these receptors correlates with airway neutrophilia and airway hyperresponsiveness (AHR)

207 Lung and airway neutrophils are a hallmark of severe disease in i

208 ies have the potential to effectively reduce airway obstruction and inflammation in allergic asthma.

209 Persistent severe airway obstruction despite massive doses of corticostero

210 Airway obstruction was defined as forced expiratory volu

211 ssive condition of chronic bronchitis, small airway obstruction, and emphysema that represents a lead

212 verse correlations with sputum eosinophilia, airway obstruction, and number of hospitalizations in as

213 PG-CAT treated mice showed amelioration in airway obstruction, reduction in neutrophil elastase and

214 hese children developed postextubation upper airway obstruction, reintubation rates were greater than

215 fore defibrillation, removal of foreign-body airway obstruction, resuscitation care for suspected opi

216 tween 5 and 19 Hz, the indices of peripheral airway obstruction.

217 l change in airway pressure generated during airway occlusion [PiMax]).

218 vealed a higher negative pressure inside the airway of Dp16 mice compared to wild-type littermates, s

219 nd exhibited immunomodulatory effects in the airways of allergic individuals.

220 LA(2) group X (sPLA(2)-X) is elevated in the airways of asthmatics and that mice lacking the sPLA(2)-

221 umbers of neutrophils are recruited into the airways of children with severe RSV disease.

222 mbda is present in the lower, but not upper, airways of patients with coronavirus disease 2019 (COVID

223 tigate immune mediator profiles in the lower airways of patients with N-ERD.

224 Here, in blood and airways of severe COVID-19 patients, we serially analyze

225 gative bacterium that commonly colonizes the airways of smokers and patients with chronic lung diseas

226 nhaled into the respiratory tract and invade airway or lung tissue.

227 pneas contributes to awakening and restoring airway patency.

228 results reinforce the importance of IL-13 in airway pathobiology and suggest that neutralization of I

229 However, the potential for DNA from airway pathogens to enter the circulation of cystic fibr

230 findings were analysed based on parenchymal, airway, pleural, mediastinal, and vascular sequelae of P

231 The upper airways present a barrier to inhaled allergens and micro

232 monary outcomes than the continuous positive airway pressure alone group.

233 n predicting 90-day mortality, baseline mean airway pressure demonstrated similar discriminative abil

234 ntaneous breathing trials, and the change in airway pressure during an occlusion maneuver to measure

235 for 2 hours (phase 2) or continuous positive airway pressure for 2 hours (phase 3), and then crossove

236 spiratory muscle strength (maximal change in airway pressure generated during airway occlusion [PiMax

237 analysis of the ISAACC (Continuous Positive Airway Pressure in Patients with ACS and OSA) study, inc

238 We tested whether a continuous positive airway pressure ventilation strategy mitigates ventilato

239 s include weight loss and exercise, positive airway pressure, oral appliances that hold the jaw forwa

240 ife support, when combined with lower Vt and airway pressures than the current standard of care, may

241 ificantly improved at 24 hours, as were peak airway pressures, intrinsic positive end-expiratory pres

242 ing of T cells in the lung revealed that the airway prime regimen induced more antigen-specific multi

243 haracterized by peak viral load in the upper airway prior to or at the time of symptom onset, an unus

244 al for clearing fungal conidia from the host airways prior to establishing disease.

245 ced in mice by preinfection chemokine-driven airway recruitment of neutrophils, which caused enhanced

246 hat regulate functionally distinct phases of airway regeneration and aging.

247 factor (NGF), a neurotrophin associated with airway remodeling and airway hyperresponsiveness.

248 miR-98) and PPARgamma levels, thus promoting airway remodeling.

249 ergic asthma in mice with females developing airway remodelling at a much earlier stage than males.

250 epithelial cells, mucus hypersecretion, and airway remodelling, and consequently might impact asthma

251 neutralization of IL-13 may reduce asthmatic airway remodelling.

252 ted TLC 134.8% vs 109.6%; P < .05) and lower airway resistance (mean %of predicted Raw 101.9% vs 199.

253 Specific airway resistance (sR(aw) ) was significantly higher in

254 A "core" airway resistome dominated by macrolide but with high pr

255 Airway responsiveness was increased by 48.1% after DBP e

256 Endogenous PAR-2 activation in submerged airway RPMI 2650 or NCI-H520 squamous cells increased in

257 months) had higher virus-induced IFN-lambda airway secretion; (b) subjects with RSV infection showed

258 12, p = 0.016) and recurrent accumulation of airway secretions (HR 2.614, p = 0.001).

259 and type 2 cytokine production in a model of airway sensitization and challenge using a complete alle

260 Airway sensitization of naive mice with RSV-infected BMD

261 vation of these cation channels expressed in airway sensory nerves.

262 In MASK-air (Mobile Airways Sentinel Network), a visual analogue scale (VAS)

263 Airway sizes and soft tissue, tongue fat, and abdominal

264 eflection resulted in similar improvement in airway skills, but better retention over time.

265 NM myosin II undergoes polymerization in airway SM and regulates contraction by catalysing the as

266 e interaction of S100A4 with NM myosin II in airway SM at the cell cortex and catalysed NM myosin fil

267 olatile odorants on the contractile state of airway smooth muscle (ASM) and uncovered a complex mecha

268 4 (RGS4), a cytoplasmic protein expressed in airway smooth muscle and bronchial epithelium that regul

269 Here, Abi1 knockdown by shRNA reduced human airway smooth muscle cell migration, which was restored

270 o by inactivating Myocardin, which prevented airway smooth muscle differentiation.

271 r demonstrate that during development, while airway smooth muscle is dispensable for epithelial branc

272 Weight loss reduced volumes of several upper airway soft tissues in subjects with obesity and OSA.

273 The major source of airway stem/progenitors other than basal-like cells rema

274 ied primary end-point was relative change in airway subepithelial eosinophils per mm(2) of basement m

275 athogens many strategies have evolved in the airways such as mucociliary clearance and cough.

276 outcomes than one based on the frequency of airway suctioning is unclear.

277 Cytokines that increased airway surface liquid pH decreased or reversed paracellu

278 pen-label randomized clinical trial of upper airway surgery vs ongoing medical management.

279 s to grass pollen (ARg) was defined as upper airway symptoms during grass pollen exposure.

280 Comparison of airway T(RM) cells and splenic effector-memory T cells t

281 d show that local environmental cues altered airway T(RM) cells to limit cytolytic function and promo

282 se vulnerability is expressed throughout the airways, the so-called unified airway hypothesis, but th

283 uman lung epithelial cells and primary human airway tissues by increasing the infectivity and stabili

284 By utilizing three-dimensional (3-D) human airway tissues to examine viral infection in a physiolog

285 gate the protease repertoire of murine lower airway tissues, primary type II alveolar epithelial cell

286 life cycle in three-dimensional (3-D) human airway tissues.

287 The COPD incidence in the lowest airway to lung quartile was significantly higher than in

288 g on G-protein-coupled receptors to regulate airway tone.

289 Increases in airway type 2 cytokine activity, including interleukin-4

290 f a new class of biologic agents that target airway type 2 inflammation has provided a new model for

291 tment, in a large part because they decrease airway type 2 inflammation.

292 iated with reduced cytokine release into the airways upon local LPS instillation.

293 aramyxoviruses enter epithelial cells of the airway using sialic acid as a receptor and cause only mi

294 Experimentally, airway vaccination induces greater efficacy than parente

295 LO circuit exerts descending regulation over airway vagal reflexes in male and female rats using a ra

296 = -0.53; P < 0.0001) independently predicted airway WA% (R(2) = 0.32; P = 0.0001).Conclusions: TAC wa

297 h greater asthma severity and was related to airway wall thickness and ventilation defects.

298 sponses may contribute to remodelling of the airway wall.

299 on, Aspergillus conidia deposit in the small airways, where they are likely to make their initial hos

300 ation of fluid and/or tissue in the lung and airways, which activated both ASICs and TRPV1 expressed