ライフサイエンスコーパス: upper airway

1 ft tissues or facial skeleton to enlarge the upper airway.

2 s on identifying sites of obstruction in the upper airway.

3 ates the mucosal innate defense of the human upper airway.

4 veillance and defense mechanism of the human upper airway.

5 s with recurrent growth of papillomas in the upper airway.

6 late trapped in a layer of mucous out of the upper airway.

7 ole in the overall respiratory health of the upper airway.

8 aryngeal movements to achieve closure of the upper airway.

9 lococcus aureus, a frequent colonizer of the upper airways.

10 des of the skin, gastrointestinal tract, and upper airways.

11 preceded by asymptomatic colonization of the upper airways.

12 lty swallowing, indicating impairment of the upper airways.

13 disturbances, particularly the impairment of upper airways.

14 lty swallowing, suggesting impairment of the upper airways.

15 iameter (D) in sleeping humans with narrowed upper airways.

16 ng its potential niche as a commensal of the upper airways.

17 viral subtypes is likely to occur in ferret upper airways.

18 respiratory tract that is used to clear the upper airways.

19 article transport and deposition (TD) in the upper airways.

20 involvement beyond mere colonization of the upper airways.

21 he presented with cardiac arrest, ice in her upper airways, a first-documented nasopharyngeal tempera

22 lecule probes to the epithelial cells of the upper airways, a multiscale computational model of the l

23 infant monkeys were inoculated with H1N1 by upper airway administration.

24 exposure and retention, specifically in the upper airways after intratracheal administration.

25 In upper airways airway surface liquid (ASL) depth and clea

26 s: To determine the effect of weight loss on upper airway anatomy in subjects with obesity and OSA.

27 These include: (1) upper airway anatomy, (2) the ability of upper airway di

28 ow OA alters AHI and four phenotypic traits (upper-airway anatomy/collapsibility and muscle function,

29 < 0.05), which was driven by improvements in upper-airway anatomy/collapsibility under passive (1.9 +

30 order and that OAs may affect more than just upper-airway anatomy/collapsibility.

31 >= 10 events/h) underwent a sleep study and upper airway and abdominal magnetic resonance imaging be

32 By evaluating both upper airway and acellular bronchoalveolar lavage sample

33 analysed the microbiota and proteomes of the upper airway and determined direct antibacterial activit

34 ogen, is naturally capable of colonizing the upper airway and sometimes disseminating to remote tissu

35 rgency room; it is usually manifested in the upper airway and the head and neck region.

36 es, LT has somehow affected the stability of upper airway and ventilatory mechanics.

37 n greatly reduce virus load in the lower and upper airways and decrease virus-induced pathological se

38 of distinct immune defence programmes in the upper airways and intestine to limit K. pneumoniae colon

39 e characterized by local inflammation of the upper airways and sinuses and is frequently divided into

40 e bacterium primarily infects the throat and upper airways and the produced diphtheria toxin (DT), wh

41 be a range of sensory symptoms suggestive of upper-airway and laryngeal neural dysfunction.

42 phalus, mucociliary clearance defects in the upper airway, and abnormal spermatogenesis.

43 y small volume (<1 mL) is instilled into the upper airways, and with programmed air ventilation of th

44 lowing were scaled by differences in initial upper airway area before swallowing.

45 us, aimed to quantitatively characterize the upper airway as well as craniofacial abnormalities in Dp

46 intensive care unit-acquired weakness, i.e., upper airway as well as extremity muscles.

47 ureus, an organism frequently colonizing the upper airways, at the human mucosal site of the disease.

48 the pool of undifferentiated progenitors of upper airways available for differentiation.

49 erapy is proposed for treating patients with upper airway bacterial rhinosinusitis.

50 the DeltaF508 mutation in readily accessible upper-airway basal stem cells (UABCs) obtained from CF p

51 muscles responsible for maintaining an open upper airway become hypotonic during REM sleep.

52 Respiratory virus detection in the upper airway by multiplex PCR assay is common in critica

53 Transient colonization of the murine upper airways by L. rhamnosus GG was demonstrated and wa

54 because edema occurring in the mucosa of the upper airways can lead to suffocation.

55 Nested case-control analyses of 115 men with upper airway cancer (including 1 nasopharyngeal cancer),

56 nd and Wales, and associations with incident upper airway cancer and leukemia were explored in nested

57 ies, with significant enrichment in lung and upper airway cancers.

58 Pathological collapsibility of the upper airways, caused by many different genetic and envi

59 en awake but experience repeated episodes of upper airway closure when asleep, in particular during R

60 sleep apnea experience repeated episodes of upper airway closure when they are asleep, in particular

61 Anatomical airway problems (upper airway collapse and adenoid hypertrophy) and funct

62 an increasingly common disorder of repeated upper airway collapse during sleep, leading to oxygen de

63 One of the key factors that triggers upper airway collapse is decreased pharyngeal dilator mu

64 ic features of the diseases that may promote upper airway collapse or heart failure.

65 e littermates, showing the potential risk of upper airway collapse.

66 orrelated with apnea severity and indices of upper airway collapsibility during NREM sleep.

67 iveness to negative epiglottic pressure, and upper airway collapsibility during passive and active co

68 to examine the pathophysiology of increased upper airway collapsibility of DS and to evaluate the ef

69 Upper airway collapsibility was also reduced with desipr

70 and measures of arousal, apnea severity and upper airway collapsibility were ascertained during NREM

71 ition, the AT was a predictor of measures of upper airway collapsibility, including the hypopnea/apne

72 rousal threshold is a predictor of increased upper airway collapsibility.

73 sing multivariate analysis, baseline passive upper-airway collapsibility and loop gain were independe

74 indings suggest that OA therapy improves the upper-airway collapsibility under passive and active con

75 philus influenzae (NTHi) are closely related upper airway commensal bacteria that are difficult to di

76 actor B was defined as a presence of chronic upper airway complications.

77 thma, gastro-oesophageal reflux disease, and upper airway conditions, and that it can be cured in mos

78 ntation could potentially be used to enhance upper airway control in the elderly.

79 reduced image distortion was shown in lungs, upper airway, cranial sinuses, and intestines because of

80 e critical to cartilage formation and normal upper airway development in mice.

81 a for reference and documents the structural upper airway differences between those with and without

82 s suggest that cholinergic signaling impairs upper airway dilator muscle activity by suppressing glut

83 (1) upper airway anatomy, (2) the ability of upper airway dilator muscles to respond to rising intrap

84 eshold, small lung volume, and dysfunctional upper airway dilator muscles.

85 able anatomy and collapsibility and enhanced upper-airway dilator muscle responses to avoid OSA.

86 cture that is mitigated by highly responsive upper-airway dilator muscles to avoid OSA.

87 The upper airway dilators are much more susceptible to a dec

88 This group with so-called severe chronic upper airway disease (SCUAD) represents a therapeutic ch

89 seen great progress in the understanding of upper airway disease and in its management.

90 Treatment-related issues of uncontrolled upper airway disease are linked with the correct choice

91 In a percentage of LAR subjects, the upper airway disease is also associated with lower airwa

92 of the available literature on occupational upper airway disease with a focus on pathophysiological

93 s on the current unmet needs in work-related upper airway disease.

94 nts with AERD, especially for the control of upper airway disease.

95 sneezing, which is blunted in patients with upper-airway disease.

96 ght recently published important articles on upper airway diseases and allergen immunotherapy.

97 The airway epithelium in asthma and upper airway diseases is dysfunctional due to disturbed

98 ce interval) than controls for incidence of: upper airway diseases, including adenotonsillitis (3.29,

99 ry IgA immunity could be impaired in chronic upper airway diseases.

100 importance to increase the awareness towards upper airway disorders in the swimming athletes and to e

101 little is known regarding its implication in upper airway disorders.

102 lerance, we isolated CD4(+) T cells from the upper airway draining lymph nodes of both OVA323-339- an

103 d are critical in maintaining patency of the upper airway during respiration.

104 ange around 37 degrees C as occur within the upper airways during infection.

105 a due to a rapid increase in pressure in the upper airways during sneezing, coughing, or vomiting, wh

106 uently, in aging Tau-P301L mice, progressive upper airway dysfunction is linked to progressive tauopa

107 Because patients with tauopathy suffer from upper airway dysfunction, the Tau-P301L mice can serve a

108 Twenty-five OSA patients underwent upper airway endoscopy during natural sleep to assess to

109 However, upper airway endoscopy is considered an aerosol-generati

110 we analyzed CCL5 (RANTES) mRNA expression in upper airway epithelial cells.

111 Despite being commonly used to collect upper airway epithelial lining fluid, nasal washes are p

112 egrins accumulate on the luminal membrane of upper-airway epithelial cells from mice and humans with

113 ted over time, we demonstrate that the human upper airway epithelium is maintained by an equipotent b

114 tensity and the pressure gradient across the upper airway (estimated with oesophageal pressure, Pes)

115 To summarize the current state of the art in upper-airway evaluation, focusing on endoscopic techniqu

116 we review the emerging inflammatory roles of upper airway fibroblasts, the majority of which appear t

117 ice underwent behavioral assays to determine upper airway function at multiple time points prior to a

118 l tissue can have widespread consequences on upper airway function.

119 Upper-airway gain was taken as the ratio of the increase

120 tly alter pharyngeal anatomy/collapsibility, upper-airway gain, or arousal threshold.

121 oyed a systems biology approach to delineate upper-airway gene network patterns underlying asthma exa

122 The upper airways have been shown to reflect colonization of

123 Here, we examine the upper airway host transcriptional response in patients w

124 ws dynamic estimation of changes in relative upper airway hydraulic diameter (D) in sleeping humans w

125 ur results provide a potential mechanism for upper airway hypotonia during REM sleep.

126 n treatment during RSV bronchiolitis reduced upper airway IL-8 levels, prolonged the time to the thir

127 Studies involving MRI of the upper airway illustrated that OSAS populations tend to h

128 Upper airway immune mediator levels were altered during

129 to negative pressure applied to the isolated upper airway in anaesthetized rats before and after micr

130 postmortem human trachea and bronchi and on upper airways in 2 compartments, cartilage and submucosa

131 It has been suggested that the upper airways (including the paranasal sinuses and nasop

132 Using mass spectrometry and murine upper airway infection models, we demonstrated that phos

133 thalmological examination (recent history of upper airway infections and/or head and neck surgeries a

134 We speculate that upper airway infections may be common precipitants of a

135 weeks of age due to overwhelming suppurative upper airway infections that were associated with neutro

136 f genetic and environmental factors, such as upper airway infections.

137 a H1N1, suggesting autoimmunity triggered by upper-airway infections.

138 f the current state of the art of control in upper airway inflammation and stressing the unmet needs

139 sponsible for the lack of control in chronic upper airway inflammation are often but not always linke

140 Persistent upper airway inflammation caused by agents inhaled in th

141 The degree of upper airway inflammation correlated with the degree of

142 Upper airway inflammation is one of the most frequent he

143 chanisms that cause persistent, exaggerated, upper airway inflammation rather than acute resolving il

144 and most frequently diagnosed etiologies of upper airway inflammation.

145 We sought to identify differences in the upper airway inflammatory signature between CRSwNP and A

146 was to identify potential differences in the upper airways inflammatory response after exposure to LM

147 respiratory distress syndrome as well as in upper-airway inflammatory diseases, such as chronic obst

148 Upper airway injury is a recognized complication of prol

149 Upper airway involvement can also lead to dyspnea and su

150 The upper airway is a complex tissue structure that is prone

151 Direct visualization of the upper airway is an important diagnostic modality in infa

152 rmine whether ciliary ACE2 expression in the upper airway is influenced by patient demographics, clin

153 bacterial colonization (or carriage) in the upper airway is the prerequisite of all these infections

154 Chronic inflammation of the upper airways is common and can arbitrarily be divided i

155 a chronic inflammatory disease affecting the upper airways, is a valuable and accessible model to inv

156 assortant viruses from tissues of the ferret upper airway, it is reasonable to conclude that continue

157 by recurrent episodes of obstruction of the upper airway leading to sleep fragmentation and intermit

158 HLOs possess upper airway-like epithelium with basal cells and immatu

159 s varies; predisposing factors include small upper airway lumen, unstable respiratory control, low ar

160 recruitment of monocyte/macrophages into the upper airway lumen, where they engulfed pneumococci.

161 unds generated by different vibrators of the upper airway may be useful indicators of obstruction sit

162 ses that disease mechanisms occurring in the upper airway may mirror lower airway events.

163 previously found that children with smaller upper airways (measured by magnetic resonance imaging wh

164 duction in tongue fat volume was the primary upper airway mediator of the relationship between weight

165 Our results suggest that upper airway microbial composition in infancy contribute

166 superior sampling method to characterize the upper airway microbiome and immune response in both chil

167 pling method for the characterization of the upper airway microbiome and immune response, we collecte

168 To characterize the upper airway microbiome, we used 16S ribosomal RNA and s

169 rging evidence indicates associations of the upper-airway microbiome with bronchiolitis severity, lit

170 infection, indicating the robustness of the upper-airway microbiome.

171 We studied upper airway microbiota at 1 week, 1 month, and 3 months

172 icant endoplasmic reticulum injury in select upper airway motoneurons.

173 m nuclei, directly or indirectly involved in upper airway motor control (i.e., the Kolliker-Fuse, per

174 Ns that might be applied to the treatment of upper airway motor deficits.

175 help in the development of therapeutics for upper airway motor disorders such as obstructive sleep a

176 TSLP-responding DC populations in the human upper airway mucosa and assess the TSLP-mediated effects

177 well as in the inflammatory response of the upper airway mucosa and in wound healing, presumably thr

178 methylation and gene expression profiles in upper airway mucosal cells and assessed AR at age 6 year

179 associated differentially methylated CpGs in upper airway mucosal cells at age 6 years, 792 of which

180 through altered DNA methylation patterns in upper airway mucosal cells.

181 nting on the cytokines and chemokines in the upper airway mucosal lining fluid of healthy neonates.

182 Human upper airway mucus layer proteins were recovered during

183 plasticity of XII motor output may increase upper airway muscle (innervated by XII nerve) tone and i

184 sible mechanism for REM sleep suppression of upper airway muscle activity.SIGNIFICANCE STATEMENT Indi

185 measure OSA severity, arousal threshold and upper airway muscle responsiveness.

186 geal anatomy/collapsibility, loop gain (LG), upper-airway muscle responsiveness (gain) and the arousa

187 without apnea exhibited a threefold greater upper-airway muscle responsiveness than both overweight/

188 ep, hypoglossal motoneurons that control the upper airway muscles are inhibited in REM sleep by the c

189 per subject, after the local anatomy of the upper airway musculature was examined by ultrasonography

190 exchange during sleep, related to transient upper airway narrowing disrupting ventilation, and causi

191 ropathy and abnormalities of ventilatory and upper airway neural control.

192 Healthy children have wide variation in upper airway neuromuscular compensatory responses and ar

193 Children with robust upper airway neuromuscular responsiveness, or a very hig

194 A range of bacteria can colonize the upper airway; nevertheless, we focus on strategies share

195 ntify clinically significant post-extubation upper airway obstruction (UAO) and differentiate subglot

196 ep apnea (OSA) is characterized by recurrent upper airway obstruction during sleep.

197 t in many neuromuscular disorders mechanical upper airway obstruction from oropharyngeal weakness con

198 recapitulate craniofacial abnormalities and upper airway obstruction of human DS and can serve as an

199 latory pressures, pulmonary dysfunction, and upper airway obstruction that occur after combined smoke

200 longer length of ventilation, postextubation upper airway obstruction, high respiratory effort postex

201 ologic disease, lower aPiMax, postextubation upper airway obstruction, higher preextubation positive

202 When children developed postextubation upper airway obstruction, reintubation rates were 47.4%

203 when these children developed postextubation upper airway obstruction, reintubation rates were greate

204 attacks, and the risk of asphyxiation due to upper airway obstruction.

205 e when these children develop postextubation upper airway obstruction.

206 mal sensory responses have been found in the upper airway of obstructive sleep apnea patients, but no

207 The rapid recruitment of ILC2s to the upper airways of allergic patients with rhinitis, and th

208 ithout a tracheal tube, because the straight upper airways of animals do not obstruct in coma.

209 ter (D) in both an in vitro model and in the upper airways of sleeping humans.

210 recruitment of ILC2s and granulocytes to the upper airways of subjects with atopy and healthy subject

211 IFN-lambda is present in the lower, but not upper, airways of patients with coronavirus disease 2019

212 As a consequence, samples taken from the upper airway often captured only a fraction of the popul

213 tact of aspirated gastric refluxate with the upper airway or by a vago-vagal reflex.

214 The Kolliker-Fuse (KF) maintains upper airway patency and a normal respiratory pattern.

215 pontine Kolliker-Fuse nucleus (KF) controls upper airway patency and regulates respiration, in parti

216 ctive of this study was to determine whether upper airway patency can be improved using chemogenetic

217 ssor muscle of the tongue and contributes to upper airway patency during inspiration.

218 Apnoea-induced LTF may preserve upper airway patency during sleep, thereby limiting furt

219 cts improve genioglossus muscle activity and upper airway patency during sleep.

220 al pressure are important for maintenance of upper airway patency in humans.

221 rength than the diaphragm, and impairment of upper airway patency is a key mechanism of extubation fa

222 which plays an important role in maintaining upper airway patency, particularly during sleep, and mod

223 GMNs, which contribute to the maintenance of upper airway patency.

224 ue and play an important role in maintaining upper airway patency.

225 uscle of the tongue, is required to maintain upper airway patency.

226 ic (passive critical closing pressure of the upper airway [Pcrit]) and nonanatomic (genioglossus musc

227 y contrast, the number of swallows evoked by upper airway/pharyngeal distensions was not significantl

228 ine the effects of zolpidem on OSA severity, upper airway physiology and next-day sleepiness and aler

229 ous studies suggested an association between upper airway pneumococcal colonization density and pneum

230 mproved adaptation of A(H7N9) virus to human upper airway poses an important threat to public health.

231 The upper airways present a barrier to inhaled allergens and

232 n is characterized by peak viral load in the upper airway prior to or at the time of symptom onset, a

233 We show that when upper airway protection requirements change, individuals

234 ogical colonization owing to the efficacy of upper airway-protective mechanisms and the host mucosal

235 Conversely, in the upper airways, Proteobacteria prime immunity through IL-

236 ies lead to primary ciliary dyskinesia, with upper-airways recurrent infections, left-right asymmetry

237 ) were evaluated as markers of activation of upper airway remodeling using image analysis, together w

238 The concept of upper airway remodelling has only recently been introduc

239 848 were used to mimic a viral insult in the upper airways represented by primary human nasal epithel

240 The mucosal lining of the upper airways represents the outer surface of the body t

241 ons to provide forced expiration and reduced upper airway resistance simultaneously.

242 ced early expiratory airflow (i.e. increased upper airway resistance) only during wake.

243 y, particularly during sleep, and modulating upper airway resistance.

244 1.3 l min(-1); P < 0.05), but did not alter upper airway responsiveness (P = 0.7).

245 Upper airway responsiveness was defined as the ratio of

246 thanol-fed rats in vivo with rGM-CSF via the upper airway restored GM-CSF receptor membrane expressio

247 ngth and smaller cross-sectional area of the upper airway, resulting in a significantly reduced upper

248 measure electrophysiological function in the upper airways, RNAscope in situ hybridization and quanti

249 Allegro con brio: it rapidly spreads in the upper airway's epithelia.

250 udied whole-genome deep sequencing of RSV in upper airway samples from an infant with severe combined

251 stinguish atopic and nonatopic phenotypes in upper airway samples.

252 pe reassortant viruses that may be shed from upper airway secretions.

253 These data suggest that T2R38 is an upper airway sentinel in innate defense and that genetic

254 <0.01), 19% had a relatively noncollapsible upper airway similar to many of the control subjects (Pc

255 eposition of fat in the tongue, compromising upper airway size.

256 geted branches of the pulmonary airway tree: upper airways, small airways (bronchioles), or the most

257 Comatose humans have upper airway soft tissue obstruction unless the head is

258 than control subjects; (3) the size of other upper airway soft tissue structures (volume of the tongu

259 hypothesis that the volume of the important upper airway soft tissue structures is heritable.

260 phoid tissue, rather than enlargement of the upper airway soft tissue structures, is the primary anat

261 ions: Weight loss reduced volumes of several upper airway soft tissues in subjects with obesity and O

262 Analysis of upper airway specimens identifies specific inflammatory

263 In contrast, upper-airway specimens from the same subjects contained

264 it the accuracy of DNA-based measurements on upper-airway specimens.

265 In the upper airways, SpyCEP expression was required for surviv

266 od-like receptor-stimulating bacteria in the upper airway (Staphylococcus aureus and Staphylococcus e

267 ted the clinical safety and effectiveness of upper-airway stimulation at 12 months for the treatment

268 p, cohort design, we surgically implanted an upper-airway stimulation device in patients with obstruc

269 In this uncontrolled cohort study, upper-airway stimulation led to significant improvements

270 without apnea have a moderately compromised upper-airway structure that is mitigated by highly respo

271 nfectious and non-infectious diseases of the upper airways, such as otitis media, adenotonsillitis, r

272 ade to achieve intubation success, including upper airway suctioning (used in 43% of attempts resulti

273 long-term efficacy, and safety of multilevel upper airway surgery for treatment of patients with OSA.

274 oup, open-label randomized clinical trial of upper airway surgery vs ongoing medical management.

275 Upper airway symptoms among responders to the terrorist

276 ARbp was defined as upper airway symptoms during birch pollen exposure.

277 hinitis to grass pollen (ARg) was defined as upper airway symptoms during grass pollen exposure.

278 Patients with particularly intensive upper airway symptoms had the highest levels of blood eo

279 In subjects who did not report upper airway symptoms, 57% had an LM score of 0, 30% had

280 ects with atopy displayed rapid induction of upper airway symptoms, an enrichment of ILC2s, eosinophi

281 1, asthma with a moderate course, intensive upper airway symptoms, and blood eosinophilia (18.9% of

282 n, their less efficient replication at human upper airway temperatures has implications for the under

283 itis (CRS) is an inflammatory disease of the upper airways that affects 10% of Europeans and American

284 In the upper airways, the involvement of RAGE remains completel

285 Glucose uptake was quantified within upper airway tissues with the standardized uptake value.

286 throughout the airways usually occur in the upper airways, tonsils, and adenoid structures that make

287 EGPA commonly presents with upper airway tract and lung involvement, peripheral neur

288 leukemia, nasopharyngeal carcinoma, or other upper airway tumors from formaldehyde exposure.

289 Identification of upper airway (UA) obstruction based on pharyngeal factor

290 at RAGE protein is highly expressed in human upper airways under normal physiology and that it is sub

291 ruction by evaluating dynamic changes in the upper airway using drug-induced sleep computed tomograph

292 Induction of IFNalpha in the upper airways via activation of TLR7 represents a novel

293 airway, resulting in a significantly reduced upper airway volume in Dp16 mice.

294 Although overall the upper airway was more collapsible in patients with OSA (

295 st-inspiratory drive (adductor motor) to the upper airways was enhanced in amplitude and duration in

296 ections related to medication (predominantly upper airway) was less likely.

297 eeks genioglossus EMG and dynamic MRI of the upper airway were performed before and after administrat

298 l in characterizing aerosol transport in the upper airways, while Monte Carlo based radiation codes a

299 pothesized that reducing inflammation in the upper airway with intranasal corticosteroid (INCS) medic

300 tis (CRS) is a multifactorial disease of the upper airways with a high prevalence (approximately 11%)