ライフサイエンスコーパス: upper airway

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

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

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

4 aryngeal movements to achieve closure of the upper airway.

5 ding on the underlying collapsibility of the upper airway.

6 l and pathogenic bacteria that reside in the upper airway.

7 tment of these muscles as stabilizers of the upper airway.

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

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

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

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

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

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

14 ns that are expressed in the oral cavity and upper airways.

15 ns that are expressed in the mouth, nose and upper airways.

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

17 preceded by asymptomatic colonization of the upper airways.

18 involvement beyond mere colonization of the upper airways.

19 lty swallowing, indicating impairment of the upper airways.

20 disturbances, particularly the impairment of upper airways.

21 lty swallowing, suggesting impairment of the upper airways.

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

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

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

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

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

27 The relation between upper airway allergic inflammation and asthma has contin

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

29 Endoscopy was used to evaluate upper airway anatomy, to confirm ISLN anaesthesia, and t

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

31 < 0.05), which was driven by improvements in upper-airway anatomy/collapsibility under passive (1.9 +

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

33 By evaluating both upper airway and acellular bronchoalveolar lavage sample

34 t target for modulating the fluid content of upper airway and nasopharyngeal secretions in disorders

35 nd the epithelia of submucosal glands in the upper airway and nasopharynx.

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

37 We did not find relationships between the upper airway and systemic compartments.

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

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

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

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

42 ubmucosal glands supply most of the mucus in upper airways, and gland serous cells are the primary si

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

46 their role in bacterial colonization of the upper airway as well as how viruses might contribute to

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 relationships of the tissues surrounding the upper airway (bone and soft tissues) in 92 normal childr

51 Their site of origin also differs: upper airway C-fibres arise predominantly from the jugul

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

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

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

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

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

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

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

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

60 Upper airway collapsibility (UAC) is increased in childr

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

62 effect of therapeutic devices and agents on upper airway collapsibility during sleep.

63 Upper airway collapsibility was also reduced with desipr

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

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

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

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

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

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

70 Upper airway critical pressure measurements correlate wi

71 Upper airway cross-sectional area obtained from acoustic

72 sized that respiratory cycle fluctuations in upper airway cross-sectional area would be larger in chi

73 ompared with control subjects: (1) a smaller upper airway cross-sectional area, particularly during i

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

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

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

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

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

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

80 ars to be related to the presence of lung or upper airway disease and anti-PR3 antibody seropositivit

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

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

83 the histopathologic characteristics of this upper airway disease in avian and mammalian species.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

98 Thus, upper airway dynamic testing during wakefulness in respo

99 per airway patency, such that measurement of upper airway dynamics using acoustic pharyngometry may c

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

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

102 ysfunction syndrome (RADS), asthma, reactive upper airways dysfunction syndrome (RUDS), gastroesophag

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

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

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

106 ins and toxins that mediate adherence to the upper airway epithelium, an essential early step in path

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

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

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

110 sts were susceptible to RSV infection of the upper airway following intranasal challenge; however, th

111 se data suggest that the middle-aged men had upper airway function midway between that of young norma

112 rons, which control tongue muscles affecting upper airway function, that is metamodulated by metabotr

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

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

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

116 to drop to nearly zero on exhalation; in the upper airways gamma is approximately 30 mN/m and constan

117 The upper airways have been shown to reflect colonization of

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

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

120 and automatic segmentation to delineate the upper airway in 20 children with obstructive sleep apnea

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

122 lung volume have an important effect on the upper airway in subjects with sleep apnea during non-REM

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

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

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

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

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

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

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

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

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

132 Persistent upper airway inflammation caused by agents inhaled in th

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

134 Upper airway inflammation is one of the most frequent he

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

136 and most frequently diagnosed etiologies of upper airway inflammation.

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

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

139 Upper airway involvement can also lead to dyspnea and su

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

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

142 f the soft tissue structures surrounding the upper airway is enlarged in patients with sleep apnea an

143 Segmental analysis demonstrated that the upper airway is restricted throughout the initial two-th

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

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

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

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

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

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

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

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

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

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

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

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

156 nt hypoxia may result in oxidative injury to upper airway motoneurons, thereby diminishing serotonerg

157 icant endoplasmic reticulum injury in select upper airway motoneurons.

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

159 dulating the capacity for neuroplasticity in upper airway motor control.

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

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

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

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

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

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

166 minantly theta EEG activity) on ventilation, upper airway muscle activation and upper airway resistan

167 does not appear to have a greater effect on upper airway muscle activity as one ages.

168 First we compared upper airway muscle activity between young and middle-ag

169 ts that the initial sleep onset reduction in upper airway muscle activity is due to loss of a 'wakefu

170 st that the initial sleep onset reduction in upper airway muscle activity is due to loss of a 'wakefu

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

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

173 ssociated with the recruitment of four major upper airway muscles (genioglossus, digastric, sternohyo

174 We conclude that LTF of upper airway muscles is an adaptive respiratory behaviou

175 idative and antioxidant capacity in selected upper airway muscles.

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

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

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

179 A prominent role for upper airway neuromuscular control mechanisms in the pat

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

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

182 Common reasons for exclusion were upper airway obstruction (13.5%) and cyanotic congenital

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

184 The model differentiates between upper airway obstruction and complications like bronchos

185 re measurements correlate with the degree of upper airway obstruction during sleep and may have a rol

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

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

188 Even though upper airway obstruction is potentially life-threatening

189 However, upper airway obstruction secondary to severe bleeding in

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

191 Two levels of upper airway obstruction were induced in ten dogs by par

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

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

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

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

196 sleep disruption that occurs in response to upper airway obstruction.

197 tory laryngeal adduction with closure of the upper airway occurs and likely functions to aid autoresu

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

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

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

201 eted protein expressed in the oropharynx and upper airways of humans, mice, rats, and cows.

202 ause epithelial cell tumors in the lower and upper airways of sheep and goats.

203 V) cause contagious cancers in the lungs and upper airways of sheep and goats.

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

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

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

207 tromyograms, videofluoroscopic images of the upper airway, oronasal airflow and respiratory inductanc

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

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

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

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

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

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

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

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

216 akefulness, active neural processes preserve upper airway patency, such that measurement of upper air

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

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

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

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

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

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

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

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

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

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

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

228 848 were used to mimic a viral insult in the upper airways represented by primary human nasal epithel

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

230 designed to assess whether elevated sleeping upper airway resistance (R(UA)) alters the ventilatory r

231 estigated muscle activity, ventilation , and upper airway resistance (UAR) during wakefulness and sle

232 tilation, upper airway muscle activation and upper airway resistance (UAR) in middle-aged and younger

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

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

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

236 iratory airflow, which they do by regulating upper-airway resistance.

237 show that serotonin-dependent plasticity in upper airway respiratory output is similar in F344 and S

238 1.3 l min(-1); P < 0.05), but did not alter upper airway responsiveness (P = 0.7).

239 Upper airway responsiveness was defined as the ratio of

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

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

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

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

244 ctive sleep apnea syndrome involves abnormal upper airway sensory input, which may be responsible for

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

246 <0.01), 19% had a relatively noncollapsible upper airway similar to many of the control subjects (Pc

247 at lung volume during wakefulness influences upper airway size and resistance, particularly in patien

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

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

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

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

252 first time family aggregation of size of the upper airway soft tissue structures has been demonstrate

253 maging in a case-control design to study the upper airway soft tissue structures in 48 control subjec

254 , our data indicate that heritability of the upper airway soft tissue structures is found in normal s

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

256 study the family aggregation of the size of upper airway soft tissue structures that are associated

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

258 Analysis of upper airway specimens identifies specific inflammatory

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

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

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

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

263 Upper airway stiffness was determined by injecting known

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

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

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

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

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

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

270 Upper airway symptoms among responders to the terrorist

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

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

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

274 1, asthma with a moderate course, intensive upper airway symptoms, and blood eosinophilia (18.9% of

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

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

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

278 smoke have been placed on the lungs and the upper airways, this finding highlights the fact that mul

279 tion is the most serious, reinfection of the upper airway throughout life is the rule.

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

281 cells, a pattern similar to that reported in upper airway tissues.

282 low transducer were placed in the lung model upper airway to measure the volume of CO2 rebreathed and

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

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

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

286 and obese rats was associated with decreased upper airway (UA) collapsibility (p < 0.05), unchanged m

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

288 The upper airway undergoes progressive changes during childh

289 he sap operon within sites of the chinchilla upper airway upon infection.

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

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

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

293 Fiberoptic imaging in an isolated, sealed upper airway was performed in 10 decerebrate cats to det

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

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

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

297 ve apnea patients have an anatomically small upper airway with augmented pharyngeal dilator muscle ac

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

299 y is due to an anatomically more collapsible upper airway with more negative pressure driven muscle a

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