ライフサイエンスコーパス: airflow

1 d have a high sampling efficiency and a high airflow.

2 HFEV(1) group to catastrophic reductions in airflow.

3 the spatiotemporal structure of the expelled airflow.

4 naturally occurs in the lung due to lateral airflow.

5 to poor asthma control and deterioration of airflow.

6 ed by the mechanical response of whiskers to airflow.

7 e their whiskers to help detect and localize airflow.

8 that rats also use whiskers to help localize airflow.

9 eath inspiratory loads, inspiratory time and airflow acceleration increased to preserve volume, and i

10 acute respiratory distress syndrome in whom airflow, airway pressure, and esophageal pressure were r

11 al fluid dynamics simulations of respiratory airflow and droplet transport in medical imaging-based d

12 Infant VmaxFRC predicted reduced airflow and infant tptef/te reduced HRCT airway caliber

13 cally presents with a diurnal variability in airflow and is a characteristic that is usually not seen

14 hanges in airway dynamics impairs expiratory airflow and leads to progressive air trapping.

15 furcation generation G9 was used to simulate airflow and particle transport within the respiratory tr

16 s that can be used to measure nasal patency, airflow and resistance, mainly peak nasal inspiratory fl

17 rons to detect increases in the wing-induced airflow and that JO neurons are involved in a response t

18 tigates the whiskers' mechanical response to airflow and the associated neural response.

19 heterogeneous chemistry, along with stagnant airflow and uninterrupted emissions from power plants an

20 e orientation of the whisker relative to the airflow, and is influenced by the whisker's resonant fre

21 te smoke (WCS) under physiological breathing airflow, are lacking.

22 arallel to perpendicular with respect to the airflow as airspeed increases.

23 was delivered with respect to initiation of airflow as variation in this parameter would influence l

24 Frontal airflow, as experienced during forward flight, causes an

25 e of oxygen dependence at 36 weeks rose, and airflows at 8 years of age were worse in 2005 than in ea

26 Modeled airflow back-trajectories suggest that the elevated conc

27 ocal fold oscillation is passively driven by airflow between the lungs and upper respiratory spaces,

28 A high airflow blower enables rapid cooling.

29 tive expiration and reduced early expiratory airflow but only during wake.

30 ir surrounding the pileus creates convective airflows capable of carrying spores at speeds of centime

31 It has long been desired to match airflow conditions during formulation evaluation to thos

32 presented directional visual, olfactory, and airflow cues known to elicit orienting behavior.

33 ence of optic flow by using only directional airflow cues, and require simultaneous odor and directio

34 y administration of azithromycin can improve airflow decline-free survival after allogeneic HSCT.

35 The primary efficacy end point was airflow decline-free survival at 2 years after randomiza

36 nistration of azithromycin resulted in worse airflow decline-free survival than did placebo; these fi

37 ithromycin vs 50 placebo) had experienced an airflow decline; 138 patients (30%) died (78 azithromyci

38 trial protocol as a significant clinical or airflow deterioration), and the secondary outcome was as

39 detection limit (~0.05 m s(-1) ), multiangle airflow differential response (0 degrees -90 degrees ),

40 y a group of CX neurons that robustly encode airflow direction and are required for proper orientatio

41 priate corrective turns following changes in airflow direction.

42 body (ventral P-FNs) are robustly tuned for airflow direction.

43 Ventral P-FNs did not generate a 'map' of airflow direction.

44 logic gates are scalable to high volumes of airflow, do not consume power at steady state, and can b

45 These findings suggest that nasal airflow entrains ketamine-dependent HFO in diverse brain

46 ently and dynamically manipulate 3D objects, airflow fields, and odor plumes in virtual reality over

47 mouth, highlighting the importance of nasal airflow for generating respiratory oscillations.

48 Observations made in westerly airflow (from parts of London where traffic is a smaller

49 tive expiration and reduced early expiratory airflow (i.e. increased upper airway resistance) only du

50 ensors capable of monitoring the environment airflow in real time are rarely reported.

51 ons project a westward shift of anticyclonic airflow in summer, but uncertainty is larger for spring

52 We aimed to compare maximal expiratory airflow in these individuals during late adolescence and

53 The expiratory time constants of regional airflows in the segmented airway tree were quantified as

54 cating that syringeal sounds are produced by airflow-induced labia and membrane vibration.

55 brain thus likely evolved in part to process airflow information.

56 nd require simultaneous odor and directional airflow input for plume following to a host volatile ble

57 smooth muscle and the subsequent decrease in airflow involve a poorly understood set of mechanical an

58 caused by HMW agents showed a higher risk of airflow limitation (1.76 [1.07-2.91]), whereas OA due to

59 patients with fixed as compared to variable airflow limitation (69.76 vs 43.84 pg/ml, P < 0.05) and

60 Most patients with airflow limitation (70.6%) had no previous spirometry te

61 measures as z-score, and a classification of airflow limitation (AL) based on this parameter has rece

62 [95% CI, 1.66-4.24]; P < .001) but not with airflow limitation (aOR, 1.07 [95% CI, .71-1.62]; P = .7

63 ng sites, aged at least 40 years, with known airflow limitation (defined as a post-bronchodilator FEV

64 xpression was also associated with increased airflow limitation (FEV1/forced vital capacity and resid

65 associated with a higher risk of subsequent airflow limitation (odds ratio [95% confidence interval]

66 ated with increased risk of incident stage 2 airflow limitation (ratio of FEV1 to forced expiratory v

67 linical history of COPD, along with moderate airflow limitation and an increased risk of exacerbation

68 ion does not mediate the association between airflow limitation and atherosclerosis.

69 Instead, airflow limitation and endothelial dysfunction seem to b

70 bronchial airway hyperreactivity and chronic airflow limitation and has been described as leading to

71 ith asthma had more respiratory symptoms and airflow limitation and higher levels of inflammatory and

72 nificantly down-regulated in smokers without airflow limitation and in patients with COPD compared wi

73 ulmonary disease, moderate-severe expiratory airflow limitation and radiologically determined bronchi

74 ributable to variation in the definitions of airflow limitation and the treatment of people with asth

75 Background Fixed airflow limitation and ventilation heterogeneity are com

76 and cardiac markers and support the role of airflow limitation as independent predictor of mortality

77 and CMH, how symptoms during life related to airflow limitation at 60-64 years, and how CMH duration

78 A measure of airflow limitation but not vital capacity was associated

79 y disease (COPD) is characterized by chronic airflow limitation caused by a combination of airways di

80 Airflow limitation compatible with chronic obstructive p

81 tinguishable, but many patients with chronic airflow limitation demonstrate features of both conditio

82 ations with decline in FEV1 and incidence of airflow limitation for adults who were free from COPD at

83 els in sputum are associated with persistent airflow limitation in asthma patients with airway eosino

84 The aim of the ALICE (Airflow Limitation in Cardiac Diseases in Europe) study

85 ) study was to investigate the prevalence of airflow limitation in patients with ischemic heart disea

86 etic factors and is strongly associated with airflow limitation in smaller airways.

87 Airway remodeling burden is not limited to airflow limitation in the assessment of COPD severity an

88 re less likely to have undergone testing for airflow limitation in the community at the time of initi

89 ne in adulthood, and development of moderate airflow limitation in the general adult population.

90 iation between atopy and post-bronchodilator airflow limitation in the general population aged 40 yea

91 iation between atopy and post-bronchodilator airflow limitation in the general population appears to

92 airways and reduced airway resistance, while airflow limitation in the LFEV(1) is due to increased ai

93 Although airflow limitation is associated with additional morbidi

94 Treatments for airflow limitation might improve survival and both respi

95 und Longitudinal progression to irreversible airflow limitation occurs in approximately 10% of patien

96 h emphysema were matched for the severity of airflow limitation of those with bronchiolitis.

97 disease (COPD) is defined by the presence of airflow limitation on spirometry, yet subjects with COPD

98 The no airflow limitation or air-trapping criteria (None) pheno

99 nt asthma (defined as wheeze and presence of airflow limitation or airway hyper-reactivity, or both).

100 ficant for spirometric phenotypes related to airflow limitation or COPD.

101 The airflow limitation phenotype (A Limit) had an FEV1/FVC z

102 ire and were classed as having or not having airflow limitation through pulmonary function tests befo

103 The prevalence of asthma with airflow limitation was 1.1% (0.9-1.4), representing 13.1

104 Airflow limitation was associated with greater respirato

105 Airflow limitation was defined as post-bronchodilator FE

106 Airflow limitation was defined as post-bronchodilator sp

107 Airflow limitation was observed in 30.5% of patients wit

108 with ischemic heart disease: 11.3% had mild airflow limitation, 15.8% moderate airflow limitation, 3

109 ator spirometry, to identify the presence of airflow limitation, 18,475 subjects (99%) were assigned

110 had mild airflow limitation, 15.8% moderate airflow limitation, 3.3% severe airflow limitation, and

111 .8% moderate airflow limitation, 3.3% severe airflow limitation, and 0.1% very severe airflow limitat

112 mpassing 8 never-smokers, 10 smokers without airflow limitation, and 12 smokers with COPD.

113 but without current or previous evidence of airflow limitation, bronchial reversibility, or airway h

114 ged 40-85 years, had moderate to very severe airflow limitation, had elevated blood eosinophil counts

115 rimarily of young, obese females with severe airflow limitation, little eosinophilic inflammation, an

116 COPD is characterized by persistent airflow limitation, neutrophilia and oxidative stress fr

117 ntiating asthma from other causes of chronic airflow limitation, such as chronic obstructive pulmonar

118 ic obstructive pulmonary disease with severe airflow limitation, symptoms of chronic bronchitis, and

119 ording to simple clinical measures (level of airflow limitation, symptoms, and frequency of previous

120 a with low cumulated smoking exposure and no airflow limitation, those with COPD, those with asthma-C

121 y variable respiratory symptoms and variable airflow limitation.

122 on was stratified by country and severity of airflow limitation.

123 ults in largely irreversible and progressive airflow limitation.

124 ditional common characteristic is reversible airflow limitation.

125 ith COPD and explore their relationship with airflow limitation.

126 ed with the AA genotype demonstrated greater airflow limitation.

127 ere airflow limitation, and 0.1% very severe airflow limitation.

128 rrelated with the type 2 immune response and airflow limitation.

129 y disease (COPD) is characterized by chronic airflow limitation.

130 post-bronchodilator measures for those with airflow limitation.

131 deration in the diagnosis of asthma based on airflow limitation.

132 lly characterized by incompletely reversible airflow limitation.

133 erized by incompletely reversible expiratory airflow limitation.

134 not associated with emphysema or severity of airflow limitation.

135 Here we use 3D airflow modelling to demonstrate that local dune topogra

136 Airflow models at length scales relevant to landform siz

137 ment periods for total symptom scores, nasal airflow, nasal secretion weight, and nasal congestion sc

138 d safety, nasal and nonnasal symptoms, nasal airflow, nasal secretions, basophil activation, and plas

139 COPD (198 [4%] of 4439) and smokers without airflow obstruction (255 [5%] of 5547).

140 To examine sex differences in the risk of airflow obstruction (a COPD hallmark) in relation to smo

141 cific incidence trends of pre-bronchodilator airflow obstruction (AO) among adults without asthma fro

142 acute exacerbation (AE) in patients without airflow obstruction (Asthma AE group).

143 ed physical activity (multisensory armband), airflow obstruction (FEV1), health status (St. George's

144 f lung for carbon monoxide (Dlco%) than with airflow obstruction (forced expiratory volume in 1 secon

145 ntial shared genetic architecture underlying airflow obstruction across individuals, irrespective of

146 acute respiratory events in smokers without airflow obstruction affect lung function decline is unkn

147 that could be related to symptom control and airflow obstruction after standardized treatment.

148 ase refers to a group of diseases that cause airflow obstruction and a constellation of symptoms, inc

149 but not total IgE, is associated with fixed airflow obstruction and a number of radiological abnorma

150 control subjects and influenced by worsening airflow obstruction and corticosteroid use.

151 al dysfunction, which results in progressive airflow obstruction and debility.

152 apoA-I and large HDLNMR particles can reduce airflow obstruction and disease severity in asthma.

153 medium-dose inhaled corticosteroids reduces airflow obstruction and improves asthma control in patie

154 begins in infancy or childhood with variable airflow obstruction and intermittent wheezing, cough, an

155 early-onset nonsevere asthma and reversible airflow obstruction and normal airway structure.

156 ized clinically by older age and more severe airflow obstruction and pathologically by a second T2 ne

157 ung function are at increased risk for fixed airflow obstruction and possibly COPD in early adulthood

158 constrict airway smooth muscle, but elicits airflow obstruction and pulmonary inflammation in patien

159 mmunological biomarkers are related to fixed airflow obstruction and radiological abnormalities in mo

160 Fixed airflow obstruction and radiological abnormalities were

161 Understanding the genetic basis of airflow obstruction and smoking behaviour is key to dete

162 In adults, differences in airflow obstruction and symptoms between SA and NONSA pe

163 Preliminary studies have shown that both airflow obstruction and systemic inflammation may contri

164 nd to lesser extent of Twist, was related to airflow obstruction and to expression of a canonical EMT

165 m the association between skin wrinkling and airflow obstruction and to identify genetic polymorphism

166 We found no association between airflow obstruction and use of solid fuels for cooking o

167 pulmonary disease, who had at least moderate airflow obstruction and were taking part in PR, were ran

168 Defining airflow obstruction as FEV1:FVC less than 0.70 provided

169 Airflow obstruction assessed from post-bronchodilator sp

170 a lung disorder characterized by progressive airflow obstruction associated with inflammation and emp

171 eling and contributes to the mucus plugs and airflow obstruction associated with severe asthma phenot

172 osing COPD in patients with mild to moderate airflow obstruction at baseline.

173 is similar to cluster T2 in terms of chronic airflow obstruction but is composed of nonsmokers.

174 d-onset persistent asthma is associated with airflow obstruction by mid-adult life, but this does not

175 for INtrinsic and EXtrinsic skin Aging) and airflow obstruction by spirometry, using the ratio of fo

176 on, airway hyperresponsiveness, and variable airflow obstruction cause cough are unclear.

177 Asthma is a disease of reversible airflow obstruction characterised clinically by wheezing

178 ontrol, recurrent exacerbations, and chronic airflow obstruction despite adequate and, in many cases,

179 Patients with moderate chronic airflow obstruction experienced a reduction in exacerbat

180 Asthmatics with persistent airflow obstruction had greater airway smooth muscle (As

181 A proportion of 26.3% of smokers without airflow obstruction had ND-E/I greater than the 90th per

182 tantial proportion of subjects without overt airflow obstruction have significant respiratory morbidi

183 Cluster analysis of adults with symptomatic airflow obstruction identifies 5 disease phenotypes, inc

184 nd significantly correlated with measures of airflow obstruction in asthma patients.

185 f the gut-lung axis can be targeted to treat airflow obstruction in asthma.

186 all conducting airways are the major site of airflow obstruction in chronic obstructive pulmonary dis

187 be a marker of neutrophilic inflammation and airflow obstruction in patients with asthma, who have a

188 ated in relation to both symptom control and airflow obstruction in severe asthmatics.

189 usceptible (n = 64) to emphysema with severe airflow obstruction in the Pittsburgh Specialized Center

190 ched among genes associated with more severe airflow obstruction in these COPD cohorts (P < 0.001), s

191 ammation and remodeling, although persistent airflow obstruction in these patients was associated wit

192 inant of GCH in ever smokers with or without airflow obstruction is active smoking.

193 Cohort studies suggest that airflow obstruction is established early in life, manife

194 In asthma, airflow obstruction is thought to result primarily from

195 ndent association between skin wrinkling and airflow obstruction of the lung.

196 have shown significant associations between airflow obstruction or COPD with a non-synonymous SNP in

197 iratory tract disease can manifest itself as airflow obstruction or viral pneumonia, which can be fat

198 th muscle function and may contribute to the airflow obstruction phenotype observed in human CF.

199 h severe uncontrolled asthma and the chronic airflow obstruction phenotype.

200 Their effects in patients with milder airflow obstruction remain unclear.

201 r matrix (ECM) processes specifically in the airflow obstruction study.

202 se of smoking, women showed a higher risk of airflow obstruction than men.

203 COPD is characterised by poorly reversible airflow obstruction usually due to cigarette smoking.

204 ver diagnosed asthma and post-bronchodilator airflow obstruction was 44.8%, 19.3% and 7.5%, respectiv

205 Airflow obstruction was assessed by FEV1% predicted.

206 Increasing PRM(FSA) in subjects without airflow obstruction was associated with increased FVC (P

207 bution relative to PRM(FSA) in those without airflow obstruction was limited by its low burden.

208 lity and the predictors of age, dyspnea, and airflow obstruction were available.

209 eparate models for subjects without and with airflow obstruction were generated using baseline clinic

210 s were obese female patients with reversible airflow obstruction who exhibited airway wall thickening

211 te-onset older male subjects with persistent airflow obstruction who exhibited significant air trappi

212 In both sexes, the association of airflow obstruction with cigarettes per day, smoking dur

213 ual emphysema at CT demonstrated progressive airflow obstruction with lower values of ratio of forced

214 To assess the association of airflow obstruction with self-reported use of solid fuel

215 The association of airflow obstruction with smoking characteristics was ass

216 The association of airflow obstruction with smoking status was stronger in

217 re was also no evidence of an association of airflow obstruction with use of solid fuels (ORmen=1.00,

218 The association of airflow obstruction with use of solid fuels for cooking

219 idence supporting the association of COPD or airflow obstruction with use of solid fuels is conflicti

220 methods with GWASs of pulmonary function and airflow obstruction would identify a broader repertoire

221 e that included IL-6 (in cases of mild or no airflow obstruction), and one that included BMP1 (in cas

222 d one that included BMP1 (in cases of severe airflow obstruction).Conclusions: Two distinct stromal g

223 In subjects without airflow obstruction, acute respiratory events were not a

224 In never- and ever-smokers without airflow obstruction, aging is associated with increased

225 common chronic lung disease characterized by airflow obstruction, airway hyperresponsiveness (AHR), a

226 and 80% had late-onset asthma, 50% had fixed airflow obstruction, and 66% showed a Th2-high phenotype

227 al-appearing lung regions in smokers without airflow obstruction, and it is associated with respirato

228 ovel candidate gene in emphysema with severe airflow obstruction, and rs61754411 is a previously unre

229 before age 18 years were more likely to have airflow obstruction, but a sex difference in this associ

230 tio Impaired Spirometry (PRISm) will develop airflow obstruction, but there are no established method

231 ve or multiplicative effects on the risk for airflow obstruction, but this has not been demonstrated

232 ight into the specific mechanisms underlying airflow obstruction, COPD, and tobacco addiction, and sh

233 to -13.2]; p=0.006), higher Body Mass Index, Airflow Obstruction, Dyspnea, and Exercise Capacity (BOD

234 to -8.556; P < 0.001), and body mass index, airflow obstruction, dyspnea, and exercise capacity inde

235 ore, -0.6 points; and BODE (body mass index, airflow obstruction, dyspnea, and exercise capacity) ind

236 OPD assessment test scores, Body-mass index, airflow Obstruction, Dyspnea, and Exercise index, or Glo

237 cted, 37 [29-45]; and BODE [body mass index, airflow obstruction, dyspnea, and exercise] index, 6 [5-

238 tive associations with emphysema with severe airflow obstruction, including a suggestive association

239 ute worsening of asthma symptoms, reversible airflow obstruction, or bronchial hyperresponsiveness af

240 ream driver, whereas in subjects with severe airflow obstruction, pathways downstream of pathological

241 exacerbations include previous exacerbation, airflow obstruction, poor overall health, home oxygen us

242 linear regression, for participants without airflow obstruction, PRM(fSAD) but not PRM(emph) was ass

243 n men and women is similarly associated with airflow obstruction, respiratory symptoms, more emphysem

244 sex), NO2 levels were associated highly with airflow obstruction, such that each 10-ppb increase in N

245 tics of chronic persistent asthma, including airflow obstruction, use of corticosteroid medications,

246 sorders encompassing different phenotypes of airflow obstruction, which might differ in their respons

247 Presence of airflow obstruction, which was defined by a baseline FEV

248 alyses were conducted to identify effects on airflow obstruction, YKL-40 levels, and asthma severity.

249 NO2 levels can be associated with increased airflow obstruction.

250 y, cell adhesion, epigenetic regulation, and airflow obstruction.

251 PRM(FSA) and age in subjects with or without airflow obstruction.

252 asthma with a history of smoking and chronic airflow obstruction.

253 ts with mild to moderate post-bronchodilator airflow obstruction.

254 iation contributing to emphysema with severe airflow obstruction.

255 stratified by asthma symptom control and by airflow obstruction.

256 ncreased in both groups with the severity of airflow obstruction.

257 with increased cough, sputum production, and airflow obstruction.

258 links between asthma and subsequent chronic airflow obstruction.

259 co smoking are risk factors for irreversible airflow obstruction.

260 sistent respiratory symptoms and progressive airflow obstruction.

261 a have additive or multiplicative effects on airflow obstruction.

262 io are considered the standard assessment of airflow obstruction.

263 ol, and apoB are associated with more severe airflow obstruction.

264 racts with SZ-AATD to significantly increase airflow obstruction.

265 richment analysis to a meta-analyzed GWAS of airflow obstruction.

266 ch share a common complication of reversible airflow obstruction.

267 d with abnormal immune responses, leading to airflow obstruction.

268 acity (FVC) ratio is used as a criterion for airflow obstruction; however, the test characteristics o

269 yses, it is important to study the effect of airflow on the parameters of lung sounds.

270 BVC profiling via dynamic (i.e., continuous airflow) or static headspace sampling using solid-phase

271 and the extent and strength of anticyclonic airflow over eastern North America varies with season.

272 tically replicate the nasal cavities and the airflow passing through them from a clinical point of vi

273 perceiving modulations of their self-induced airflow patterns as they enter a ground or wall effect.

274 Maximal expiratory airflow peaks early in the third decade of life, then gr

275 including: misalignments, propeller-induced airflows, power loss, intermodal crosstalk, and system b

276 lse responses convolved with the respiratory airflow predict the classical respiration-locked firing

277 realize highly sensitive detection in a wide airflow range (0.05-7.0 m s(-1) ).

278 The numerical results illustrate that airflow rate distribution at the right lung of a realist

279 n in the context of evolutionarily important airflow-sensing behaviors and olfactory search.

280 , an ultrasensitive and flexible all-textile airflow sensor based on fabric with in situ grown carbon

281 Besides, the fluffy fabric airflow sensor can be combined with a pristine fabric ai

282 Furthermore, the airflow sensor can be directly integrated into clothing

283 believed that the ultrasensitive all-textile airflow sensor holds great promise for applications in s

284 ensor can be combined with a pristine fabric airflow sensor to realize highly sensitive detection in

285 ceptionally large contact area, endowing the airflow sensor with superior properties including ultral

286 However, wearable airflow sensors capable of monitoring the environment ai

287 he mix breath velocity and individual breath airflow signals from the two nostrils.

288 These findings suggest a population code for airflow speed and direction and open new avenues for stu

289 whisker's vibration changes as a function of airflow speed: vibrations transition from parallel to pe

290 reath signals such as temperature, humidity, airflow, stress and strain.

291 asks via a biosecure closed-loop circulating airflow system.

292 B4) phase under topographic confinement with airflow that can induce a shear force and temperature gr

293 data (n = 135); level 3 (L3), which included airflow, thoracoabdominal bands, body position, electroc

294 The pattern of airflow through adulthood for individuals born very pret

295 nts suggest that ventral P-FNs inherit their airflow tuning from neurons that provide input from the

296 Lower airflow values are present by spirometry for prepubertal

297 ensors, monitoring increasing and decreasing airflow velocity, and alerting blind people walking outs

298 Expiratory airflow was measured at 8 years of age, and values were

299 adband, passive, low-cost approach to detect airflow with full fidelity over a frequency bandwidth th

300 dimensional spider silk captures fluctuating airflow with maximum physical efficiency (Vsilk/Vair app