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1 ch share a common complication of reversible airflow obstruction.
2 io are considered the standard assessment of airflow obstruction.
3 ol, and apoB are associated with more severe airflow obstruction.
4 richment analysis to a meta-analyzed GWAS of airflow obstruction.
5 the presence of comorbidities compared with airflow obstruction.
6 the lungs that leads to progressive chronic airflow obstruction.
7 d with abnormal immune responses, leading to airflow obstruction.
8 erapy in 5,887 smokers with mild to moderate airflow obstruction.
9 der characterized by incompletely reversible airflow obstruction.
10 r (3) maldistribution of inspired gases with airflow obstruction.
11 ding onto the development and persistence of airflow obstruction.
12 d implicate the HTR4 gene in the etiology of airflow obstruction.
13 scular inflammation and largely irreversible airflow obstruction.
14 compartments correlated with the severity of airflow obstruction.
15 xacerbations, independent of the severity of airflow obstruction.
16 l as mucus hypersecretion, which can lead to airflow obstruction.
17 vital capacity (FEV(1)/FVC), an indicator of airflow obstruction.
18 , spirometry should be performed to diagnose airflow obstruction.
19 re most evident in patients with more severe airflow obstruction.
20 ikely amplifies inflammation and progressive airflow obstruction.
21 d biosynthesis correlated with the degree of airflow obstruction.
22 lead to bronchial lymphedema and exaggerated airflow obstruction.
23 ated with exposure intensity, independent of airflow obstruction.
24 re asthma, likely contribute to irreversible airflow obstruction.
25 well as mucus hypersecretion with subsequent airflow obstruction.
26 ure intensity, independent of ex-smoking and airflow obstruction.
27 derate airflow obstruction and 2.61 for mild airflow obstruction.
28 group may disclose novel mechanisms of fixed airflow obstruction.
29 n and did not correlate with the severity of airflow obstruction.
30 rment of the diffusion capacity (DL(CO)) and airflow obstruction.
31 n is not a major risk factor for progressive airflow obstruction.
32 /- 15 yr (mean +/- SD) with fixed expiratory airflow obstruction.
33 guish between infants with and those without airflow obstruction.
34 arly evident in patients with severe chronic airflow obstruction.
35 a risk factor for the development of chronic airflow obstruction.
36 way remodeling seen in patients with chronic airflow obstruction.
37 ce by 2 weeks of age and was associated with airflow obstruction.
38 ased risk of developing chronic irreversible airflow obstruction.
39 NO2 levels can be associated with increased airflow obstruction.
40 y, cell adhesion, epigenetic regulation, and airflow obstruction.
41 PRM(FSA) and age in subjects with or without airflow obstruction.
42 asthma with a history of smoking and chronic airflow obstruction.
43 ts with mild to moderate post-bronchodilator airflow obstruction.
44 sistent respiratory symptoms and progressive airflow obstruction.
45 iation contributing to emphysema with severe airflow obstruction.
46 stratified by asthma symptom control and by airflow obstruction.
47 ncreased in both groups with the severity of airflow obstruction.
48 with increased cough, sputum production, and airflow obstruction.
49 links between asthma and subsequent chronic airflow obstruction.
50 racts with SZ-AATD to significantly increase airflow obstruction.
51 co smoking are risk factors for irreversible airflow obstruction.
52 a have additive or multiplicative effects on airflow obstruction.
53 r human study subjects developed significant airflow obstruction 10 min postexposure which persisted
57 To examine sex differences in the risk of airflow obstruction (a COPD hallmark) in relation to smo
59 nchodilators was associated with more severe airflow obstruction, a predominantly solid pattern of LA
60 ntial shared genetic architecture underlying airflow obstruction across individuals, irrespective of
62 acute respiratory events in smokers without airflow obstruction affect lung function decline is unkn
63 ogeneic hematopoietic stem cell transplants, airflow obstruction (AFO) remains a significant complica
64 s that may be involved in the development of airflow obstruction after hematopoietic cell transplanta
67 etric abnormalities, and was correlated with airflow obstruction, air trapping, and diffusing capacit
69 isease of the lung characterized by variable airflow obstruction, airway hyperresponsiveness (AHR), a
70 common chronic lung disease characterized by airflow obstruction, airway hyperresponsiveness (AHR), a
72 vel of CerS2 was associated with significant airflow obstruction, airway inflammation, and increased
73 irways hyperresponsiveness (AHR), reversible airflow obstruction, airway remodeling, and episodic exa
74 arette smoking correlated more strongly with airflow obstruction among PI*SZ than PI*ZZ subjects.
75 ted a maximum LOD score of 2.09 for moderate airflow obstruction and 2.61 for mild airflow obstructio
76 ase refers to a group of diseases that cause airflow obstruction and a constellation of symptoms, inc
77 but not total IgE, is associated with fixed airflow obstruction and a number of radiological abnorma
79 se characterized by intermittent, reversible airflow obstruction and airway hyperresponsiveness (AHR)
83 8 (LOD = 1.36) and 19 (LOD = 1.09) for mild airflow obstruction and chromosomes 19 (LOD = 1.21) and
84 vided increased evidence for linkage of mild airflow obstruction and chronic bronchitis to several ge
85 tives of these early-onset COPD probands for airflow obstruction and chronic bronchitis was performed
86 t PiMZ heterozygotes have significantly more airflow obstruction and COPD than PiMM individuals and c
90 iated with a significantly increased risk of airflow obstruction and emphysema but the risk of chroni
91 medium-dose inhaled corticosteroids reduces airflow obstruction and improves asthma control in patie
92 human deoxyribonuclease 1 (rhDNase) reduces airflow obstruction and improves mucociliary clearance i
93 racterize the kinetics of grain dust-induced airflow obstruction and inflammation in the lower respir
94 begins in infancy or childhood with variable airflow obstruction and intermittent wheezing, cough, an
95 response (BDR) reflects the reversibility of airflow obstruction and is recommended as an adjunctive
97 ingle inhalation challenge of CDE results in airflow obstruction and lower respiratory tract inflamma
98 e (COPD) is characterized by the presence of airflow obstruction and lung destruction with airspace e
100 ized clinically by older age and more severe airflow obstruction and pathologically by a second T2 ne
101 ung function are at increased risk for fixed airflow obstruction and possibly COPD in early adulthood
102 constrict airway smooth muscle, but elicits airflow obstruction and pulmonary inflammation in patien
103 mmunological biomarkers are related to fixed airflow obstruction and radiological abnormalities in mo
106 ve effects of etoricoxib on allergen-induced airflow obstruction and sputum eosinophils, basal lung f
108 inophilic airway inflammation contributes to airflow obstruction and symptoms in some patients with C
109 Preliminary studies have shown that both airflow obstruction and systemic inflammation may contri
110 positively with the severity of inflammatory airflow obstruction and the level of methacholine airway
111 nd to lesser extent of Twist, was related to airflow obstruction and to expression of a canonical EMT
112 m the association between skin wrinkling and airflow obstruction and to identify genetic polymorphism
113 particular showed a direct correlation with airflow obstruction and treatment requirement in patient
115 pulmonary disease, who had at least moderate airflow obstruction and were taking part in PR, were ran
116 e that included IL-6 (in cases of mild or no airflow obstruction), and one that included BMP1 (in cas
117 nstrated reduced diffusing capacity; 20% had airflow obstruction, and 20% had chest restriction.
118 and 80% had late-onset asthma, 50% had fixed airflow obstruction, and 66% showed a Th2-high phenotype
120 yper-responsiveness, incompletely reversible airflow obstruction, and asthma-related school and work
121 al-appearing lung regions in smokers without airflow obstruction, and it is associated with respirato
122 smooth muscle bronchoconstriction leading to airflow obstruction, and mucous hypersecretion are clini
123 ously that lower respiratory tract symptoms, airflow obstruction, and neutrophilic airway inflammatio
124 d in lungs of never smokers, smokers without airflow obstruction, and patients with COPD by reverse t
125 ovel candidate gene in emphysema with severe airflow obstruction, and rs61754411 is a previously unre
126 ilic inflammation, the attributes of chronic airflow obstruction, and the notion of corticosteroid in
127 cific incidence trends of pre-bronchodilator airflow obstruction (AO) among adults without asthma fro
129 as detected on computed tomography (CT), and airflow obstruction are inversely related to left ventri
131 se findings help to explain heterogeneity of airflow obstruction as well as why, in people with asthm
133 a lung disorder characterized by progressive airflow obstruction associated with inflammation and emp
134 eling and contributes to the mucus plugs and airflow obstruction associated with severe asthma phenot
140 before age 18 years were more likely to have airflow obstruction, but a sex difference in this associ
141 tio Impaired Spirometry (PRISm) will develop airflow obstruction, but there are no established method
142 ve or multiplicative effects on the risk for airflow obstruction, but this has not been demonstrated
143 us by goblet cells, which leads to worsening airflow obstruction by luminal obstruction of small airw
144 d-onset persistent asthma is associated with airflow obstruction by mid-adult life, but this does not
145 for INtrinsic and EXtrinsic skin Aging) and airflow obstruction by spirometry, using the ratio of fo
146 essure support ventilation in the setting of airflow obstruction can be accompanied by marked variati
147 revalence of the broader category of chronic airflow obstruction (CAO), defined as asthma, chronic br
151 LOD = 1.70) and 19 (LOD = 1.54) for moderate airflow obstruction, chromosomes 8 (LOD = 1.36) and 19 (
152 d one that included BMP1 (in cases of severe airflow obstruction).Conclusions: Two distinct stromal g
153 atopoietic stem cell transplantation-related airflow obstruction, consensus diagnostic criteria, and
154 ight into the specific mechanisms underlying airflow obstruction, COPD, and tobacco addiction, and sh
155 ontrol, recurrent exacerbations, and chronic airflow obstruction despite adequate and, in many cases,
156 a have frequent exacerbations and persistent airflow obstruction despite treatment with inhaled gluco
159 to -13.2]; p=0.006), higher Body Mass Index, Airflow Obstruction, Dyspnea, and Exercise Capacity (BOD
160 total score (SGRQ), and the body mass index, airflow obstruction, dyspnea, and exercise capacity (BOD
161 to -8.556; P < 0.001), and body mass index, airflow obstruction, dyspnea, and exercise capacity inde
162 ore, -0.6 points; and BODE (body mass index, airflow obstruction, dyspnea, and exercise capacity) ind
163 OPD assessment test scores, Body-mass index, airflow Obstruction, Dyspnea, and Exercise index, or Glo
164 cted, 37 [29-45]; and BODE [body mass index, airflow obstruction, dyspnea, and exercise] index, 6 [5-
165 The BODE index (including body-mass index, airflow obstruction, dyspnoea, and exercise capacity) wa
166 ecreased lung function and increased odds of airflow obstruction, even in participants who had never
167 esent in symptomatic infants with reversible airflow obstruction, even in the presence of atopy.
168 c airway disease characterized by paroxysmal airflow obstruction evoked by irritative stimuli on a ba
170 predicted, FEV(1)/FVC < 90% predicted], mild airflow obstruction (FEV(1) < 80% predicted, FEV(1)/FVC
171 ion, the patients with LDA continued to show airflow obstruction (FEV(1)% predicted = 65.4 +/- 2.9).
172 ed physical activity (multisensory armband), airflow obstruction (FEV1), health status (St. George's
174 health and functional impact of undiagnosed airflow obstruction for subjects in the general populati
175 f lung for carbon monoxide (Dlco%) than with airflow obstruction (forced expiratory volume in 1 secon
176 or qualitative phenotypes including moderate airflow obstruction [forced expiratory volume at one sec
177 cts with asthma who smoke or who have severe airflow obstruction from linkage analysis, as well as in
178 fied ADO index (including age, dyspnoea, and airflow obstruction) from the Swiss cohort, and validate
180 A proportion of 26.3% of smokers without airflow obstruction had ND-E/I greater than the 90th per
181 f of the estimated 24 million Americans with airflow obstruction have received a COPD diagnosis, and
182 tantial proportion of subjects without overt airflow obstruction have significant respiratory morbidi
183 morbidity, more severe BDR and BHR, greatest airflow obstruction, high smoking prevalence, higher sym
184 acity (FVC) ratio is used as a criterion for airflow obstruction; however, the test characteristics o
185 isease characterized, in part, by reversible airflow obstruction, hyperresponsiveness and inflammatio
186 Cluster analysis of adults with symptomatic airflow obstruction identifies 5 disease phenotypes, inc
191 all conducting airways are the major site of airflow obstruction in chronic obstructive pulmonary dis
192 y therapy caused significant improvements in airflow obstruction in eosinophilic asthma, but not in p
193 fferences in gene expression were related to airflow obstruction in epithelial cells (C3, ALOX5AP, CC
194 Spirometry should not be used to screen for airflow obstruction in individuals without respiratory s
195 be a marker of neutrophilic inflammation and airflow obstruction in patients with asthma, who have a
196 ar-capillary membrane function and increases airflow obstruction in patients with LVD but not in norm
198 at spirometry should be obtained to diagnose airflow obstruction in patients with respiratory symptom
199 hyperreactivity (AHR, defined by exaggerated airflow obstruction in response to bronchoconstrictors),
201 nchitis to several genomic regions; for mild airflow obstruction in smokers only, the maximum LOD was
202 function, greater risk of the development of airflow obstruction in smokers, a predisposition to lowe
203 en Pneumocystis colonization and severity of airflow obstruction in smokers, suggesting a possible pa
204 usceptible (n = 64) to emphysema with severe airflow obstruction in the Pittsburgh Specialized Center
206 ched among genes associated with more severe airflow obstruction in these COPD cohorts (P < 0.001), s
207 ammation and remodeling, although persistent airflow obstruction in these patients was associated wit
209 ay inflammation, airway wall remodeling, and airflow obstruction in this prevalent disease syndrome.
211 Although asthma typically induces reversible airflow obstruction, in some patients airflow obstructio
212 tive associations with emphysema with severe airflow obstruction, including a suggestive association
218 exposed to organic dusts, the progression of airflow obstruction is related to the endotoxin concentr
220 defined by irreversible airflow obstruction; airflow obstruction is typically determined by reduction
221 isorder marked by inflammation and recurrent airflow obstruction, is associated with elevated levels
222 ed, which provided additional support for an airflow obstruction locus in that region with a non-para
224 -parametric multipoint approach for moderate airflow obstruction (LOD = 2.13) and mild airflow obstru
225 EBC LXA4 levels correlate with the degree of airflow obstruction measured by using FEV1 (r = 0.28, P
226 The cardinal feature of COPD is persistent airflow obstruction, measured by reductions in quantitat
227 hort: the body-mass index (B), the degree of airflow obstruction (O) and dyspnea (D), and exercise ca
228 the two study groups by Day 6 for indices of airflow obstruction obtained from gamma-camera images of
232 th all-cause mortality among persons without airflow obstruction or COPD in a general population samp
233 have shown significant associations between airflow obstruction or COPD with a non-synonymous SNP in
235 with isolated diaphragm weakness but without airflow obstruction or hyperinflation, a group that woul
236 ot appear to be a significant determinant of airflow obstruction or lower airway inflammation followi
237 iratory tract disease can manifest itself as airflow obstruction or viral pneumonia, which can be fat
238 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 th muscle function and may contribute to the airflow obstruction phenotype observed in human CF.
243 exacerbations include previous exacerbation, airflow obstruction, poor overall health, home oxygen us
244 linear regression, for participants without airflow obstruction, PRM(fSAD) but not PRM(emph) was ass
246 n men and women is similarly associated with airflow obstruction, respiratory symptoms, more emphysem
247 cal CT can accurately demonstrate reversible airflow obstruction resulting from airway hyperreactivit
248 ations of asthma are thought to be caused by airflow obstruction resulting from airway inflammation,
249 .16, 1.03-1.32), and incompletely reversible airflow obstruction (RR 1.28, 1.04-1.57) than did those
253 sex), NO2 levels were associated highly with airflow obstruction, such that each 10-ppb increase in N
254 f an EEG arousal accentuated the response to airflow obstruction, such that the PAT amplitude decreas
255 provide evidence for significant linkage to airflow obstruction susceptibility loci on chromosomes 2
256 of the small airways leading to progressive airflow obstruction, termed bronchiolitis obliterans syn
258 syndrome (BOS) is a condition of progressive airflow obstruction that affects a majority of lung tran
259 ic obstructive pulmonary disease (COPD) have airflow obstruction that leads to dynamic lung hyperinfl
260 CHRNA5/3 region as a genetic risk factor for airflow obstruction that may be independent of smoking a
261 conclude that in the absence of significant airflow obstruction the volume of transplanted immature
262 tory and physical examination for predicting airflow obstruction; the value of spirometry for screeni
263 tics of chronic persistent asthma, including airflow obstruction, use of corticosteroid medications,
266 COPD is characterised by poorly reversible airflow obstruction usually due to cigarette smoking.
268 ver diagnosed asthma and post-bronchodilator airflow obstruction was 44.8%, 19.3% and 7.5%, respectiv
271 Increasing PRM(FSA) in subjects without airflow obstruction was associated with increased FVC (P
273 ealth and functional status with undiagnosed airflow obstruction was independently associated with se
280 Categories of diagnosed and undiagnosed airflow obstruction were defined using questionnaire res
281 eparate models for subjects without and with airflow obstruction were generated using baseline clinic
282 of emphysema on CT scanning and more severe airflow obstruction were linearly related to impaired le
284 The agreement was less in the infants with airflow obstruction where the N2 washout gave slightly h
285 smoked pipes or cigars had increased odds of airflow obstruction whether they had also smoked cigaret
286 sorders encompassing different phenotypes of airflow obstruction, which might differ in their respons
288 s were obese female patients with reversible airflow obstruction who exhibited airway wall thickening
289 te-onset older male subjects with persistent airflow obstruction who exhibited significant air trappi
290 edominance of patients with mild to moderate airflow obstruction who would not experience additional
292 ual emphysema at CT demonstrated progressive airflow obstruction with lower values of ratio of forced
296 re was also no evidence of an association of airflow obstruction with use of solid fuels (ORmen=1.00,
298 idence supporting the association of COPD or airflow obstruction with use of solid fuels is conflicti
299 methods with GWASs of pulmonary function and airflow obstruction would identify a broader repertoire
300 alyses were conducted to identify effects on airflow obstruction, YKL-40 levels, and asthma severity.