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1 IPF) is a progressive and fatal interstitial lung disease.
2 e treatment of acute lung injury and chronic lung disease.
3 ial effects on wheezing, asthma, and chronic lung disease.
4 e components further differ depending on the lung disease.
5 udy has yet examined the mycobiome in fungal lung disease.
6 te investigation of subclinical interstitial lung disease.
7 uce the risk of progressing to more advanced lung disease.
8 ects of human lung development and pediatric lung disease.
9 important pathobiological factor in early CF lung disease.
10 s, and 1 patient died of severe interstitial lung disease.
11 , destructive skin lesions, and interstitial lung disease.
12 tive outcome measures that capture and track lung disease.
13 jury and in human tissues from subjects with lung disease.
14 ted with abnormal lung perfusion in early CF lung disease.
15 find that SARS-CoV infection causes enhanced lung disease.
16 s no other family history of asthma or other lung disease.
17 that are critical for protection from severe lung disease.
18 mic toxicity in patients with refractory MAC lung disease.
19 opathy, cerebrovascular disease, and chronic lung disease.
20 progression of tissue injury seen in chronic lung disease.
21 development may set the stage for subsequent lung disease.
22 humanized model for pre-clinical studies of lung disease.
23 d potential therapeutic targets for neonatal lung disease.
24 change in structure associated with advanced lung disease.
25 infants who subsequently went on to develop lung disease.
26 expressing mice, a well-established model of lung disease.
27 has a high mortality associated with severe lung disease.
28 ary hypertension due to left-sided heart and lung disease.
29 healthy children) from the progression of CF lung disease.
30 so, whether it is associated with subsequent lung disease.
31 damage in the etiology of flavorings-related lung disease.
32 totype of chronic, progressive, and fibrotic lung disease.
33 utic target in the management of RSV-induced lung disease.
34 ent for the diagnosis of diffuse parenchymal lung disease.
35 hanges in these histologic features indicate lung disease.
36 n health and as altered by acute and chronic lung disease.
37 setting of scleroderma-related interstitial lung disease.
38 ay generations were observed in end-stage CF lung disease.
39 d through endoscopy from 14 patients without lung disease.
40 d pathological signs indicative of end-stage lung disease.
41 as possible therapeutic targets for treating lung disease.
42 5) has been consistently linked to heart and lung disease.
43 hen they are smear-negative or lack cavitary lung disease.
44 ), with most due to progressive interstitial lung disease.
45 by the investigator was due to interstitial lung disease.
46 individuals as well as patients with chronic lung disease.
47 pulmonary fibrosis (IPF) is a deadly chronic lung disease.
48 structive pulmonary disease and occupational lung disease.
49 05 benchmark for all outcomes except chronic lung disease.
50 increase in the work of breathing in chronic lung disease.
51 (CFTR) channel, which can result in chronic lung disease.
52 these chemokine pathways could help improve lung disease.
53 lung physiology consistent with interstitial lung disease.
54 for EHF in regulating epithelial function in lung disease.
55 SPNs in populations with endemic infectious lung disease.
56 cularly phenotype patients with interstitial lung disease.
57 tational age, birth weight, and less chronic lung disease.
58 tion for reducing the burden of occupational lung diseases.
59 acute and chronic inflammatory and fibrotic lung diseases.
60 has been linked to the worsening of ongoing lung diseases.
61 rvention and/or prevention of silica-induced lung diseases.
62 during wound healing and is dysregulated in lung diseases.
63 ypoxic PH and potentially other inflammatory lung diseases.
64 inform the development of new therapies for lung diseases.
65 fibrosis is the hallmark of the interstitial lung diseases.
66 ould underlie the chronicity of inflammatory lung diseases.
67 n cystic fibrosis (CF) and other obstructive lung diseases.
68 ular regulation and function of autophagy in lung diseases.
69 s to the pathogenesis and treatment of human lung diseases.
70 thological fibroblasts and myofibroblasts in lung diseases.
71 thogenesis of Th2-driven asthma and allergic lung diseases.
72 portant trigger of acute episodes of chronic lung diseases.
73 re of cystic fibrosis (CF) and other chronic lung diseases.
74 BEC) is essential for understanding numerous lung diseases.
75 of patients with other progressive fibrotic lung diseases.
76 f transport in persons with muco-obstructive lung diseases.
77 le of the respiratory epithelium in multiple lung diseases.
78 D (Global Initiative for Chronic Obstructive Lung Disease) 0-4 was as follows: 41.8 (47.7), 53.8 (57.
79 l class IV (1.25; 1.03-1.52), severe chronic lung disease (1.67; 1.35-2.05), nonfemoral access site (
80 amyotrophic lateral sclerosis, 44 (4.5%) had lung disease, 26 (2.6%) had heart disease, and 9 (0.9%)
81 lowest rates seen among patients with severe lung disease (51.4%), those undergoing dialysis (47.7%),
83 s in breath samples can potentially indicate lung disease activity and help in the study of airway in
85 ATIONALE: Mechanisms contributing to chronic lung disease after preterm birth are incompletely unders
86 nd Severe Sepsis Risk Score included chronic lung disease, age 75 years or older, peripheral artery d
87 England, and South Atlantic for interstitial lung disease; along the southern half of the Mississippi
88 ere dysfunction and humans with interstitial lung disease also accumulate excess chitin polymers in t
90 urvey to determine the prevalence of chronic lung disease among adults 18 years or older in Malawi, u
91 hage, necrotizing enterocolitis, and chronic lung disease among infants less than 33 weeks' gestation
92 ears) including 4 patients with interstitial lung disease and 3 patients with cutaneous clinical feat
93 ears) including 4 patients with interstitial lung disease and 3 patients with cutaneous clinical feat
94 reviewed consecutive patients with end-stage lung disease and a height of 65 inches or less who under
96 saving option for patients with interstitial lung disease and acute respiratory failure provided they
97 e analysis of all patients with interstitial lung disease and acute respiratory failure treated with
99 lls (iPSCs) would provide valuable models of lung disease and facilitate precision therapies for airw
100 , preterm infants frequently develop chronic lung disease and have a significantly increased risk of
101 multidisciplinary diagnosis of interstitial lung disease and may prove useful in the diagnosis of IP
102 y the investigators, one due to interstitial lung disease and one as a result of multiorgan failure t
104 PD) is characterized by lifelong obstructive lung disease and profound, refractory bronchospasm.
105 ute to understanding the role of exosomes in lung disease and provide suggestions for highly warrante
107 ivo contribution of IL-17 in cystic fibrosis lung disease and the therapeutic validity of attenuating
110 e first introduce representative obstructive lung diseases and examine limitations of currently avail
112 l and clinical research networks in fibrotic lung disease, and create a global lung fibrosis initiati
113 esearch and clinical practice in obstructive lung disease, and drug discovery platforms was invited t
114 fore discharge, NDI, moderate-severe chronic lung disease, and severe retinopathy of prematurity.
115 city or echolucency on neuroimaging, chronic lung disease, and stage 3 or higher retinopathy of prema
117 progressive scleroderma-related interstitial lung disease, and the present preference for mycophenola
118 International Union Against Tuberculosis and Lung Disease, and the World Health Organization also par
119 ferential diagnoses from a choice of diffuse lung diseases, and chose likelihoods (censored at 5% and
120 c output from arteriovenous fistula, hypoxic lung diseases, and metabolic derangements associated wit
122 NDI (aOR, 1.27; 95% CI, 0.78-2.06), chronic lung disease (aOR, 1.36; 95% CI, 0.78-2.39) or severe re
123 hloride levels, failure to thrive (FTT), and lung disease are characteristic features of cystic fibro
125 ract infections and exacerbations of chronic lung diseases are commonly caused by nontypeable Haemoph
127 es, the proximal causes of many occupational lung diseases are well understood and they should be ame
128 thogen in patients with cystic fibrosis (CF) lung disease as well as non-CF bronchiectasis and chroni
129 pportive therapy consistent with any serious lung disease, as no specific drugs have been approved as
130 Lymphangioleiomyomatosis (LAM) is a fatal lung disease associated with germline or somatic inactiv
131 e lung disease, the phenotype of obstructive lung disease associated with work-related organic dust e
133 heart catheterization, medications, chronic lung disease, bleeding diathesis, and immunodeficiency.
134 ntial for the treatment of M. intracellulare lung disease, but optimization of treatment regimens is
136 5 yr) and the Canadian Cohort of Obstructive Lung Disease (CanCOLD) study (n = 1,551 subjects; study
137 y worldwide, the history of asbestos-induced lung disease casts a long shadow over fibrous materials
139 ry aspergillosis (IPA) is a life-threatening lung disease caused by the fungus Aspergillus fumigatus,
141 is a chronic, progressive and fatal fibrotic lung disease characterized by profound changes in stem c
142 erbate fibrogenic pathways in the setting of lung diseases characterized by epithelial cell dysfuncti
143 ution between 2004 and 2014 for interstitial lung disease, chronic obstructive pulmonary disease, or
145 ral mitral regurgitation, moderate or severe lung disease, dialysis, and severe tricuspid regurgitati
146 brosis is a kind of devastating interstitial lung disease due to the limited therapeutic strategies.
147 irway closure has important implications for lung disease, especially asthma; in particular, the pros
148 g (18)F-FDG PET quantification approaches in lung diseases, focusing on methods to account for variat
151 or stage 2 Global initiative for Obstructive Lung Disease (GOLD) COPD who had been clinically stable
152 he Global Initiative for Chronic Obstructive Lung Disease (GOLD) spirometric category (1-4) on the ba
153 on Global Initiative for Chronic Obstructive Lung Disease guidelines, 461 patients (17.6%) had mild,
154 3 patients with Mycobacterium intracellulare lung disease had an initial microbiological response and
156 Knowledge of genetic origins of obstructive lung diseases has made inhaled gene therapy an attractiv
157 all parts of the world, left-sided heart and lung diseases have become the most frequent causes of pu
158 status, older age, higher ejection fraction, lung disease, home oxygen use, lower mean aortic valve g
159 sease (HR, 1.20; 95% CI, 1.04-1.39), chronic lung disease (HR, 1.16; 95% CI, 1.01-1.34), and discharg
160 e, recurrent hyponatremia, infantile FTT and lung disease identified deleterious variants in each CA1
161 echanisms underlying dyspnea in interstitial lung disease (ILD) and chronic obstructive pulmonary dis
162 DPO) in patients with fibrosing interstitial lung disease (ILD) and determine whether there are diffe
163 fic signatures across end-stage interstitial lung disease (ILD) cases, (2) characterize ILD subgroups
164 s (IPF) is a progressive, fatal interstitial lung disease (ILD) characterized by abnormal extracellul
170 sm to delay or prevent the development of CF lung disease in a manner independent of CF transmembrane
171 e UK) evaluated cases of diffuse parenchymal lung disease in a two-stage process between Jan 1, and O
172 nce imaging (MRI) were shown to detect early lung disease in CF; however, the relationship between th
173 summarizes what we have learned about early lung disease in children with CF and discusses the impli
174 RATIONALE: Early onset and progression of lung disease in children with cystic fibrosis (CF) indic
181 eful surveillance tool to monitor structural lung disease in preschool and school-age children with C
182 produced modest improvements in radiographic lung disease in subjects with G551D-CFTR mutations.
184 the mechanisms leading to the development of lung disease in the setting of neonatal necrotizing ente
185 biopsies performed annually for interstitial lung disease in the United States, two-thirds of which w
187 t and/or progression of chronic inflammatory lung diseases including asthma, chronic obstructive pulm
188 hysiological hallmarks of severe obstructive lung diseases including chronic obstructive pulmonary di
189 eudomonas aeruginosa colonization in chronic lung disease, including cystic fibrosis (CF) and chronic
190 uman immune cells can induce features of RSV lung disease, including mucus hyperplasia, in murine lun
192 ggest involvement of pendrin in inflammatory lung diseases, including cystic fibrosis (CF), perhaps b
194 ession in patients with CF and other chronic lung diseases, including the role respiratory viral infe
195 to SARS-CoV and how it may be implicated in lung disease induced by other highly pathogenic respirat
196 We used a transgenic mouse model of chronic lung disease induced by the overexpression of transformi
198 n used for noninvasive diagnosis of a fungal lung disease (IPA) of humans, an approach with enormous
199 igate the hypothesis that flavorings-related lung disease is caused by in vivo protein damage, we cor
202 t diagnostic approach to diffuse parenchymal lung disease is crucial if clinical trial data are to be
204 ective surgical lung biopsy for interstitial lung disease is just under 2% but significantly higher f
205 Thus, our findings establish that fibrotic lung disease is mediated, in part, by senescent cells, w
209 nnective tissue disease-related interstitial lung disease (kappaw=0.73 [0.68-0.78]); moderate for non
210 lar disease, chronic kidney disease, chronic lung disease, liver disease, and cancer) and all-cause m
211 e (>/=70%) have higher prevalence of chronic lung disease, lower birth weight, and longer nursery sta
212 lungs indicates continuous infection in MAC lung disease (MAC-LD), but its clinical significance has
213 r disease, diabetes mellitus, liver disease, lung disease, malignancy, other organ transplantation, a
214 to understanding the pathogenesis of chronic lung disease may reside in deciphering the complex inter
215 he findings support that chronic obstructive lung diseases may have at least part of their origins in
216 entres with scleroderma-related interstitial lung disease meeting defined dyspnoea, pulmonary functio
217 STING N153S mice lacking IRF3 also developed lung disease, myeloid cell expansion, and T cell cytopen
219 ilzomib group (pneumonia [n=2], interstitial lung disease [n=1], septic shock [n=1], and unknown [n=1
225 bronchopulmonary dysplasia (BPD), a chronic lung disease of prematurity that often leads to sequelae
231 e lung clearance index to reflect structural lung disease on the basis of chest computed tomography a
232 -affected individuals experience progressive lung disease or cardiac and nervous system involvement (
236 e heart disease, stroke, chronic obstructive lung disease, or cancer at the time they answered this b
237 clinically significant trauma, occupational lung disease, or reportable disease, and did not signifi
239 (MMP-7) has been implicated in interstitial lung disease pathobiology and proposed as a diagnostic a
240 llations and endogenous PaO2 oscillations in lung-diseased patients have different origins, it is lik
241 f invasive aspergillosis, a frequently fatal lung disease primarily affecting immunocompromised indiv
242 acterize a new subtype of congenital diffuse lung disease, provide a histological correlate, and supp
245 The incidence of interstitial and malignant lung diseases remains unacceptably high because control
248 sitivity pneumonitis (OHP) is an immunologic lung disease resulting from lymphocytic and frequently g
250 DI, and there were no differences in chronic lung disease, retinopathy of prematurity, or NDI among s
252 ings support a role for CXCL1 and IL-8 in CF lung disease severity and identify STAT3 as a modulating
253 CXCL1 and IL8 polymorphisms with changes in lung disease severity in patients with CF (n = 6365; IL8
256 et Global Initiative for Chronic Obstructive Lung Disease spirometric criteria for lung-function impa
257 in Global Initiative for Chronic Obstructive Lung Disease stage 1, where each exacerbation was associ
259 D (Global Initiative for Chronic Obstructive Lung Disease stage I to II) before and after treatment w
260 D (Global Initiative for Chronic Obstructive Lung Disease stage II-IV) underwent hyperpolarized (129)
262 D (Global Initiative for Chronic Obstructive Lung Disease) stages I-IV: 9.4, 42.5, 37.5, and 10.5%, r
265 in the CanCOLD (Canadian Cohort Obstructive Lung Disease) study, with at least 12 months of exacerba
266 sults are used for diagnosing common chronic lung diseases such as asthma and chronic obstructive pul
267 tructive pulmonary disease, and interstitial lung diseases such as idiopathic pulmonary fibrosis.
268 Applications in patients with obstructive lung diseases, such as asthma and chronic obstructive pu
271 nent feature of asthma and other obstructive lung diseases that is minimally affected by current trea
272 e to a significant proportion of obstructive lung disease, the phenotype of obstructive lung disease
274 ertension due to left-sided heart disease or lung disease, the use of pulmonary vasodilator treatment
276 sis for the development of this occupational lung disease through the ability of Be to induce posttra
278 stablished mouse model of severe obstructive lung diseases, to produce lower-mortality but pathophysi
279 characterized by vasculopathy, interstitial lung disease, ulcerative skin lesions, and premature dea
280 More than one third of patients with chronic lung disease undergoing lung transplantation have pre-ex
281 f patients who presented to the interstitial lung disease unit of the Royal Brompton and Harefield NH
282 ans were evaluated for CF-related structural lung disease using the Perth-Rotterdam Annotated Grid Mo
283 ranscripts encoded by genes implicated in CF lung disease was measured in a variety of P. aeruginosa
286 epithelial (HTBE) cells from donors without lung disease were cultured to determine pro-inflammatory
287 he metabolic syndrome, and chronic heart and lung disease were independently associated with a higher
289 infection led to susceptibility to asthmatic lung disease when mice subsequently re-encountered aeroa
292 fibrosing interstitial pneumonia, is a fatal lung disease with a median survival time of 3-5 years.
295 nary fibrosis (IPF) is a chronic age-related lung disease with high mortality that is characterized b
296 nary fibrosis (IPF) is a chronic progressive lung disease with high mortality, uncertain cause, and f
299 PD) are highly prevalent chronic obstructive lung diseases with an associated high burden of disease.
300 itial pneumonias (fIIP) are a group of fatal lung diseases with largely unknown etiology and without
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