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1 e response play roles in the pathogenesis of idiopathic pulmonary fibrosis.
2 em cells (LR-MSC) plays an important role in idiopathic pulmonary fibrosis.
3 were not correlated with disease severity of idiopathic pulmonary fibrosis.
4 RNA-related collagen V overexpression during idiopathic pulmonary fibrosis.
5 there is consideration of their use to treat idiopathic pulmonary fibrosis.
6 eir relationship with disease progression in idiopathic pulmonary fibrosis.
7 as chronic obstructive pulmonary disease and idiopathic pulmonary fibrosis.
8 proves the feasibility of clinical trials in idiopathic pulmonary fibrosis.
9 interstitial lung diseases, particularly for idiopathic pulmonary fibrosis.
10 n clinical trials and to guide management of idiopathic pulmonary fibrosis.
11 tween healthy controls and participants with idiopathic pulmonary fibrosis.
12 ease, and interstitial lung diseases such as idiopathic pulmonary fibrosis.
13 ration of two new drugs for the treatment of idiopathic pulmonary fibrosis.
14 s, thus avoiding surgery in the diagnosis of idiopathic pulmonary fibrosis.
15 ng inflammation characteristic of asthma and idiopathic pulmonary fibrosis.
16 or of or against treatment interventions for idiopathic pulmonary fibrosis.
17 of scar tissue in the lungs of patients with idiopathic pulmonary fibrosis.
18 gnatures were associated with progression of idiopathic pulmonary fibrosis.
19 l, dyspnea, and death from any cause or from idiopathic pulmonary fibrosis.
20 fibroblasts from the lungs of patients with idiopathic pulmonary fibrosis.
21 stress is observed in lungs of patients with idiopathic pulmonary fibrosis.
22 engths are associated with worse survival in idiopathic pulmonary fibrosis.
23 as a diagnostic and prognostic biomarker of idiopathic pulmonary fibrosis.
24 progression-free survival, in patients with idiopathic pulmonary fibrosis.
25 treatment of human lung diseases, including idiopathic pulmonary fibrosis.
26 ine and acute exacerbations in patients with idiopathic pulmonary fibrosis.
27 es in interstitial lung disorders other than idiopathic pulmonary fibrosis.
28 tient receiving immunosuppression because of idiopathic pulmonary fibrosis.
29 ly as compared with placebo in patients with idiopathic pulmonary fibrosis.
30 epigenetic silencing of cyclooxygenase-2 in idiopathic pulmonary fibrosis.
31 rbates chronic pulmonary diseases, including idiopathic pulmonary fibrosis.
32 affect risk stratification of patients with idiopathic pulmonary fibrosis.
33 nd diseased lungs of patients suffering from idiopathic pulmonary fibrosis.
34 tivators of telomerase in therapies to treat idiopathic pulmonary fibrosis.
35 e gene encoding mucin 5B, is associated with idiopathic pulmonary fibrosis.
36 6 integrin is central to the pathogenesis of idiopathic pulmonary fibrosis.
37 everal cancers and other diseases, including idiopathic pulmonary fibrosis.
38 cause of the fibrotic changes that underlie idiopathic pulmonary fibrosis.
39 reatment options available for patients with idiopathic pulmonary fibrosis.
40 ated in fibroblasts from human subjects with idiopathic pulmonary fibrosis.
41 was also induced in myofibroblasts in human idiopathic pulmonary fibrosis.
42 dyskeratosis congenita, aplastic anemia, and idiopathic pulmonary fibrosis.
43 idiopathic cases of organ fibrosis, such as idiopathic pulmonary fibrosis.
44 telomere lengths of the Dallas patients with idiopathic pulmonary fibrosis (1.33 [SD 0.25]) were simi
45 erlying lung diseases included COPD (44.8%), idiopathic pulmonary fibrosis (22.9%), interstitial lung
46 on of mesenchymal cells are the hallmarks of idiopathic pulmonary fibrosis, a devastating disease of
48 ncological indications and diseases, such as idiopathic pulmonary fibrosis, a number may hold promise
51 transplant (aHR, 1.3; 95% CI, 1.0-1.7), and idiopathic pulmonary fibrosis (aHR, 1.4; 95% CI, 1.0-1.8
52 been suggested as a beneficial treatment for idiopathic pulmonary fibrosis, although data from placeb
53 ently used to inhibit TGF-beta signalling in idiopathic pulmonary fibrosis, ameliorated BK dysfunctio
54 incidence, prevalence, and mortality risk of idiopathic pulmonary fibrosis among US Medicare benefici
55 f two effective treatments for patients with idiopathic pulmonary fibrosis, an accurate diagnosis is
56 or adults aged 40-80 years with well-defined idiopathic pulmonary fibrosis and 5% or less honeycombin
58 elevated in lung biopsies from patients with idiopathic pulmonary fibrosis and bleomycin (BLM)-induce
59 during TGF-beta1-induced differentiation of idiopathic pulmonary fibrosis and CCD-19Lu fibroblasts.
60 ribute to EMT, ATII cells from patients with idiopathic pulmonary fibrosis and chronic obstructive pu
61 ought to contribute towards diseases such as idiopathic pulmonary fibrosis and chronic obstructive pu
62 and potential risk factors for diagnosis of idiopathic pulmonary fibrosis and death between 2001 and
63 ed vasculitis, systemic lupus erythematosus, idiopathic pulmonary fibrosis and dengue haemorrhagic fe
64 itoring disease progression in patients with idiopathic pulmonary fibrosis and emphysema extent great
67 mary fibroblasts obtained from patients with idiopathic pulmonary fibrosis and human lung CCD-19Lu fi
68 erstitial pneumonia pattern is a hallmark of idiopathic pulmonary fibrosis and is essential for its d
69 ibrotic areas of lungs of both patients with idiopathic pulmonary fibrosis and mice that are subjecte
71 ge-scale real applications in breast cancer, idiopathic pulmonary fibrosis and pan-cancer methylation
72 h 31, 2012, 189 had a confirmed diagnosis of idiopathic pulmonary fibrosis and were included in subse
73 onsible for collagen V overexpression during idiopathic pulmonary fibrosis, and these miRNAs may serv
74 also increased in the lungs of patients with idiopathic pulmonary fibrosis as compared to in normal h
75 atrix (ECM) turnover predicts progression of idiopathic pulmonary fibrosis as determined by change in
76 e up-regulated in the lungs of patients with idiopathic pulmonary fibrosis as well as in wound healin
77 ession, in telomere-related diseases such as idiopathic pulmonary fibrosis, as well as in mice and ot
78 irfenidone to Confirm Efficacy and Safety in Idiopathic Pulmonary Fibrosis (ASCEND 016; 52 weeks)-for
79 he etiology of degenerative diseases such as idiopathic pulmonary fibrosis, bone marrow failure, and
80 ngths are found in a subset of patients with idiopathic pulmonary fibrosis, but their clinical signif
81 everal chronic pulmonary diseases, including idiopathic pulmonary fibrosis, chronic obstructive pulmo
82 ndings were validated in the two independent idiopathic pulmonary fibrosis cohorts (Chicago and San F
83 in serum and lung tissue from patients with idiopathic pulmonary fibrosis compared to healthy volunt
84 ted levels in lung tissue from patients with idiopathic pulmonary fibrosis compared with control lung
85 in leukocytes in the lungs of patients with idiopathic pulmonary fibrosis compared with control lung
86 e increased in the serum of individuals with idiopathic pulmonary fibrosis compared with healthy cont
87 ns were related to subsequent progression of idiopathic pulmonary fibrosis (defined as death or decli
88 ative to control participants, patients with idiopathic pulmonary fibrosis demonstrate excessive mono
89 -onset ILD in India, followed by CTD-ILD and idiopathic pulmonary fibrosis; diagnoses varied between
90 dyskeratosis congenita, aplastic anemia, and idiopathic pulmonary fibrosis disrupt the binding betwee
91 d the apoptotic susceptibility of normal and idiopathic pulmonary fibrosis fibroblasts; blocked TGF-b
92 Drug Administration (FDA)-approved drug for idiopathic pulmonary fibrosis, for its therapeutic effec
93 on CT in a cohort of patients with suspected idiopathic pulmonary fibrosis from a previous randomised
94 d a pooled cohort study of 517 patients with idiopathic pulmonary fibrosis from three IPFnet multicen
95 n, 102 women; mean age, 69 years +/- 9) with idiopathic pulmonary fibrosis from two institutions.
96 placebo-controlled trials of IFN-gamma-1b in idiopathic pulmonary fibrosis (GIPF-001 [NCT00047645] an
98 ently published placebo-controlled trials in idiopathic pulmonary fibrosis have established that pirf
99 nsplant-free survival time for patients with idiopathic pulmonary fibrosis (HR 0.22 [95% CI 0.08-0.63
100 terstitial lung disease diagnoses other than idiopathic pulmonary fibrosis (HR 0.73 [0.16-3.41]; p=0.
101 ght not be necessary to reach a diagnosis of idiopathic pulmonary fibrosis if high-resolution CT scan
106 likely to be useful in routine management of idiopathic pulmonary fibrosis in the medium-term future
109 pplying the concept of precision medicine to idiopathic pulmonary fibrosis, in particular to search f
110 ty (FVC) or vital capacity, in patients with idiopathic pulmonary fibrosis; in the third trial, this
111 onchoalveolar lavage fluid of a patient with idiopathic pulmonary fibrosis, indicating that these rea
112 h fibrosing ILD, including 456 patients with idiopathic pulmonary fibrosis (IPF) (men, 366; women, 90
114 Despite shared environmental exposures, idiopathic pulmonary fibrosis (IPF) and chronic obstruct
115 ) cause telomere diseases including familial idiopathic pulmonary fibrosis (IPF) and dyskeratosis con
116 target genes are increased in patients with idiopathic pulmonary fibrosis (IPF) and in animal models
118 parenchymal lung diseases (DPLD), including idiopathic pulmonary fibrosis (IPF) and sarcoidosis, are
119 ious cause, such as the devastating diseases idiopathic pulmonary fibrosis (IPF) and scleroderma.
120 or the computed tomographic (CT) features of idiopathic pulmonary fibrosis (IPF) and to gain insight
121 ry-related hospitalizations of patients with idiopathic pulmonary fibrosis (IPF) are more frequent th
122 lung injury is related to poor outcome, and idiopathic pulmonary fibrosis (IPF) can be regarded as a
124 ted that lung fibroblasts from patients with idiopathic pulmonary fibrosis (IPF) exhibit a hypermotil
125 rom the lungs of the patients suffering from idiopathic pulmonary fibrosis (IPF) exhibit enhanced FXI
127 urgical lung biopsy, patients diagnosed with idiopathic pulmonary fibrosis (IPF) in clinical practice
182 yofibroblastic differentiation of normal and idiopathic pulmonary fibrosis (IPF) lung fibroblasts.
183 rs, individuals might be diagnosed as having idiopathic pulmonary fibrosis (IPF) or chronic (fibrotic
184 In this exploratory analysis, adults with idiopathic pulmonary fibrosis (IPF) or chronic obstructi
185 pulmonary hypertension (PH) in patients with idiopathic pulmonary fibrosis (IPF) or chronic obstructi
190 geal reflux (GER) is higher in patients with idiopathic pulmonary fibrosis (IPF) than in matched cont
191 significance of a first-choice diagnosis of idiopathic pulmonary fibrosis (IPF) versus not IPF for M
193 B cells are involved in the pathogenesis of idiopathic pulmonary fibrosis (IPF), a progressive, rest
194 gs of human donors and patients with COPD or idiopathic pulmonary fibrosis (IPF), as well as in cigar
195 ides an updated approach to the diagnosis of idiopathic pulmonary fibrosis (IPF), based on a systemat
196 Mortality prediction is well studied in idiopathic pulmonary fibrosis (IPF), but little is known
197 BAL of patients with stable and progressive idiopathic pulmonary fibrosis (IPF), defined as <5% and
199 are effective in slowing the progression of idiopathic pulmonary fibrosis (IPF), it remains a debili
200 Although aging is a known risk factor for idiopathic pulmonary fibrosis (IPF), the pathogenic mech
201 of lung fibrosis and in human subjects with idiopathic pulmonary fibrosis (IPF), we observed activat
202 expressed in lung tissues from patients with idiopathic pulmonary fibrosis (IPF), whereas PIAS4 prote
203 Current prediction models of mortality in idiopathic pulmonary fibrosis (IPF), which are based on
204 trol (fibrosis-free) donors or patients with idiopathic pulmonary fibrosis (IPF), which is a very agg
205 in PBMCs and lung tissues from patients with idiopathic pulmonary fibrosis (IPF), which was confirmed
230 and trafficking has a newly defined role in idiopathic pulmonary fibrosis (IPF); however, the contri
231 y has been implicated in the pathogenesis of idiopathic pulmonary fibrosis (IPF); however, the repert
241 hese preliminary data suggest progression of idiopathic pulmonary fibrosis is associated with the pre
243 A central pathway in the pathogenesis of idiopathic pulmonary fibrosis is epithelial injury leadi
246 we believe that the future of management for idiopathic pulmonary fibrosis lies in the development of
249 bryonic fibroblasts (MEFs) and rat and human idiopathic pulmonary fibrosis lung fibroblasts with siRN
251 en shown to be highly expressed in AECs from idiopathic pulmonary fibrosis lungs although its role is
252 by both mesothelial and mesenchymal cells in idiopathic pulmonary fibrosis lungs but has limited or n
253 te that some disease progression pathways in idiopathic pulmonary fibrosis may represent partial reve
254 nnual incidence and cumulative prevalence of idiopathic pulmonary fibrosis, median survival time of p
255 ficantly higher in patients with progressive idiopathic pulmonary fibrosis (n=32) than in those with
257 ficantly higher in patients with progressive idiopathic pulmonary fibrosis (n=71) than in patients wi
259 open surgery, and a provisional diagnosis of idiopathic pulmonary fibrosis or connective tissue disea
260 al cohort study (PROFILE), participants with idiopathic pulmonary fibrosis or idiopathic non-specific
263 stingly, and of potential relevance to human idiopathic pulmonary fibrosis, PARP activity in lung fib
264 s upregulated in peripheral blood cells from idiopathic pulmonary fibrosis patients and correlated wi
265 P activity in lung fibroblasts isolated from idiopathic pulmonary fibrosis patients was significantly
266 pment and differentially expressed miRNAs in idiopathic pulmonary fibrosis patients, some of which we
274 d mortality (0.0237), and treatment-emergent idiopathic-pulmonary-fibrosis-related (0.0132) mortality
275 ent-emergent all-cause mortality (p=0.0420), idiopathic-pulmonary-fibrosis-related mortality (0.0237)
276 0.35 [0.17-0.72; 0.0029]; treatment-emergent idiopathic-pulmonary-fibrosis-related mortality 0.32 [0.
277 ll-cause mortality 0.45 [0.24-0.83; 0.0094]; idiopathic-pulmonary-fibrosis-related mortality 0.35 [0.
278 is-related mortality, and treatment-emergent idiopathic-pulmonary-fibrosis-related mortality at weeks
279 ity, treatment-emergent all-cause mortality, idiopathic-pulmonary-fibrosis-related mortality, and tre
280 -myofibroblast differentiation/activation in idiopathic pulmonary fibrosis remain poorly understood.
281 e, and was replicated in the two independent idiopathic pulmonary fibrosis replication cohorts (Chica
282 Present guidelines for the diagnosis of idiopathic pulmonary fibrosis require histological confi
283 bo-Clinical Studies Assessing Pirfenidone in Idiopathic Pulmonary Fibrosis: Research of Efficacy and
285 kers to Estimate Time-progression (COMET) in idiopathic pulmonary fibrosis study were followed up for
286 ical Markers to Estimate Time-Progression in Idiopathic Pulmonary Fibrosis) study were used to conduc
287 TH, were higher in lungs from patients with idiopathic pulmonary fibrosis than in control individual
288 24) at baseline were higher in patients with idiopathic pulmonary fibrosis than in healthy controls.
289 Additionally, we demonstrate that in human idiopathic pulmonary fibrosis there is increased pulmona
290 tudy, we randomly assigned 555 patients with idiopathic pulmonary fibrosis to receive either oral pir
292 irfenidone to Confirm Efficacy and Safety in Idiopathic Pulmonary Fibrosis] trial), including all pat
293 radiation-induced pulmonary fibrosis and in idiopathic pulmonary fibrosis, two diseases considered t
295 elomere length and survival in patients with idiopathic pulmonary fibrosis was independent of age, se
296 ndpoint for clinical trials in patients with idiopathic pulmonary fibrosis who have mild-to-moderate
297 to the preservation of FVC in patients with idiopathic pulmonary fibrosis with mild-to-moderate impa
298 trial, we randomly assigned patients who had idiopathic pulmonary fibrosis with mild-to-moderate impa
300 research is to develop a method to diagnose idiopathic pulmonary fibrosis without the patient having
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