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1 BOS also directly affects the mental health and physical
2 BOS also directly affects the mental health and physical
3 BOS and normal lung tissues were assessed for HA localiz
4 BOS could be treated by eliminating production of interl
5 BOS has a 5-year prevalence of approximately 45% and is
6 BOS is associated with increased cytotoxic/pro-inflammat
7 BOS is associated with increased cytotoxic/proinflammato
8 BOS is associated with many deleterious consequences, in
9 BOS LR-MSCs also demonstrated resistance to the inhibito
10 BOS+ patients revealed increased development of HLA clas
11 BOS, but especially RAS patients, experienced more frequ
12 BOS-free survival in intention-to-treat (ITT) analysis w
13 (bronchiolitis obliterans syndrome level 0 [BOS 0]), early CLAD (BOS 0p), and late-stage CLAD (BOS 1
14 LVs per bronchiole: with infiltrates, 5.00 (BOS), 9.00 (RAS), 4.00 (control), P = 0.62; without infi
15 rom 35 LTx recipients (n = 22 stable, n = 13 BOS) and healthy controls (n = 25) were cultured as prim
17 BOS, and 8 stable pediatric LTxR, 16 AR, 17 BOS, and 16 stable adult LTxR were included for validati
18 lpha, and IL-2R were serially analyzed in 31 BOS+ and matched 31 BOS- patients using quantitative mul
19 serially analyzed in 31 BOS+ and matched 31 BOS- patients using quantitative multiplex bead immunoas
20 activating factor (BAFF) in 136 patients (46 BOS, 41 no cGVHD, 49 cutaneous cGVHD) to define novel bi
24 ft seems to have a protective effect against BOS, whereas de novo acquisition of microbial population
25 n sCD30 levels during BOS development in all BOS+ patients, compared to BOS- (mean 139.8+/-10.7 vs. 1
26 (MCs) derived from fibrotic lung allografts (BOS MCs) demonstrated constitutive nuclear beta-catenin
27 wer in patients in the BOS 0p (P = .025) and BOS 1-3 groups (P = .003) than it was in the patients wi
31 irculating miRNAs occurs in LTxR with AR and BOS, suggesting that they can provide not only important
38 h of associations between BAL parameters and BOS in order to provide a comprehensive and systematic a
42 ously active and inhibited preferentially by BOS, suggesting that area X disinhibits dopaminergic neu
45 selectivity for the originally crystallized BOS after exposure to distorted feedback and during decr
52 red with patients who subsequently developed BOS, consistently had a significantly increased percenta
53 sized that patients who ultimately developed BOS would have elevations in these chemokines before los
55 rker for HCT patients at risk for developing BOS at an early stage and could allow improvement of pat
58 cutoff point >9% was optimal for diagnosing BOS in patients with first drop of pulmonary function te
59 miR-144, and miR-155 strongly discriminated BOS from stable LTxR (P < 0.001 for all comparisons).
60 ity to interrogate the lung allograft during BOS development and identify potential disease mechanism
63 significant elevation in sCD30 levels during BOS development in all BOS+ patients, compared to BOS- (
65 it clear that some patients with established BOS might in fact benefit from such therapy due to its v
71 rejection was a significant risk factor for BOS stages 1 and 2, but not stage 3 or death, in the uni
75 3%) and significantly increased the risk for BOS (p < 0.0001, HR = 3.2, 95% CI 2.3-4.6) and death (p
88 ytokines IL-1beta, IL-2, IL-12, and IL-15 in BOS+ patients, compared to BOS- and normal subjects.
94 se the knowledge gained from BAL analyses in BOS through increased sample sizes, covariant adjustment
95 h infection and pseudomonal colonizations in BOS and RAS compared with control (P=0.0090 and P=0.0034
96 to leverage analysis of BAL constituents in BOS may offer great potential to provide additional in-d
99 thase enzymes were significantly elevated in BOS versus normal lung tissues and both lavage fluid and
104 ls of TIMP-bound MMP-8 and -9 were higher in BOS than in good outcome recipients, suggesting activity
112 bronchitis was more prevalent in subjects in BOS stage 0p and BOS stages 1-3 at the time of biopsy.
113 oids remain the backbone of therapy for IPS, BOS, and BOOP, TNF inhibition may augment management of
116 cted serially from BOS+ (n = 20) and matched BOS- (n = 20) lung transplant (LT) patients were analyze
120 litis obliterans syndrome [BOS]-neutrophilic BOS-restrictive allograft syndrome [RAS]) have been iden
121 m non-neutrophilic BOS, 17 from neutrophilic BOS, and 20 from RAS using classic enzyme-linked immunos
122 % neutrophils were elevated in neutrophilic BOS and RAS compared to stable and non-neutrophilic BOS
123 compared to stable, whereas in neutrophilic BOS IL-1beta (P<0.001), IL-1Ralpha (P<0.01), IL-7 (P<0.0
125 RAS compared to stable and non-neutrophilic BOS patients, whereas also the % eosinophils was elevate
126 20 patients suffering from non-neutrophilic BOS, 17 from neutrophilic BOS, and 20 from RAS using cla
128 ha-SMA and collagen I when compared with non-BOS controls, consistent with a stable in vivo fibrotic
131 als and diminish the harmful consequences of BOS, both for critical care health-care professionals an
132 als and diminish the harmful consequences of BOS, both for critical care healthcare professionals and
134 trated a significantly faster development of BOS (P=0.005) compared with patients with no virus detec
135 und to be associated with the development of BOS and allograft fibrosis after lung transplantation.
136 x was associated with earlier development of BOS and may have negative impact on outcome after double
137 eholders to help mitigate the development of BOS in critical care health-care professionals and dimin
138 eholders to help mitigate the development of BOS in critical care healthcare professionals and dimini
141 ty did not impact the time to development of BOS or RAS in lung transplantation (low vs high LVD: 38.
143 strongly associated with the development of BOS within 2 years of transplant (23.4% vs. 7.7% in thos
144 und to be associated with the development of BOS, but these studies need to be replicated in independ
145 ified as risk factors for the development of BOS, it is unclear whether large-airway lymphocytic infl
146 injury appears central to the development of BOS, little is known regarding the specific epithelial c
157 omarkers for the prediction and diagnosis of BOS are urgently needed to improve patients' prognosis.
158 ion of Pseudomonas preceded the diagnosis of BOS in 14 of 18 (78%) and by a median of 204 days (95% c
164 ranslational studies using a murine model of BOS demonstrated increased expression of IL-13 and its r
165 vo mouse orthotopic lung transplant model of BOS, antagonism of the LPA receptor (LPA1) or ATX inhibi
172 ys a significant role in the pathogenesis of BOS, we investigated whether soluble CD30 (sCD30), a T-c
175 E-score was associated with greater risk of BOS (adjusted hazard ratio, 1.76; 95% confidence interva
176 ransplant depression had an elevated risk of BOS (hazard ratio [HR], 1.91; 95% confidence interval [9
177 olymorphism was associated with more risk of BOS (relative risk, 8.6 [2.2-33.5], P<0.0001) and decrea
184 relationship between microbial populations, BOS, and other covariates was explored using PERMANOVA a
185 ophil chemoattractant in posttransplantation BOS and provide opportunities for the development of uni
188 lactic therapy with AZI actually may prevent BOS and improve FEV1 after LTx, most likely through its
192 assigned 32 HSCT recipients with mild/severe BOS to receive budesonide/formoterol or placebo for 6 mo
193 espond more strongly to the bird's own song (BOS) than to other sounds, and area X is critical for th
194 uditory presentation of the bird's own song (BOS), possibly providing a permanent referent for song m
196 s the ability of budesonide oral suspension (BOS), a novel muco-adherent topical steroid formulation,
199 gnosis of bronchiolitis obliterans syndrome (BOS) after allogeneic hematopoietic cell transplant (HCT
200 tment for bronchiolitis obliterans syndrome (BOS) after allogeneic hematopoietic stem cell transplant
202 edom from bronchiolitis obliterans syndrome (BOS) and graft survival were compared between patients w
204 edom from bronchiolitis obliterans syndrome (BOS) at three years was similar in those undergoing a vi
205 opment of bronchiolitis obliterans syndrome (BOS) following lung transplantation has been correlated
206 ssociated bronchiolitis obliterans syndrome (BOS) in a murine model, we hypothesized that T follicula
207 onset of bronchiolitis obliterans syndrome (BOS) in consecutive lung transplant recipients 61 years
209 o prevent bronchiolitis obliterans syndrome (BOS) in many patients, primarily a disease of the small
210 o prevent bronchiolitis obliterans syndrome (BOS) in many patients, primarily a disease of the small
211 The term bronchiolitis obliterans syndrome (BOS) is a clinical surrogate for the histopathologic dia
214 enting as bronchiolitis obliterans syndrome (BOS) or restrictive allograft syndrome (RAS) is the majo
215 ejection, bronchiolitis obliterans syndrome (BOS) remain major limiting factors for lung transplantat
218 ns and by bronchiolitis obliterans syndrome (BOS), a form of chronic rejection linked in part to micr
220 me (IPS), bronchiolitis obliterans syndrome (BOS), and bronchiolitis obliterans organizing pneumonia
221 ifests as bronchiolitis obliterans syndrome (BOS), but no biomarker can currently predict the progres
222 ated with bronchiolitis obliterans syndrome (BOS), but the effect of pseudomonas on BOS and death has
223 n, termed bronchiolitis obliterans syndrome (BOS), is the major cause of poor outcomes after lung tra
224 sented by bronchiolitis obliterans syndrome (BOS), is the single most important factor that limits th
225 ubsequent bronchiolitis obliterans syndrome (BOS), mortality and graft loss for up to 15 years posttr
229 nd during bronchiolitis obliterans syndrome (BOS), we hypothesized that the type 2 immune mediated re
230 lity, and bronchiolitis obliterans syndrome (BOS)-free survival were analyzed up to 36 months after t
240 idence of bronchiolitis obliterans syndrome (BOS): 1/43 in the Everolimus group and 8/54 in the MMF g
241 efined as bronchiolitis obliterans syndrome [BOS]) is considered to reflect the evolution of chronic
242 tructive (bronchiolitis obliterans syndrome [BOS]) or a restrictive lung function defect (restrictive
243 enotypes (bronchiolitis obliterans syndrome [BOS]-neutrophilic BOS-restrictive allograft syndrome [RA
248 these complementary results illustrate that BOS involves a selective alteration in the distribution
251 n was significantly lower in patients in the BOS 0p (P = .025) and BOS 1-3 groups (P = .003) than it
255 nsitioning from lung transplant (state 1) to BOS (state 2), from transplant (state 1) to death (state
257 evelopment in all BOS+ patients, compared to BOS- (mean 139.8+/-10.7 vs. 14.8+/-2.7 U/ml, P < 0.001).
259 lung fluid of patients with BOS compared to BOS-free controls, in cross-sectional and longitudinal a
261 that accumulation of HA could contribute to BOS by directly activating innate immune signaling pathw
269 likelihood of transition from transplant to BOS was increased by acute rejection, CXCL5, and the int
273 candidate miRNAs in 14 LTxR with AR, 7 with BOS, and compared them against 13 stable pediatric LTxR
275 nce of profibrotic mediators associated with BOS, including transforming growth factor-beta and IL-13
282 brushings were collected from patients with BOS (n = 10), stable lung transplant patients (n = 18),
283 brushings were collected from patients with BOS (n=10), stable lung transplant patients (n=18) and h
285 positive for BOS 0-p FEV(1) in patients with BOS (sensitivity) was 71% at 2 years before the onset of
288 y reduced in the lung fluid of patients with BOS compared to BOS-free controls, in cross-sectional an
293 elevated in lung transplant recipients with BOS when compared with those without BOS and healthy con
295 sa is common particularly in recipients with BOS, but a possible etiological relationship remains une
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