ライフサイエンスコーパス: BOS

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 decreased SIRT1 in peripheral blo

7 BOS is associated with increased cytotoxic/pro-inflammat

8 BOS is associated with increased cytotoxic/proinflammato

9 BOS is associated with many deleterious consequences, in

10 BOS LR-MSCs also demonstrated resistance to the inhibito

11 BOS+ patients revealed increased development of HLA clas

12 BOS, but especially RAS patients, experienced more frequ

13 BOS-free survival in intention-to-treat (ITT) analysis w

14 (bronchiolitis obliterans syndrome level 0 [BOS 0]), early CLAD (BOS 0p), and late-stage CLAD (BOS 1

15 LVs per bronchiole: with infiltrates, 5.00 (BOS), 9.00 (RAS), 4.00 (control), P = 0.62; without infi

16 rom 35 LTx recipients (n = 22 stable, n = 13 BOS) and healthy controls (n = 25) were cultured as prim

17 vs high LVD: 38.5 vs 86.0 months, P = 0.15 [BOS]; 60.5 vs 69.5 months, P = 0.80 [RAS]).

18 BOS, and 8 stable pediatric LTxR, 16 AR, 17 BOS, and 16 stable adult LTxR were included for validati

19 lpha, and IL-2R were serially analyzed in 31 BOS+ and matched 31 BOS- patients using quantitative mul

20 serially analyzed in 31 BOS+ and matched 31 BOS- patients using quantitative multiplex bead immunoas

21 activating factor (BAFF) in 136 patients (46 BOS, 41 no cGVHD, 49 cutaneous cGVHD) to define novel bi

22 ontrol), P = 0.62; without infiltrates, 4.5 (BOS), 0.00 (RAS), 4.56 (control), P = 0.74).

23 In addition, 6 AR, 7 BOS, and 8 stable pediatric LTxR, 16 AR, 17 BOS, and 16

24 (median number of LVs per bronchiole: 4.75 (BOS), 6.47 (RAS), 4.25 (control), P = 0.97).

25 ft seems to have a protective effect against BOS, whereas de novo acquisition of microbial population

26 n sCD30 levels during BOS development in all BOS+ patients, compared to BOS- (mean 139.8+/-10.7 vs. 1

27 (MCs) derived from fibrotic lung allografts (BOS MCs) demonstrated constitutive nuclear beta-catenin

28 wer in patients in the BOS 0p (P = .025) and BOS 1-3 groups (P = .003) than it was in the patients wi

29 re prevalent in subjects in BOS stage 0p and BOS stages 1-3 at the time of biopsy.

30 potential noninvasive biomarkers for AR and BOS after pediatric LTx.

31 s) that associate with development of AR and BOS in pediatric lung transplant recipients (LTxR).

32 irculating miRNAs occurs in LTxR with AR and BOS, suggesting that they can provide not only important

33 elated with increased GC B cells, cGVHD, and BOS.

34 f endobronchial lymphocytic inflammation and BOS may have mechanistic implications.

35 a marker of type I alveolar cell injury and BOS.

36 Diagnostic criteria for IPS and BOS have been established, although optimal treatment st

37 depletion, B cells remained in the lung, and BOS was not reversed.

38 transplant recipients with good outcome and BOS using a multiplex immunoassay.

39 h of associations between BAL parameters and BOS in order to provide a comprehensive and systematic a

40 n 1 second were identified and classified as BOS or RAS.

41 phocytic bronchiolitis were compared between BOS, RAS, and stable patients.

42 lls, in lung transplant recipients with BOS, BOS-free patients and in donor controls.

43 ously active and inhibited preferentially by BOS, suggesting that area X disinhibits dopaminergic neu

44 erans syndrome level 0 [BOS 0]), early CLAD (BOS 0p), and late-stage CLAD (BOS 1-3).

45 ), early CLAD (BOS 0p), and late-stage CLAD (BOS 1-3).

46 selectivity for the originally crystallized BOS after exposure to distorted feedback and during decr

47 sis of National Institutes of Health-defined BOS diagnosed a median of 11 mo after HCT.

48 ns were significantly more likely to develop BOS than those who cleared these antibodies.

49 ey were significantly less likely to develop BOS than those who had persistent antibodies.

50 fidence interval, 4%-21%]), and 20 developed BOS (32%, [95% confidence interval, 21%-45%]).

51 ansplant recipients who eventually developed BOS.

52 Sixty (57%) subjects developed BOS.

53 red with patients who subsequently developed BOS, consistently had a significantly increased percenta

54 sized that patients who ultimately developed BOS would have elevations in these chemokines before los

55 y after transplantation in LTR who developed BOS (P=0.015).

56 rker for HCT patients at risk for developing BOS at an early stage and could allow improvement of pat

57 ecipients from those subsequently developing BOS within the first 2 years posttransplantation.

58 Patients with newly diagnosed BOS had significantly higher percentages of CD19(+)CD21(

59 cutoff point >9% was optimal for diagnosing BOS in patients with first drop of pulmonary function te

60 miR-144, and miR-155 strongly discriminated BOS from stable LTxR (P < 0.001 for all comparisons).

61 ity to interrogate the lung allograft during BOS development and identify potential disease mechanism

62 old decline in IL-10 levels was found during BOS development.

63 significant elevation in sCD30 levels during BOS development in all BOS+ patients, compared to BOS- (

64 sinophilia were randomized to receive either BOS 2 mg or placebo twice daily for 12 weeks.

65 it clear that some patients with established BOS might in fact benefit from such therapy due to its v

66 0, are elevated in patients with established BOS.

67 lung recipients with or without established BOS.

68 For BOS and BOOP in particular, therapy has been based upon

69 For BOS vs placebo, change in DSQ score was -14.3 vs -7.5 (P

70 endobronchial biopsies as a risk factor for BOS and mortality.

71 n FEV1) resulted in even greater hazards for BOS and death.

72 es for the screening of early predictors for BOS.

73 3%) and significantly increased the risk for BOS (p < 0.0001, HR = 3.2, 95% CI 2.3-4.6) and death (p

74 test, are subsequently at increased risk for BOS and worse overall survival.

75 tification of patients at increased risk for BOS.

76 prospectively identify patients at risk for BOS.

77 Few prospective trials for BOS have been performed, with current therapy based on o

78 plant (state 1) to death (state 3), and from BOS (state 2) to death (state 3).

79 Freedom from BOS was significantly shorter in those patients without

80 CT may noninvasively differentiate RAS from BOS.

81 Sera collected serially from BOS+ (n = 20) and matched BOS- (n = 20) lung transplant

82 Transition from BOS to death was affected by the length of time in state

83 Furthermore, BOS LR-MSCs were found to be defective in their ability

84 ring from chronic rejection, of which 79 had BOS and 24 were diagnosed with RAS.

85 In BOS, persistent alloimmune injury and chronic airway inf

86 and lymphocytic bronchiolitis (P=0.0006) in BOS and RAS versus control.

87 ytokines IL-1beta, IL-2, IL-12, and IL-15 in BOS+ patients, compared to BOS- and normal subjects.

88 f metalloproteinases (TIMPs), is abnormal in BOS.

89 ls were found in the small distal airways in BOS compared with stable patients and controls.

90 ls were found in the small distal airways in BOS compared with stable patients and controls.

91 tes target the small and/or large airways in BOS.

92 tes target the small and/or large airways in BOS.

93 se the knowledge gained from BAL analyses in BOS through increased sample sizes, covariant adjustment

94 loss of SIRT1 in T, NK-like, and NK cells in BOS patients compared with stable patients and controls

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

97 dy was underpowered to prove a difference in BOS-free survival.

98 proline-glycine-proline (PGP) is elevated in BOS patient bronchoalveolar lavage (BAL) fluid.

99 thase enzymes were significantly elevated in BOS versus normal lung tissues and both lavage fluid and

100 as of intraluminal small airways fibrosis in BOS lung tissue.

101 contribute to the development of fibrosis in BOS.

102 m these lymphocyte subsets was also found in BOS.

103 m these lymphocyte subsets was also found in BOS.

104 ls of TIMP-bound MMP-8 and -9 were higher in BOS than in good outcome recipients, suggesting activity

105 ls of TIMP-bound MMP-8 and -9 were higher in BOS.

106 x and demonstrated a significant increase in BOS development (47% vs. 14%).

107 , -8, and -9 were significantly increased in BOS compared to good outcome recipients.

108 BAL neutrophilia in BOS and RAS were elevated at days 360, 540, and 720 vers

109 Silencing NFAT1 in BOS MCs suppressed ATX expression, and sustained overexp

110 nts, whereas no active MMPs were observed in BOS recipients.

111 neutrophil chemoattractant capacity seen in BOS BAL fluid.

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

114 In this study we demonstrate that many BOS(+) patients (12 of 36) develop Abs reactive to epith

115 Due to lack of specific markers, BOS is diagnosed clinically.

116 cted serially from BOS+ (n = 20) and matched BOS- (n = 20) lung transplant (LT) patients were analyze

117 litis obliterans syndrome [BOS]-neutrophilic BOS-restrictive allograft syndrome [RAS]) have been iden

118 m non-neutrophilic BOS, 17 from neutrophilic BOS, and 20 from RAS using classic enzyme-linked immunos

119 % neutrophils were elevated in neutrophilic BOS and RAS compared to stable and non-neutrophilic BOS

120 compared to stable, whereas in neutrophilic BOS IL-1beta (P<0.001), IL-1Ralpha (P<0.01), IL-7 (P<0.0

121 ect any differences between non-neutrophilic BOS and stable patients.

122 RAS compared to stable and non-neutrophilic BOS patients, whereas also the % eosinophils was elevate

123 20 patients suffering from non-neutrophilic BOS, 17 from neutrophilic BOS, and 20 from RAS using cla

124 OS secreted significantly less PGE2 than non-BOS LR-MSCs.

125 ha-SMA and collagen I when compared with non-BOS controls, consistent with a stable in vivo fibrotic

126 ater development not only of RAS but also of BOS.

127 To raise awareness of BOS, the Critical Care Societies Collaborative (CCSC) de

128 als and diminish the harmful consequences of BOS, both for critical care health-care professionals an

129 als and diminish the harmful consequences of BOS, both for critical care healthcare professionals and

130 ence, causative factors, and consequences of BOS.

131 trated a significantly faster development of BOS (P=0.005) compared with patients with no virus detec

132 und to be associated with the development of BOS and allograft fibrosis after lung transplantation.

133 x was associated with earlier development of BOS and may have negative impact on outcome after double

134 eholders to help mitigate the development of BOS in critical care health-care professionals and dimin

135 eholders to help mitigate the development of BOS in critical care healthcare professionals and dimini

136 We demonstrate that development of BOS is associated with increased levels of TIMP-1 and -2

137 The development of BOS is related to an imbalance of personal characteristi

138 ty did not impact the time to development of BOS or RAS in lung transplantation (low vs high LVD: 38.

139 Development of BOS was dependent upon T cells expressing the chemokine

140 strongly associated with the development of BOS within 2 years of transplant (23.4% vs. 7.7% in thos

141 und to be associated with the development of BOS, but these studies need to be replicated in independ

142 ified as risk factors for the development of BOS, it is unclear whether large-airway lymphocytic infl

143 injury appears central to the development of BOS, little is known regarding the specific epithelial c

144 eriod are associated with the development of BOS.

145 important risk factor for the development of BOS.

146 e results with the subsequent development of BOS.

147 infection, contribute to the development of BOS.

148 genetic polymorphisms in the development of BOS.

149 idual variability seen in the development of BOS.

150 ssociated with the subsequent development of BOS.

151 a novel marker to monitor the development of BOS.

152 5 were higher (P < 0.05) with development of BOS.

153 recipients in relation to the devlopment of BOS.

154 omarkers for the prediction and diagnosis of BOS are urgently needed to improve patients' prognosis.

155 ion of Pseudomonas preceded the diagnosis of BOS in 14 of 18 (78%) and by a median of 204 days (95% c

156 from individuals at the time of diagnosis of BOS.

157 at 3 months only in LTR who remained free of BOS (P=0.003).

158 were associated with an increased hazard of BOS.

159 the central events in immunopathogenesis of BOS following human lung transplantation.

160 their instrumental role in the initiation of BOS process and potential targeted therapies.

161 were derived from bronchoalveolar lavage of BOS patients.

162 vo mouse orthotopic lung transplant model of BOS, antagonism of the LPA receptor (LPA1) or ATX inhibi

163 lso elevated in patients before the onset of BOS.

164 pithelial cell Ab precedes clinical onset of BOS.

165 However, the pathogenesis of BOS remains unclear.

166 ys a significant role in the pathogenesis of BOS, we investigated whether soluble CD30 (sCD30), a T-c

167 cores were the only score type predictive of BOS (P < 0.01).

168 E-score was associated with greater risk of BOS (adjusted hazard ratio, 1.76; 95% confidence interva

169 ransplant depression had an elevated risk of BOS (hazard ratio [HR], 1.91; 95% confidence interval [9

170 olymorphism was associated with more risk of BOS (relative risk, 8.6 [2.2-33.5], P<0.0001) and decrea

171 A trend toward reduced risk of BOS was observed in recipients with posttransplant anxie

172 to the same genera may increase the risk of BOS.

173 re not as strongly associated with a risk of BOS.

174 antially increased incidence and severity of BOS.

175 t the onset of allograft rejection acting on BOS specific features.

176 sibly silencing Uva exerted little effect on BOS-evoked activity in HVC neurons.

177 rome (BOS), but the effect of pseudomonas on BOS and death has not been well defined.

178 Up to now there is no effective therapy once BOS is established.

179 relationship between microbial populations, BOS, and other covariates was explored using PERMANOVA a

180 ophil chemoattractant in posttransplantation BOS and provide opportunities for the development of uni

181 ay augment management of IPS and potentially BOS as well.

182 sisted after multivariate adjustment for pre-BOS AR and lymphocytic bronchiolitis burden.

183 lactic therapy with AZI actually may prevent BOS and improve FEV1 after LTx, most likely through its

184 Until recently, BOS and other psychological disorders in critical care h

185 Until recently, BOS and other psychological disorders in critical care h

186 +/- 10; 37 +/- 10; 30 +/- 10) (mean +/- SEM BOS, stable, control, respectively) (P < 0.05 for all).

187 ent in the FEV1 in patients with mild/severe BOS after allogeneic HSCT.

188 assigned 32 HSCT recipients with mild/severe BOS to receive budesonide/formoterol or placebo for 6 mo

189 espond more strongly to the bird's own song (BOS) than to other sounds, and area X is critical for th

190 uditory presentation of the bird's own song (BOS), possibly providing a permanent referent for song m

191 uditory presentation of the bird's own song (BOS).

192 s the ability of budesonide oral suspension (BOS), a novel muco-adherent topical steroid formulation,

193 Burnout syndrome (BOS) occurs in all types of health-care professionals an

194 Burnout syndrome (BOS) occurs in all types of healthcare professionals and

195 gnosis of bronchiolitis obliterans syndrome (BOS) after allogeneic hematopoietic cell transplant (HCT

196 tment for bronchiolitis obliterans syndrome (BOS) after allogeneic hematopoietic stem cell transplant

197 Bronchiolitis obliterans syndrome (BOS) after lung transplantation (LTx) results from bronc

198 edom from bronchiolitis obliterans syndrome (BOS) and graft survival were compared between patients w

199 fested as bronchiolitis obliterans syndrome (BOS) and worse posttransplant survival.

200 edom from bronchiolitis obliterans syndrome (BOS) at three years was similar in those undergoing a vi

201 opment of bronchiolitis obliterans syndrome (BOS) following lung transplantation has been correlated

202 ssociated bronchiolitis obliterans syndrome (BOS) in a murine model, we hypothesized that T follicula

203 onset of bronchiolitis obliterans syndrome (BOS) in consecutive lung transplant recipients 61 years

204 opment of bronchiolitis obliterans syndrome (BOS) in human lung allografts.

205 o prevent bronchiolitis obliterans syndrome (BOS) in many patients, primarily a disease of the small

206 o prevent bronchiolitis obliterans syndrome (BOS) in many patients, primarily a disease of the small

207 Bronchiolitis obliterans syndrome (BOS) is a condition of progressive airflow obstruction t

208 Bronchiolitis obliterans syndrome (BOS) is the primary limiting factor for long-term surviv

209 enting as bronchiolitis obliterans syndrome (BOS) or restrictive allograft syndrome (RAS) is the majo

210 ring from bronchiolitis obliterans syndrome (BOS) or restrictive allograft syndrome (RAS) who underwe

211 ejection, bronchiolitis obliterans syndrome (BOS) remain major limiting factors for lung transplantat

212 Bronchiolitis obliterans syndrome (BOS), a condition of irreversible small airway fibrosis,

213 ns and by bronchiolitis obliterans syndrome (BOS), a form of chronic rejection linked in part to micr

214 Bronchiolitis obliterans syndrome (BOS), a process of fibro-obliterative occlusion of the s

215 me (IPS), bronchiolitis obliterans syndrome (BOS), and bronchiolitis obliterans organizing pneumonia

216 ifests as bronchiolitis obliterans syndrome (BOS), but no biomarker can currently predict the progres

217 ated with bronchiolitis obliterans syndrome (BOS), but the effect of pseudomonas on BOS and death has

218 n, termed bronchiolitis obliterans syndrome (BOS), is the major cause of poor outcomes after lung tra

219 sented by bronchiolitis obliterans syndrome (BOS), is the single most important factor that limits th

220 ubsequent bronchiolitis obliterans syndrome (BOS), mortality and graft loss for up to 15 years posttr

221 Bronchiolitis obliterans syndrome (BOS), pathognomonic for chronic graft-versus-host diseas

222 Bronchiolitis obliterans syndrome (BOS), the clinical correlate of chronic rejection after

223 Bronchiolitis obliterans syndrome (BOS), the major cause of death on lung transplantation,

224 lity, and bronchiolitis obliterans syndrome (BOS)-free survival were analyzed up to 36 months after t

225 opment of bronchiolitis obliterans syndrome (BOS).

226 re termed bronchiolitis obliterans syndrome (BOS).

227 known as bronchiolitis obliterans syndrome (BOS).

228 e risk of bronchiolitis obliterans syndrome (BOS).

229 actor for bronchiolitis obliterans syndrome (BOS).

230 opment of bronchiolitis obliterans syndrome (BOS).

231 opment of bronchiolitis obliterans syndrome (BOS).

232 on termed bronchiolitis obliterans syndrome (BOS).

233 edom from bronchiolitis obliterans syndrome (BOS).

234 correlate bronchiolitis obliterans syndrome (BOS).

235 idence of bronchiolitis obliterans syndrome (BOS): 1/43 in the Everolimus group and 8/54 in the MMF g

236 lografts (bronchiolitis obliterans syndrome [BOS]) and proinflammatory cytokines by steroid-resistant

237 efined as bronchiolitis obliterans syndrome [BOS]) is considered to reflect the evolution of chronic

238 tructive (bronchiolitis obliterans syndrome [BOS]) or a restrictive lung function defect (restrictive

239 enotypes (bronchiolitis obliterans syndrome [BOS]-neutrophilic BOS-restrictive allograft syndrome [RA

240 ejection (bronchiolitis obliterans syndrome, BOS).

241 ing PV systems, including balance of system (BOS) components.

242 end-of-life recycling of balance of system (BOS).

243 We hypothesized that BOS would involve preferential injury to the secretory C

244 these complementary results illustrate that BOS involves a selective alteration in the distribution

245 We have reported that BOS is associated with a lack of suppression of cytotoxi

246 We have reported that BOS is associated with a lack of suppression of cytotoxi

247 n was significantly lower in patients in the BOS 0p (P = .025) and BOS 1-3 groups (P = .003) than it

248 ophil counts were 156 and 130 per hpf in the BOS and placebo groups, respectively.

249 group (24 +/- 8%, P = 0.009), but not in the BOS TxP group (53 +/- 10%, P = 0.97).

250 sCD30 levels declined in the BOS+ patients but were still elevated compared to BOS- (

251 nsitioning from lung transplant (state 1) to BOS (state 2), from transplant (state 1) to death (state

252 patients but were still elevated compared to BOS- (48.52+/-5.04 vs. 7.19+/-2.9, P < 0.0001).

253 evelopment in all BOS+ patients, compared to BOS- (mean 139.8+/-10.7 vs. 14.8+/-2.7 U/ml, P < 0.001).

254 -12, and IL-15 in BOS+ patients, compared to BOS- and normal subjects.

255 lung fluid of patients with BOS compared to BOS-free controls, in cross-sectional and longitudinal a

256 g transplant recipients with BOS compared to BOS-free or donor controls.

257 that accumulation of HA could contribute to BOS by directly activating innate immune signaling pathw

258 ts receiving a lung retransplantation due to BOS or RAS were collected.

259 ht unique immunological processes leading to BOS and RAS.

260 antigen (HLA) alloimmunity and predispose to BOS.

261 ker can currently predict the progression to BOS.

262 The time to BOS or graft loss was analyzed in relation to the positi

263 The average time to BOS was 3.4 years.

264 te the association between sRAGE and time to BOS, defined according to ISHLT guidelines.

265 likelihood of transition from transplant to BOS was increased by acute rejection, CXCL5, and the int

266 ntions that may be used to prevent and treat BOS.

267 The molecular mechanisms underlying BOS are poorly understood and disease-specific biomarker

268 nd use, and increased metal depletion unless BOS recycling is ensured.

269 e also genotyped using the Axion Genome-Wide BOS 1 Array Plate (AffyHD).

270 candidate miRNAs in 14 LTxR with AR, 7 with BOS, and compared them against 13 stable pediatric LTxR

271 While CAS was not associated with BOS or worse survival, it remains an important complicat

272 nce of profibrotic mediators associated with BOS, including transforming growth factor-beta and IL-13

273 with cystic fibrosis is not associated with BOS.

274 -MSCs, a failure of which is associated with BOS.

275 onstrate highly replicable associations with BOS.

276 r in RAS (median, 2.6; n = 29) compared with BOS (median, 1.0; n = 15) and stable patients (median, 0

277 mphocytic bronchiolitis in RAS compared with BOS (P=0.031).

278 cell activation marker, would correlate with BOS.

279 tic fibrosis, was negatively correlated with BOS.

280 natural killer (NK) cells from patients with BOS (n = 10), stable lung transplant patients (n = 11),

281 brushings were collected from patients with BOS (n = 10), stable lung transplant patients (n = 18),

282 brushings were collected from patients with BOS (n=10), stable lung transplant patients (n=18) and h

283 trend toward higher values in patients with BOS (room air, P = .06; 100% oxygen, P = .08).

284 (P = .003) than it was in the patients with BOS 0.

285 stions to optimize therapy for patients with BOS after HCT.

286 y reduced in the lung fluid of patients with BOS compared to BOS-free controls, in cross-sectional an

287 epithelial cells obtained from patients with BOS compared to transplant patients without BOS and cont

288 However, only a portion of the patients with BOS demonstrate detectable anti-donor-HLA Abs.

289 MSCs isolated from patients with BOS demonstrated increased expression of alpha-SMA and c

290 LR-MSCs from patients with BOS secreted significantly less PGE2 than non-BOS LR-MSC

291 irway epithelium obtained from patients with BOS, particularly with SAEC.

292 y reduced in lung transplant recipients with BOS compared to BOS-free or donor controls.

293 ra cells, in lung transplant recipients with BOS, BOS-free patients and in donor controls.

294 sa is common particularly in recipients with BOS, but a possible etiological relationship remains une

295 entrations were increased in recipients with BOS.

296 stituents in lung transplant recipients with BOS.

297 Treatment with BOS was well tolerated in adolescent and young adult pat

298 ation and included patients with and without BOS.

299 MSCs) derived from patients with and without BOS.

300 BOS compared to transplant patients without BOS and controls, suggesting an intrinsic defect.