ライフサイエンスコーパス: lung

1 s in the process of tumor engraftment in the lung.

2 on of apoptosis-resistant fibroblasts in the lung.

3 and natural killer (NK) cells present in the lung.

4 ring gene expression was not observed in the lung.

5 hils and its pro-inflammatory effects in the lung.

6 nfection results in virus replication in the lung.

7 primary and metastatic sites, including the lung.

8 erent cell types are maintained in the adult lung.

9 o platelets within thrombi in infected mouse lungs.

10 crophages from fibrotic compared with normal lungs.

11 d phosphorylated-STAT3 in Mtb-infected mouse lungs.

12 viors such as oblique, vertical, and lateral lunging.

13 gastrointestinal (31.8%), brain (22.7%), or lung (20.7%).

14 incidence rates were 1.49 per 100000 in the lung, 3.56 per 100000 in gastroenteropancreatic sites, a

15 The most common infection sources were lung (43%) and urinary tract (17%); in 22% of cases, inf

16 Eosinophils isolated from the lungs A. alternata-challenged mice are cytokine-enriched

17 C vulnerable to glycolytic inhibition, while lung ADC exhibits significant glucose independence.

18 to the human BRAF(D594A) mutation) triggers lung adenocarcinoma in vivo, indicating that BRAF-inacti

19 oncoding RNA (lncRNA), metastasis-associated lung adenocarcinoma transcript 1 (Malat1), in ischemic s

20 In clinical specimens of lung adenocarcinoma, low KLF10 expression associated wit

21 promoting cancer cell invasive phenotypes in lung adenocarcinoma, lung squamous cell carcinoma and br

22 r the racial groups in five cancers, such as lung adenocarcinoma.

23 mutation and transcript were most common in lung adenocarcinoma.

24 ial impact of 19 well-defined DCAFs in human lung adenocarcinomas (LuADCs) using integrative omics an

25 ow in mice and cancer patients (n = 70) that lung adenocarcinomas increase bone stromal activity in t

26 CAF-enriched tumors in a compendium of 1,586 lung adenocarcinomas, the presence of the 425-gene signa

27 umour progression when activated in advanced lung adenocarcinomas.

28 -inflammatory and tissue repair genes in the lungs after helminth infection or in the gut after induc

29 OPD) is regarded as a disease of accelerated lung aging.

30 s (Annexin V positivity, P < .005), and less lung allergic inflammation (number of lung eosinophils,

31 morphological abnormalities: e.g., disrupted lung alveolarization, atrophy of intestinal villus and c

32 ells (AEC2s), the facultative progenitors of lung alveoli, from human PSCs.

33 h amplified AMPhi-induced PMN migration into lung alveoli.

34 ed during 2010 to 2015 were 5.7 Gy for whole lung and 4.4 Gy for whole heart.

35 ve tissues (ovary, testis, and prostate) and lung and colon tissues from both female and male mice.

36 on CD11b(+) pulmonary dendritic cells in the lung and draining lymph nodes in wild-type BALB/c mice a

37 ction map on a radiological image of a human lung and forms an interactive resource for the scientifi

38 global changes in mRNA abundance in healthy lung and lung lesions and in the lymphoid tissues bronch

39 ters for NSCLC lesions as well as for normal lung and muscle.

40 y during the pathogenesis of cancers such as lung and pancreatic adenocarcinomas.

41 sEphrin-B2) as a new profibrotic mediator in lung and skin fibrosis.

42 Fibrosis in lung and skin leads to progressive bronchiolitis obliter

43 mpanied by a reduced mycobacterial burden in lung and spleen and a prolonged overall survival in anim

44 tations of severe BCG disease and maintained lung and spleen organ integrity, which was accompanied b

45 increase in alveolar macrophage cells in the lungs and airways, early induction of virus specific ant

46 B. cenocepacia infection in cystic fibrosis lungs and serves as a valuable resource for understandin

47 s that may be sites of infection such as the lungs and soft tissues.

48 mucosal immune responses were induced in the lungs and the genital tract with the optimized GC-coated

49 hronized across distant locations within the lung, and are preceded by long-duration waves of airway

50 fan patients enrolled in the National Heart, Lung, and Blood Institute GenTAC (Genetically Triggered

51 Although the National Heart, Lung, and Blood Institute increased funding of career de

52 with FDCM or IDCM using the National Heart, Lung, and Blood Institute-funded Pediatric Cardiomyopath

53 -chip system, comprised of liver, heart, and lung, and highlight examples of inter-organ responses to

54 lacenta and cord blood at delivery, in fetal lung, and in buccal epithelium and blood during childhoo

55 but significant target expression in tumor, lung, and stomach was confirmed by immunohistochemistry.

56 s in addition to antigen and to identify the lung antigen-presenting cell (APC) types that sustain th

57 order: hyperinflation, 6 cm H2O above; open lung approach, 2 cm H2O above; and collapse, 6 cm H2O be

58 idify and warm the air before it reaches the lungs are of key importance.

59 ood and the lung rather than residing in the lung as bona fide tissue-resident CD69(+) NK cells.

60 Areas of increased lung attenuation are a novel risk factor for ILD hospita

61 RATIONALE: Areas of increased lung attenuation visualized by computed tomography are a

62 and profound defect in lung development with lung buds failing to undergo branching morphogenesis and

63 ans), melanoma (69 patients, 271 scans), and lung cancer (84 patients, 286 scans).

64 [AUC]) between individuals with and without lung cancer (death), and (3) clinical usefulness (net be

65 t frequently mutated genes in non-small cell lung cancer (NSCLC) and is commonly comutated with oncog

66 scription and tumor growth in non-small-cell lung cancer (NSCLC).

67 These data uncover a direct role for RANK in lung cancer and may explain why female sex hormones acce

68 KRAS-mutated lung cancer cell clones were stably silenced for LSD1 ex

69 We have analyzed a panel of 17 KRAS mutant lung cancer cell lines classified as K-Ras-dependent or

70 ues and its expression level is critical for lung cancer cell proliferation, which may serve as a pro

71 aling and triggered apoptosis in KRAS-mutant lung cancer cells and inhibited tumor growth in murine m

72 s the migratory and invasive capabilities of lung cancer cells in vitro and in vivo.

73 kappaB and Akt signaling pathways sensitizes lung cancer cells to cisplatin-induced apoptosis, we for

74 ne tumor models, in primary human breast and lung cancer cells, and in deposited expression data.

75 ich increased cisplatin-induced apoptosis in lung cancer cells.

76 ous cell lung carcinoma in the International Lung Cancer Consortium (N=60,586, meta-analysis P=0.0095

77 y explain why female sex hormones accelerate lung cancer development.

78 Six-year lung cancer incidence and mortality risk predictions wer

79 ing pesticides evaluated was associated with lung cancer incidence.

80 Lung cancer is the leading cause of cancer death in the

81 Late-stage diagnosis of lung cancer occurs 95% of the time due to late manifest

82 py combined with radiation in Non-Small Cell Lung Cancer patients for use in clinical trial design.

83 ntify radiosensitivity in 134 non-small-cell lung cancer patients, by using K-Means clustering to gro

84 , which may serve as a prognostic marker for lung cancer patients.

85 tion serves as a critical immunomodulator in lung cancer progression, acting to drive immune escape v

86 n between an index of vitamin B6 levels with lung cancer risk.

87 pplying risk-based eligibility would improve lung cancer screening efficacy.

88 fits, harms, and feasibility of implementing lung cancer screening policies based on risk prediction

89 ries need to set a timeline for implementing lung cancer screening.

90 Canada, implemented a policy to regionalize lung cancer surgery at 14 designated hospitals, enforced

91 042522) showed significant associations with lung cancer susceptibility with strong cumulative epidem

92 ouble-positive human NCI-H358 non-small cell lung cancer target tumors over single-positive, non-targ

93 Here, using human lung cancer tissue microarrays and fresh frozen tissues,

94 eport that PIPKIgamma is highly expressed in lung cancer tissues and its expression level is critical

95 Thus, small-cell lung cancer tumours generate their own microenvironment

96 eous HER3 overexpressing H441 non-small cell lung cancer xenograft.

97 logically confirmed limited-stage small-cell lung cancer, Eastern Cooperative Oncology Group performa

98 may heighten immunotherapeutic responses in lung cancer, offering findings with immediate implicatio

99 of GDH1 on AMPK is evident in LKB1-deficient lung cancer, where AMPK activation predominantly depends

100 mous epithelial cells of smokers, but not in lung cancer.

101 registry data to identify incident cases of lung cancer.

102 and evolution in early-stage non-small cell lung cancer.

103 ultiple immunocompetent orthotopic models of lung cancer.

104 d risk factor in various cancers, especially lung cancer.

105 antification in patients with non-small cell lung cancer.

106 cer and the death rate was second to that of lung cancer.

107 motherapy in select patients with small-cell lung cancer.

108 rrest and increased radiochemosensitivity in lung cancer.

109 ntly associated with a higher risk of future lung cancer.Significance: This large cohort study firmly

110 To target KRas in lung cancers we used a systems approach of integrating a

111 These include kidney, heart, and lung candidates who are highly-allosensitized.

112 ociated with increased risk of squamous cell lung carcinoma in the International Lung Cancer Consorti

113 nical trials for the treatment of small cell lung carcinoma, was synthesized using this strategy.

114 ssion of Kras(G12V) and Braf(D631A) in mouse lung cells markedly enhances tumour initiation, a phenom

115 osis, which is ameliorated by restoration of lung chitinase activity by genetic or therapeutic approa

116 In the swine model, lung collapse and intratidal recruitment/derecruitment o

117 2.1-fold, and 1.8-fold differences shown for lung, colorectal, and breast cancers, respectively.

118 significantly higher drug deposition in the lung compared with the existing formulations.

119 mean number of detected cells in irradiated lungs compared to control, although the latter did not r

120 duced infiltration of Ag-specific T cells in lungs compared with M. tuberculosis-infected WT mice.

121 expression, and reduced inflammation in the lungs compared with transfers into Rag1(-)(/-) mice expr

122 of neutrophil chemoattractant CXCL1 in their lungs compared with wild-type mice.

123 sing on methods to account for variations in lung components and the interpretation of the derived pa

124 phorylation and IL-6 expression in the mouse lungs, consistent with expression of ESAT-6, IL-6 and ph

125 On day 3, widespread areas of patchy lung consolidation were found on CT, with a drastic incr

126 optimizing nucleic acid yields in CT-guided lung core needle biopsies used for genomic analysis, the

127 the ability of alveolar macrophages to limit lung damage during influenza infection.

128 Similarly, LRP-1 expression by CD11b(+) lung DCs was significantly reduced in HDM-challenged WT

129 Quantitative measures of the mean lung density had the highest correlation with coefficien

130 Between months 24 and 48, the rate of lung density loss was reduced in delayed-start patients

131 enuated cellular apoptosis (caspase-3/7) and lung deposition of collagen and C' (C5b-9).

132 nfection by Pseudomonas leads to progressive lung destruction ultimately requiring lung transplantati

133 previously recognized aspects of post-natal lung development and revealed several insights, includin

134 erm led to a specific and profound defect in lung development with lung buds failing to undergo branc

135 As we show by applying TPS to study mouse lung development, the points selected by TPS can be used

136 ATIONALE: Mechanisms contributing to chronic lung disease after preterm birth are incompletely unders

137 , preterm infants frequently develop chronic lung disease and have a significantly increased risk of

138 on Global Initiative for Chronic Obstructive Lung Disease guidelines, 461 patients (17.6%) had mild,

139 nding of the pathogenesis and progression of lung disease in cystic fibrosis (CF).

140 Extubation is often unsuccessful owing to lung disease or inadequate respiratory drive.

141 f invasive aspergillosis, a frequently fatal lung disease primarily affecting immunocompromised indiv

142 attention on the role of EHF in modifying CF lung disease severity.

143 IPF) is a progressive and fatal interstitial lung disease.

144 t and/or progression of chronic inflammatory lung diseases including asthma, chronic obstructive pulm

145 g (18)F-FDG PET quantification approaches in lung diseases, focusing on methods to account for variat

146 of patients with other progressive fibrotic lung diseases.

147 which the majority of NK cells in the human lung dynamically move between blood and the lung rather

148 In the lung, ENaC is responsible for movement of sodium.

149 esis and progressive atrophy of the proximal lung endoderm with complete epithelial loss at later sta

150 ties and dose-dependently counteracted acute lung eosinophilia in an experimental animal model.

151 d less lung allergic inflammation (number of lung eosinophils, P < .005).

152 s essential for buffering Nkx2.1 expression, lung epithelial cell identity, and tissue homeostasis.

153 terized by the loss and aberrant function of lung epithelial cells.

154 ifferentiate human pluripotent stem cells to lung epithelium rely on passing through progenitor state

155 rget gene the liver X receptor (LXR)alpha in lung fibroblasts and macrophages.

156 e immunized BALB/c mice with senescent mouse lung fibroblasts and screened for antibodies that recogn

157 ring of lipogenic or myogenic populations of lung fibroblasts during fibrosis formation and resolutio

158 estigate alignment and migration of skin and lung fibroblasts from SSc patients and healthy controls.

159 on of integrin and Src kinase interaction to lung fibrosis has not been mechanistically investigated.

160 Lung fibrosis is an unabated wound healing response char

161 improved understanding of the mechanisms of lung fibrosis, and offers hope that similar approaches w

162 in fibrotic mice arrested the progression of lung fibrosis, attenuated cellular apoptosis (caspase-3/

163 miR-155(-/-) mice developed exacerbated lung fibrosis, increased collagen deposition, collagen 1

164 y disease (COPD) is characterized by reduced lung function and is the third leading cause of death gl

165 gen therapy during the newborn period and in lung function at 8 years of age in children whose birth

166 um and breast milk with allergic disease and lung function at ages 12 and 18 years.

167 ithelial cells may be a mechanism leading to lung function decline in a subset of children with asthm

168 n smokers without airflow obstruction affect lung function decline is unknown.

169 , reduces asthma exacerbations, and improves lung function for patients with severe eosinophilic asth

170 ht help to explain why TNF blockade improves lung function in only some patients with asthma.

171 week periods twice per year, coinciding with lung function testing.

172 Lung function was significantly better in lung grafts on

173 A/X31 H3N2 led to prolonged deterioration of lung function, aggravated mucus production, peri-vascula

174 cts were monitored for respiratory symptoms, lung function, and nasal viral load.

175 ally acute, Koch phenomenon-like reactions), lung function, or radiology attributable to vaccine were

176 ropy between nicotine dependence and COPD or lung function.

177 Our findings demonstrate that lung gammadelta T cells provide an early source of innat

178 Lung function was significantly better in lung grafts on EVLP with a LF than in lungs on EVLP with

179 erwise, if the fissure was incomplete or the lung had an emphysematous appearance, patients were rand

180 17A and anti-IL-13 Fab' fragments within the lungs had a major impact on their residence time, with t

181 signaling in AT2 cells, contributing to both lung homeostasis and tumor initiation.

182 integrins or alpha4 integrins did not affect lung ILC2 numbers.

183 the potential for this process to influence lung immunity as well.

184 ith cytotoxic function, the role of which in lung immunity is unclear.

185 bacteria within the microbiota that regulate lung immunity, and delineate the host signaling axis the

186 y of MtbDeltasigH, delivered directly to the lungs, in the setting of HIV co-infection.

187 d augment pathogenic immune responses in the lung, including activation of proinflammatory IL-17-prod

188 nsparent juvenile zebrafish to model mucosal lung infection and show that C. albicans and P. aerugino

189 stridium orbiscindens) promote resistance to lung infection through Nod2 and GM-CSF.

190 Seven (47%) had bilateral lung infiltrates.

191 acked red blood cells (pRBCs) and subsequent lung inflammation after transfusion.

192 t in DC homeostasis, is required to modulate lung inflammation and bacterial burden in TB.

193 ibility to silver nanoparticle-induced acute lung inflammation in mice.

194 Robust lung inflammation is one of the prominent features in th

195 th increased airway and tissue eosinophilia, lung inflammation, and IL-4, IL-5, IL-13, and IgE produc

196 mately 92 cluster in ILC2s displayed reduced lung inflammation.

197 In the immature lung, inflammation and injury disrupt the epithelial-mes

198 minent features in the pathogenesis of acute lung injury (ALI).

199 ctive ventilation is used to prevent further lung injury in patients on invasive mechanical ventilati

200 ry that is similar to the ventilator-induced lung injury observed in mechanically ventilated patients

201 data suggest that these patients may develop lung injury that is similar to the ventilator-induced lu

202 jected into a rat model of radiation-induced lung injury via endotracheal (ET) or intravascular (IV)

203 , cigarette smoke, silica, or sepsis-induced lung injury.

204 eroxia/reactive oxygen species (ROS)-induced lung injury.

205 increased IL-1beta, IL-6, and IL-8 in fetal lung, intestine, and brain, and morphological abnormalit

206 aturation, and migration in mucosal tissues (lungs, intestines), associated lymph nodes (LNs), and ot

207 These results demonstrate a lung-intrinsic, herniation-independent cause of PH in CD

208 l SPECT/CT-based MMP-targeted imaging of the lungs is feasible and reflects pulmonary inflammation.

209 toma cells significantly reduced whole body, lung, kidney and liver metastases in an experimental met

210 hanges in mRNA abundance in healthy lung and lung lesions and in the lymphoid tissues bronchial lymph

211 Interestingly, histological analysis of lung lesions from Muc4(ko)/NDL mice revealed a reduced a

212 One hundred fifteen patients with lung lesions were then prospectively included and assess

213 1 but are initially devoid of differentiated lung lineage markers.

214 of LSD1 to an altered expression pattern of lung-lineage specific transcription factors and genes, w

215 dent lung recruitment correlate with altered lung lining fluid composition independent of age or geno

216 Imaging revealed numerous metastases in the lungs, liver, and brain.

217 early compartment-independent activation of lung macrophages toward a conserved hypoxia program, wit

218 are used primarily in germ cell, breast and lung malignancies, oxaliplatin is instead used almost ex

219 -LXA4 injected mice displayed reduced LV and lung mass to body weight ratios and improved ejection fr

220 Human lung mast cells readily recover from a desensitized stat

221 Glucocorticoids are vital for lung maturation.

222 impaired CCL2 production and diminished both lung MDSC presence and tumor growth.

223 ouse models can be used to interrogate human lung metabolome changes.

224 cells, mice lacking PITPalpha develop fewer lung metastases due to a reduction of fibrin formation s

225 endothelial KLF2 results in dysregulation of lung microvascular homeostasis and contributes to lung p

226 In a mouse lung model of KRas(G12D)-driven adenomas, we find that c

227 whereby oral AM80 administration suppressed lung mucosa-associated Tfh and autoantibody responses by

228 4 resulted in enhanced L. pneumophila in the lungs of infected mice but not within cultured host cell

229 (uPA) and the uPA receptor in AECs from the lungs of IPF patients, and in mice with bleomycin, cigar

230 monocyte macrophages and neutrophils in the lungs of male mice, and depletion of inflammatory monocy

231 Furthermore, gammadelta T cells from the lungs of mice reinfected with B. pertussis produced sign

232 ng units (CFU) in vitro and <1000 CFU in the lungs of mice.

233 As the inflammation in the lungs of the sanroque mice could have been influenced by

234 ter in lung grafts on EVLP with a LF than in lungs on EVLP without a LF.

235 ctivating mutations are initiating events in lung oncogenesis.

236 Patients with lung or colorectal cancer often exhibit leukocytosis.

237 irculating cell-free DNA of 59 patients with lung or colorectal cancer.

238 ulation of epithelial fluid transport in the lung, pancreas and other organs in cystic fibrosis (CF).

239 g tiny (<1 mm) micrometastases in the liver, lung, pancreas, kidneys, and bone, that have disseminate

240 Less QV, especially in upper lung parts, and correlation to vital capacity and to mar

241 sed by using in vivo models of IL-13-induced lung pathology and in vitro culture of murine fibroblast

242 microvascular homeostasis and contributes to lung pathology in ARDS.

243 cerbated inflammatory response and extensive lung pathology.

244 tro to generate and isolate human primordial lung progenitors that express NKX2-1 but are initially d

245 an appropriate Vt is an essential part of a lung-protective MV strategy.

246 Lung-protective ventilation is used to prevent further l

247 Furthermore, OVA-exposed lung Ptx3(-/-) CD4 T cells exhibit an increased producti

248 lung dynamically move between blood and the lung rather than residing in the lung as bona fide tissu

249 Model-predicted deficits in PEEP-dependent lung recruitment correlate with altered lung lining flui

250 positive end-expiratory pressure trial after lung recruitment was determined.

251 (AMR) is an increasingly recognized form of lung rejection.

252 effects on epithelial cell regeneration and lung repair during fibrosis.

253 mmasome activation together with accelerated lung repair.

254 Lung resection material from a separate group of subject

255 RV pressure-volume measurements, along with lung, RV histological, and protein analyses.

256 ulmonary vasculature in a decellularized rat lung scaffold.

257 l carcinomas (oesophageal, head and neck and lung) significantly promote cancer cell proliferation, m

258 0(10) colony-forming units were found in the lungs, spleen, and liver.

259 at a critical reliance on glycolysis renders lung SqCC vulnerable to glycolytic inhibition, while lun

260 invasive phenotypes in lung adenocarcinoma, lung squamous cell carcinoma and breast carcinoma cancer

261 ecific ventilation (sVlow) and the remaining lung (sVhigh) were quantified and compared.

262 sought to understand whether maintenance of lung TH17 inflammation requires environmental agents in

263 Whether regions of the lung that appear normal using traditional computed tomog

264 asthma is a chronic Th2 inflammation in the lungs that constricts the airways and presents as coughi

265 impairs metastasis of carcinoma cells to the lung, thereby providing insights into the mechanisms of

266 senescence markers are detectable within IPF lung tissue and senescent cell deletion rejuvenates pulm

267 There was no effect of MCH on fetal plasma/lung tissue cortisol concentrations, nor genes regulatin

268 Flow cytometric analysis of lung tissue from H2 R-deficient animals revealed increas

269 nflux and IL-4, IL-5 and IL-13 production in lung tissue, as well as TH2 cell activation.

270 d with gene expression of HHIP and FAM13A in lung tissue, respectively; and were genome-wide signific

271 miR-101 expression was determined in lung tissues from patients with IPF and mice with bleomy

272 BRBP is reduced in LuADCs compared to normal lung tissues.

273 ated hemoglobin [HbA1c]) and survival in all lung transplant (LTx) recipients and those with either p

274 Rates for death or double-lung transplant and the composite rates for death, doubl

275 cted from patients with BOS (n = 10), stable lung transplant patients (n = 18), and healthy aged-matc

276 ected in the bronchoalveolar lavage fluid of lung transplant patients diagnosed with IA that received

277 Thus, immunosuppressive strategies for lung transplant recipients need to be tailored based on

278 the impact of pretransplant sensitization on lung transplant recipients.

279 nt and the composite rates for death, double-lung transplant, or restenosis at 36 months were 5% and

280 act the time to development of BOS or RAS in lung transplantation (low vs high LVD: 38.5 vs 86.0 mont

281 essive lung destruction ultimately requiring lung transplantation (LT).

282 ent of donor-specific antibodies (DSA) after lung transplantation is associated with antibody mediate

283 y was most outspoken in the first year after lung transplantation.

284 Solitary kidney, liver, heart, and lung transplants performed between January 1, 2011, and

285 IL-33 dysregulated lung Treg cells and impaired immunologic tolerance to in

286 rophages and reduces CD8+ T cells to promote lung tumor growth.

287 ssion of NFS1, whereas metastatic or primary lung tumours do not.

288 Adenosquamous lung tumours, which are extremely poor prognosis, may re

289 e imaging that provide measurement of distal lung ventilation reflecting small-airway disease.

290 acerbate allergic inflammation in the murine lung via a TLR2/TLR4/MyD88-signaling pathway.

291 ddition, they showed superior protection and lung viral reduction against lethal viral challenge.

292 re time product, and we estimated changes in lung volumes and ventilation homogeneity by electrical i

293 Results QV of the entire lungs was lower for patients with CF than for control su

294 Extravascular lung water was indexed to predicted body weight (EVLWPBW

295 Formalin-fixed sections of the lungs were analyzed using fluorescence imaging, autoradi

296 kocyte recruitment and activation within the lungs were not significantly attenuated nor were a host

297 odoplanin were constitutively present in the lung, whereas the GPVI ligands fibrin and histone were i

298 n promotes molecular maturation of the fetal lung, which may be an adaptive response in preparation f

299 suring a median of 20 mm (range, 5-47 mm) in lung window CT images were analyzed.

300 ), and gas fraction (Fgas) in the 25% of the lung with the lowest specific ventilation (sVlow) and th