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1 /= 0.05) of the endothelin A receptor in the lung tissue.
2 and temporal changes in lipid composition in lung tissue.
3  infiltration and cytokine production in the lung tissue.
4 uid, and the endothelium of blood vessels in lung tissue.
5 ide gels in the range of normal and fibrotic lung tissue.
6 e modifications were increased in plasma and lung tissue.
7 poptosis both in cultured cells and in mouse lung tissue.
8 or in response to actual normal and fibrotic lung tissue.
9 and 6 +/- 6% (CT [not + poorly inflated]) of lung tissue.
10 ) genotyping and targeted gene expression in lung tissue.
11 ignificantly elevated levels of TNF-alpha in lung tissue.
12 ansferase (3-MST), in comparison to adjacent lung tissue.
13 NAs in a safe and effective manner to target lung tissue.
14 onary microvascular ECFCs from human and rat lung tissue.
15 expression (mRNA) quantitative trait loci in lung tissue.
16 urements in bronchoalveolar lavage fluid and lung tissue.
17 ownregulation of Notch2 compared with normal lung tissue.
18 ol to isolate resident ECFCs from the distal lung tissue.
19  and pathways underlying the associations in lung tissue.
20 e models of lung fibrosis and fibrotic human lung tissue.
21 pecific genes underlying the GWAS signals in lung tissue.
22 ed, followed by quantitative analysis of the lung tissue.
23 ith gene expression of PDE4D and TMEM176A in lung tissue.
24 gene correction is detected in the nasal and lung tissue.
25  with evidence of efficient penetration into lung tissue.
26 IL-5 and IL-13 in bronchoalveolar lavage and lung tissue.
27 cursors were detected in primary cultures of lung tissue.
28  epithelial TGF-beta1 immunostaining in COPD lung tissue.
29 ung injury with two-photon imaging of intact lung tissue.
30 ers by immunohistochemical assessment of IPF lung tissue.
31 lasma may be interrogated in lieu of BALF or lung tissue.
32 anhydrases, which were also expressed in LAM lung tissue.
33 ced EP4 mRNA expression in pulmonary ECs and lung tissue.
34 ed a robust expression of FOXD3-AS1 in mouse lung tissue.
35 performed eQTL and co-expression analyses in lung tissue.
36 ical density of surfactant positive cells in lung tissue.
37 es, bone marrow-derived dendritic cells, and lung tissue.
38 trations were determined in fetal plasma and lung tissue.
39 oduction of reactive oxygen species (ROS) in lung tissue.
40 asts, and the adventitia of blood vessels in lung tissue.
41 accumulation of M2 macrophages in irradiated lung tissues.
42 ed in NSCLC samples compared with tumor-free lung tissues.
43 cinoma tissues compared with adjacent normal lung tissues.
44 used to assess CtBP1 expression in the whole-lung tissues.
45 3(R172H/+); AdCre) in comparison with normal lung tissues.
46  and human adventitial fibroblasts and mouse lung tissues.
47 red: 67 primary NSCLCs and 18 matched normal lung tissues.
48 ed as an eQTL in human primary monocytes and lung tissues.
49 storing a favorable immunological balance in lung tissues.
50 luid and proinflammatory cytokines levels in lung tissues.
51 regs are rapidly mobilized into the inflamed lung tissues.
52 method to obtain single-cell suspension from lung tissues.
53 cell carcinomas, but not expressed in normal lung tissues.
54 es long enough to be transported into deeper lung tissues.
55 BRBP is reduced in LuADCs compared to normal lung tissues.
56 d autoimmunity that mainly targeted skin and lung tissues.
57 romotes wound repair in adipose, muscle, and lung tissues.
58 ofibroblast differentiation in vivo in mouse lung tissues.
59 s and were immunologically well tolerated by lung tissues.
60 , this pattern mirrored that observed in IPF lung tissues.
61 1 lung adenocarcinomas (LUAD) and 156 normal lung tissues.
62  lung cancer cell lines compared with normal lung tissues.
63  much lower than that in the adjacent normal lung tissues.
64 .5 (PGP9.5) and, for the first time in human lung tissue, 200-kD neurofilament subunit.
65 -associated radioactivity located within the lung tissue (23.3+/-4.7%) compared to the lung fluid (16
66  bacterial invasion from the airway into the lung tissue, a blunted inflammatory cytokine and neutrop
67  influx of inflammatory neutrophils into the lung tissue and airways.
68 sinophilia, the increase of cytokines in the lung tissue and antigen-specific T cell proliferation, b
69  NCTC 7466 by reducing the bacterial load in lung tissue and blood.
70 ped by multicolor flow cytometry in digested lung tissue and bronchoalveolar lavage (BAL) simultaneou
71 trometry-based metabolic profiling of serum, lung tissue and bronchoalveolar lavage fluid (BALF) from
72 ression signature for COPD was identified in lung tissue and compared with the Connectivity Map.
73 sponse causes DC retention in the peripheral lung tissue and contributes to injury.
74 cular cells and various types of PH-diseased lung tissue and determined that ECM stiffening resulted
75 wnstream signaling pathways were profiled in lung tissue and fibroblasts from the TbetaRIIDeltak-fib
76 tion in BMPRII expression is observed in SSc lung tissue and fibroblasts.
77 omplementary studies examined SSc or control lung tissue and fibroblasts.
78 ntified Nrf2-dependent genes and pathways in lung tissue and in recruited neutrophils.
79 isome-related protein and gene expression in lung tissue and isolated lung fibroblasts between human
80                            NK cells in human lung tissue and matched peripheral blood from 132 subjec
81 t endobronchial coils compress emphysematous lung tissue and may improve lung function, exercise tole
82 cho-epithelial cells (pBEC), explanted human lung tissue and mouse lungs were infected with different
83 ks at 2mg/kg, antimiR-145 accumulated in rat lung tissue and reduced expression of endogenous miR-145
84 umber and properties of NK cells resident in lung tissue and reveal a role for NK cells in limiting l
85 senescence markers are detectable within IPF lung tissue and senescent cell deletion rejuvenates pulm
86  case definitions, poor access to pathologic lung tissue and to specimens from fatal cases, poor diag
87 phy-mass spectrometry metabolic profiling of lung tissue and urine.
88 tial metabolites were captured in mice sera, lung tissues and BALF, including purines, pyrimidines, a
89 olite signatures were observed in mice sera, lung tissues and BALF, indicating the molecular differen
90                                              Lung tissues and blood samples were collected from rats
91                            Analysis of human lung tissues and primary human lung fibroblasts indicate
92               Human IPAH and control patient lung tissues and pulmonary artery smooth muscle cells (P
93 d IL-6, in the bronchoalveolar lavage or the lung tissue, and histology.
94 lung histology, serology, gene expression in lung tissue, and measurement of lung function.
95 dentical to that amplified from the original lung tissue, and phylogenetic analysis of the full-lengt
96 ammation in bronchoalveolar lavage (BAL) and lung tissue, and total free IgE in serum samples were an
97 ages, mouse bronchoalveolar lavage fluid and lung tissues, and AHR in mice.
98 ract also significantly reduces TGF-beta1 in lung tissues, and this effect is accompanied by decrease
99   Interstitial macrophages (IMs) inhabit the lung tissue, are not recovered with BAL, are shorter-liv
100 in (FST), a stress responsive gene, in mouse lung tissue as well as in human lung epithelial cells (A
101 n was reduced in human and experimental COPD lung tissues as well as in primary human ATII cells from
102 nflux and IL-4, IL-5 and IL-13 production in lung tissue, as well as TH2 cell activation.
103 and signaling through both hematopoietic and lung tissue-associated T prostanoid (TP) receptors.
104                                              Lung tissue, bronchoalveolar lavage fluid (BALF) and dra
105                       Silica-induced SPP1 in lung tissue, bronchoalveolar lavage, and serum increased
106 sections, stretch increased Cela1 binding to lung tissue by 46%.
107 berculosis, we characterized infected murine lung tissue by transcriptomic profiling and confocal ima
108                                 Within whole lung tissue, C. burnetii preferentially replicated in hA
109                                              Lung tissue can robustly regenerate functional alveolar
110 nia remains challenging because the infected lung tissue cannot usually be sampled for testing.
111  protease gene expression profiling in whole lung tissue, cathepsin K gene expression was 40-fold ove
112 d lack of SP-D reduced NK cell IFN-gamma and lung tissue CCL21 mRNA expression and impaired DC homing
113               Our supervised method for thin lung tissue classified NETs with sensitivity/specificity
114  (BAL) and increased collagen content in the lung tissue compared to saline controls.
115 nd had impaired expansion of ILC2 in damaged lung tissue compared with wild-type controls.
116   There was no effect of MCH on fetal plasma/lung tissue cortisol concentrations, nor genes regulatin
117 l as by CT scan: (3) decrease in noninflated lung tissue (CT [not inflated]); and (4) decrease in non
118 36 on influenza virus replication in a human lung tissue culture model and observed strong inhibition
119 ATII cells in vitro and in three-dimensional lung tissue cultures ex vivo.
120  elastogenic components in three-dimensional lung tissue cultures ex vivo.
121  carcinogen, urethane, resulted in increased lung tissue damage and inflammation, K-Ras oncogenic mut
122        LR12 also attenuated inflammation and lung tissue damage by reducing histopathologic changes,
123             This indicates that SIV produces lung tissue damage through destruction of IMs, whereas t
124 attendant bacterial infections contribute to lung tissue damage, respiratory insufficiency, and ultim
125 kocytes, resulting in acute inflammation and lung tissue damage.
126 assive cell death of IMs that contributed to lung tissue damage.
127 ere, we evaluated infection of ex vivo human lung tissue, defining a valuable approach for characteri
128 en identified GbbLCV-1 in post-mortem infant lung tissues demonstrating histopathological lesions con
129 TB) is characterized by oxidative stress and lung tissue destruction by matrix metalloproteinases (MM
130 gly, inhibition of WNT-5A in vivo attenuated lung tissue destruction, improved lung function, and res
131 ed with clinical and radiological markers of lung tissue destruction.
132 tensities from brain and to some extent also lung tissue, differences which may be ascribed to bindin
133                                         COPD lung tissue displayed significantly elevated CCR2 levels
134 ion of innate immune cell recruitment to the lung tissue during bacteremic pneumonia.
135 sized that IL-17A is increased in peripheral lung tissue during end-stage COPD and also directly cont
136  (BLT) reconstitution method, in addition to lung tissue engraftment, giving altogether a realistic m
137 T5C3B risk allele was associated with higher lung tissue expression (P = 1.09 x 10(-41)).
138   SNP rs734556 was associated with decreased lung tissue expression of SERPINE2, a susceptibility gen
139 TRAP activity in murine macrophage and human lung tissue extracts.
140 D8 T cells persisted in peripheral blood and lung tissue for at least 24 weeks and trafficked to mult
141            MicroRNA array profiling of human lung tissue found elevation of microRNAs associated with
142 e genetic architecture of gene expression in lung tissue from 1111 individuals.
143          DSP gene expression was measured in lung tissue from 334 subjects with IPF and 201 control s
144 e from patients with IPF (n=46) than that in lung tissue from controls (n=51).
145                  Flow cytometric analysis of lung tissue from H2 R-deficient animals revealed increas
146                                           In lung tissue from human patients with asthma, we observed
147 patients who survive sudden, massive loss of lung tissue from necrotizing pneumonia or acute respirat
148  with increased expression of AKAP13 mRNA in lung tissue from patients who had lung resection procedu
149                                           In lung tissue from patients with acute respiratory distres
150 ling and metabolic pathways are disrupted in lung tissue from patients with chronic obstructive pulmo
151 n, levels of which are elevated in serum and lung tissue from patients with idiopathic pulmonary fibr
152 P13 mRNA expression was 1.42-times higher in lung tissue from patients with IPF (n=46) than that in l
153                                              Lung tissue from patients with schistosomiasis-associate
154                                              Lung tissue from patients with schistosomiasis-associate
155                                           In lung tissue from pulmonary fibrosis patients with relati
156 were assessed in parallel using fresh-frozen lung tissue from sibling rats of the same cages.
157 , and genome-wide chromatin accessibility in lung tissue from two genetically divergent inbred mouse
158                     Furthermore, we analyzed lung tissues from 21 patients with CF and chronic obstru
159 zing 461 lung adenocarcinomas and 156 normal lung tissues from 3 separate cohorts.
160  environmental particulates (anthracosis) in lung tissues from asbestos exposed and control patients.
161                                  Analysis of lung tissues from Berkeley sickle (BK-SS) mice showed in
162  H9N2 virus to human cells and attachment to lung tissues from humans and mouse.
163 r tuberculosinyladenosine in serum and whole lung tissues from infected mice and sputum, cerebrospina
164 nd the expression of TREM-1 was increased in lung tissues from mice with pulmonary fibrosis.
165  activator protein 1 (AP-1) was increased in lung tissues from mouse after BLM injection and in mouse
166 enhances binding affinity to human cells and lung tissues from mouse and humans.
167                                              Lung tissues from patients with emphysema, and from spon
168         FIEL1 protein is highly expressed in lung tissues from patients with idiopathic pulmonary fib
169         miR-101 expression was determined in lung tissues from patients with IPF and mice with bleomy
170                                S1P levels in lung tissues from patients with PAH and pulmonary arteri
171 and histopathological analysis and processed lung tissues from patients with tuberculosis through the
172                       Analysis of plasma and lung tissues from SEB-exposed mice treated with abatacep
173 sion profiling on a large sample of resected lung tissues from subjects with severe COPD.
174 e associated with less severe BHR and higher lung tissue gene expression.
175 eutics in silico that could reverse the COPD lung tissue gene signature.
176      The system genetics approach identified lung tissue genes driving the variation in lung function
177 tissues targeted by MHV68 indicated that the lung tissue has a lower level of enzymatic UNG activity
178                  Moreover, the non-malignant lung tissues have higher microbiota alpha diversity than
179 , but the early events of its development in lung tissues have not been investigated, and S1P functio
180 otal phospholipid, PC, and disaturated PC in lung tissue homogenate, bronchoalveolar lavage fluid, an
181         In vivo, 2CA dramatically suppressed lung tissue hypercitrullination, inflammatory cell recru
182 been defined as the pressure across only the lung tissue (i.e., the pressure difference between the a
183  HA and HC-HA (i) from asthmatic and control lung tissue, (ii) in bronchoalveolar lavage fluid obtain
184 e and reveal a role for NK cells in limiting lung tissue ILC2s and preventing allergic inflammatory r
185 g Th2 cells but an increase of Th17 cells in lung tissue in comparison with recipients sensitized wit
186 es were strikingly reduced in both blood and lung tissue in relation to corticosteroid therapy and vi
187 monstrate the upregulation of these genes in lung tissue in response to highly pathogenic IAV infecti
188  lung organoids (HLOs) resembled human fetal lung tissue in vitro.
189 that loss of miR-140 is a marker of fibrotic lung tissue in vivo one-year post-radiation treatment.
190 ibited the LPS-triggered NF-kappaB levels in lung tissue in vivo.
191 ad2/Smad3, and the deposition of collagen in lung tissues in a bleomycin-induced model of pulmonary f
192 anine and long-term adenoma formation in the lung tissues in A/J mice.
193 gnaling would control pneumococcal burden in lung tissues in an experimental pneumonia model.
194 X30 was expressed in normal and peri-tumoral lung tissues in which SOX30 was unmethylated, but was si
195                           We harvested human lung tissues in which we assessed calcification lesions
196 ingle-cell suspensions derived from neonatal lung tissue included populations that expressed either S
197 ulated genes and pathways in neutrophils and lung tissue, including those involved in redox stress re
198  and demonstrate that nonspecific binding to lung tissue increases with lipophilicity.
199        Transcriptional and protein assays of lung tissue indicated p38(MAPK)-dependent activation of
200 h fIIP and affect expression of HLA genes in lung tissue, indicating that the potential genetic risk
201                                              Lung tissue inflammation and mucus production were asses
202 ldren-namely complex surfactant dysfunction, lung tissue inflammation, loss of lung volume, increased
203  better aeration distribution, and minimized lung tissue inhomogeneities.
204 kg) had reduced viral titers and showed less lung tissue injury, despite 24- to 72-h-delayed treatmen
205  LPA1 is involved in pathways leading, after lung tissue injury, to pulmonary fibrosis instead of nor
206              Therefore, we hypothesized that lung-tissue injury can lead to lung-restricted immunity
207                                     In human lung tissues, intercellular adhesion molecule-1, vascula
208 ent findings suggest that the poorly aerated lung tissue is an important target of the perpetuation o
209 d establishing a working diagnosis of IPF if lung tissue is not available.
210                      In later stages, normal lung tissue is replaced by a large amount of young colla
211  NPSH in nasal, thoracic extrapulmonary, and lung tissues; it also induced the oxidant stress respons
212 heterogeneity, and the paucity of early ARDS lung tissue limit some applications of the rapidly evolv
213 d viral loads and restricted viral spread in lung tissues, limited lung damage, and decreased inflamm
214        Staining of fibrotic and normal human lung tissue localized DSP to airway epithelia.
215 el of tumor necrosis factor-alpha in ventral lung tissue (median [interquartile range], 17.7 pg/mg [8
216                                    The human lung tissue microbiota remains largely uncharacterized,
217                   Here, we apply a series of lung tissue motion analyses, to achieve regional pulmona
218                                     In human lung tissues, numbers of pericytes are substantially inc
219                                              Lung tissue obtained from 13 non-CLAD patients served as
220  passage cultures of human ECs isolated from lung tissues obtained from patients with iPAH and contro
221 action and mRNA microarray, respectively, on lung tissue of 30 patients (screening cohort) encompassi
222 nt hantavirus, named Nova virus (NVAV), from lung tissue of a European mole (Talpa europaea), capture
223 ress-dependent pathways are activated in the lung tissue of C57/BL6J-betaENaC-Tg mice.
224 pectroscopy (LC/MS-MS) on plasma, urine, and lung tissue of Hhip (+/-) heterozygotes and wild type (H
225                  No B cells were detected in lung tissue of Lactobacillus-primed B cell deficient muM
226 d the levels of IL-17, IL-4 and IL-13 in the lung tissue of OVA-challenged mice.
227 P-C) is a novel amyloid protein found in the lung tissue of patients suffering from interstitial lung
228           To identify dysregulated miRNAs in lung tissue of patients with chronic obstructive pulmona
229 SIV infection on AMs in BAL fluid and IMs in lung tissue of rhesus macaques.
230 L1 expression was significantly decreased in lung tissue of the silica-exposed animals compared to co
231  mesenchymal stem cells (LR-MSCs) and in the lung tissues of a pulmonary fibrosis model.
232 ters were obtained from nasal turbinates and lung tissues of directly inoculated animals.
233 evated levels of CCN1 mRNA were confirmed in lung tissues of IPF subjects undergoing lung transplanta
234 release and more severe tissue injury in the lung tissues of LKB1 KO mice than in those of control mi
235 mulation, AAT1 expression and SO2 content in lung tissues of rat were reduced in shunt rats with high
236 iated the excessive collagen accumulation in lung tissues of shunt rats.
237 istress syndrome but preserved E-cadherin in lung tissue only in extrapulmonary acute respiratory dis
238 ity to peptide fusion inhibitors in the host lung tissue or animal, but the same fusion inhibitors ha
239 tors in murine bronchoalveolar lavage fluid, lung tissue, or human nasal polyp tissue were analyzed b
240 s invasive, which allows imaging of the same lung tissue over a period of weeks.
241 3-fold increased (95% CI = 1.91-2.71) in IPF lung tissue (P < 0.0001).
242 d overexpressed in LAM compared with control lung tissue (P </= 0.0001).
243 erase, polypeptide 5 (B4GALT5) expression in lung tissue (P = 1.18 x 10(-17)).
244 0) of normal and 8.0% (2/25) of peri-tumoral lung tissues (P<0.01).
245 th an increased Th2 response and exacerbated lung tissue pathology.
246 ially expressed between fibrotic and control lung tissue (Q < 0.001), many of which are involved in i
247  of superoxide dismutase-2, thereby reducing lung tissue reactive oxidative species concentrations.
248 H2O) needed to restore poorly and nonaerated lung tissue, reestablishing lung elastance and oxygenati
249 lyzed gene expression data obtained from the Lung Tissue Research Consortium and correlated RXFP1 gen
250 d with gene expression of HHIP and FAM13A in lung tissue, respectively; and were genome-wide signific
251 jury combined with loss of Tregs can lead to lung-tissue-restricted immunity.
252                        Histopathology of the lung tissues revealed extensive pulmonary edema and vasc
253  of murine and human paired normal-malignant lung tissues revealed marked upregulation of CP110 in ma
254 iles of lung microbiota in 165 non-malignant lung tissue samples from cancer patients.
255 ata resources, and examined expression using lung tissue samples from patients with IPF and controls.
256  trait locus (eQTL) analysis in 1,425 normal lung tissue samples highlights RNASET2, SECISBP2L and NR
257  genes with the greatest variation among 133 lung tissue samples identified five distinct clusters of
258                                       Within lung tissue samples the microbiome was compared with res
259 hial alveolar lavage (BAL) fluid; sputum and lung tissue samples; and pleural and spinal fluids.
260  analyses of viral nucleoprotein staining of lung tissue sections and dissociated lung cells.
261                      Primary distal PAVSMCs, lung tissue sections from unused donor (control) and idi
262             Our unsupervised method for thin lung tissue sections in murine fungal pneumonia achieved
263                                     NTN(-/-) lung tissues showed higher levels of neutrophils, cytoki
264 over, immunohistochemical analysis of paired lung tissues showed PC overexpression in cancer cells ra
265 M-IPIV group had increased CD4(+) T cells in lung tissue, significantly increased coagulation, decrea
266                      Freshly resected paired lung tissue slices cultured in 13C6-glucose or 13C5,15N2
267 s, and infiltrating of inflammatory cells in lung tissues; specific airway resistance (sRaw) response
268                                     In human lung tissue specimens both DP1 and DP2 receptors were lo
269 ection of IL-17A and IL-17F was performed in lung tissue specimens collected from patients with Globa
270 n pulmonary vasculature resistance caused by lung tissue stretch.
271 ed with high expression of CLPTM1L in normal lung tissue, suggesting that cis-regulation of CLPTM1L m
272 level of expression of their target genes in lung tissue; termed eSNPs.
273 l recruitment, and a lower bacterial load in lung tissue than mice infected with wild-type P. aerugin
274 n induces greater long-term damage to normal lung tissue than the relative equivalent dose of low-LET
275 nd had reduced leukocyte infiltration in the lung tissue than their WT littermates.
276                           In mouse and human lung tissues, the expression level and location of IL-6
277 es and conduct new RNA sequencing studies of lung tissue to identify and characterize new fIIP risk l
278 nfection-induced exacerbation also increased lung tissue TSLP (P < 0.05).
279 er model, we showed that, relative to normal lung tissues, tumor stroma contains higher levels of hyd
280              Furthermore, the limitations of lung tissue under simple mechanical loading are also not
281 lso impaired viral clearance, with increased lung tissue viral RNA copy numbers (4.7 x 10(5) copies [
282  to a Siglec-F(high) CD11c(low) phenotype in lung tissue was associated with eosinophil recruitment t
283                         We found that normal lung tissue was characterized predominantly by saturated
284        At 138 days, gene expression in fetal lung tissue was determined by quantitative RT-PCR.
285 tral confocal microscopy of human and murine lung tissue was performed to localize Syk expression.
286                     E-cadherin expression in lung tissue was reduced in volume-controlled ventilation
287 ofluorescence approach, rarely used in human lung tissue, was used with antibodies specific to protei
288 n vivo grown HLOs with fetal and adult human lung tissue, we found that in vivo transplanted HLOs had
289  respiratory distress syndrome had a greater lung tissue weight and recruitability than patients with
290 ells in the bronchoalveolar lavage fluid and lung tissue were assessed.
291                      Blood, bone marrow, and lung tissue were collected 4 hours after injury and huma
292              Grams of water per grams of dry lung tissue were determined in the lungs harvested 1 hou
293             Bronchoalveolar lavage (BAL) and lung tissue were examined for inflammation, mucus produc
294     Miners with severe disease and available lung tissue were identified through investigator outreac
295                                          The lung tissues were assessed for airway inflammation and m
296 ssion of the NLRP3 inflammasome and P2X7R in lung tissues, whereas it enhances expression of superoxi
297 biomechanical and genetic alterations in the lung tissue which lead to lung fibrosis.
298 iscriminate between control and GOLD stage 4 lung tissue, which included known pathogens such as Haem
299                                The volume of lung tissue with increased relaxation times was determin
300 rison of the effects of myosin inhibition on lung tissue with that of polyacrylamide gels suggests th

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