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1 ble to airway obstruction (nose < bronchi << bronchioles).
2 thin single segments and, indeed, individual bronchioles.
3 natomical structure known as the respiratory bronchioles.
4 ation, and increases NK cell infiltration in bronchioles.
5 d primary human cultures from trachea versus bronchioles.
6 dysplastic and sloughed cells in respiratory bronchioles.
7 o widespread papillary adenocarcinoma in the bronchioles.
8 10+ papillary adenocarcinomas throughout the bronchioles.
9 ited transgene expression to the respiratory bronchioles.
10 wed severe immune cell infiltration into the bronchioles.
11 n as stem/progenitor cells for repair in the bronchioles.
12 carcinomas restricted to proximal and distal bronchioles.
13 and likely interacts with the Clara cells of bronchioles.
14 .4 +/- 1.6% of the epithelial cells in large bronchioles.
15 hils into the walls and lumen of bronchi and bronchioles.
16 sive extracellular matrix of the bronchi and bronchioles.
17 endocrine cells involving distal bronchi and bronchioles.
18 lial cells of the injury target zone, distal bronchioles.
19 pithelial cells of the trachea, bronchi, and bronchioles.
20 nodules with adjoining thickened and dilated bronchioles.
21 atal asthmatics, 30% and 38% of pre-terminal bronchioles, 29% and 34% of terminal bronchioles, and 33
22 n control subjects (median number of LVs per bronchiole: 4.75 (BOS), 6.47 (RAS), 4.25 (control), P =
23  centrilobular region, and small bronchi and bronchioles), abnormal findings (reticulation, tiny nodu
24  enlargement of airspaces distal to terminal bronchioles accompanied by destruction of alveolar walls
25 s distinct from those of peripheral airways (bronchioles, acini, and alveoli), were established well
26 of cells contributing to renewal of terminal bronchioles after Clara cell depletion.
27 chiole wall and low collagen around the lung bronchioles after Ova-allergen challenge further confirm
28 sal cell progenitors migrate out of terminal bronchioles, aiding alveolar regeneration.
29 y response that promotes airway fibrosis via bronchiole airway epithelial damage and obliteration.
30 f the alpha(4)beta(1) ligand, VCAM-1, on the bronchioles, allowing direct access of the leukocytes to
31 docrine cells, make up the epithelium of the bronchioles along the conducting airways.
32            However, no tumors develop in the bronchioles, although recombination occurs throughout th
33 ensive single-cell atlas highlights terminal bronchiole alveolar attachments as the initial site of t
34 ng in vivo, human lung stem cells form human bronchioles, alveoli, and pulmonary vessels integrated s
35 diated communication between the organotypic bronchiole and cultures of Aspergillus fumigatus and Pse
36 P)-2 in epithelial cells lining the terminal bronchioles and alveolar ducts as well as macrophages an
37 reactivity in epithelial cells lining distal bronchioles and alveolar ducts, sites of initial lung de
38 infection, P. aeruginosa enters the terminal bronchioles and alveoli and comes into contact with alve
39            The distal lung contains terminal bronchioles and alveoli that facilitate gas exchange.
40 t lungs resulted in the expression of GFP in bronchioles and alveoli within 5 days.
41 losis is initially deposited in the terminal bronchioles and alveoli, as well as following release fr
42 ted the lumen, epithelium, and adventitia of bronchioles and bronchi in lungs of calves with BLAD com
43 enchymal cells and acinar buds and decreased bronchioles and dilated airspaces in SPC-PDGFA transgeni
44 ubpopulation formed clusters within terminal bronchioles and exhibited enriched clonogenic organoid g
45 similar strong PD-L1 expression signature in bronchioles and functionally active AMs compared to pati
46  an enrichment in methylated ACE2 in hamster bronchioles and lung macrophages, a signature associated
47  COVID-19 in both morphologically identified bronchioles and microcysts, and MUC5B accumulated in dam
48  DNA synthesis in the epithelium of terminal bronchioles and more proximal airways.
49 by contraction of the smooth muscle walls in bronchioles and pulmonary arteries and aggregation of pl
50 s to humans, with well developed respiratory bronchioles and submucosal glands.
51 -expressing stem cell population in terminal bronchioles and support the notion that regiospecific st
52 nd Main Results: The numbers of transitional bronchioles and terminal bronchioles per milliliter of l
53  of alveolar attachments of the transitional bronchioles and terminal bronchioles was also lower in p
54 e sparing larger airways as well as terminal bronchioles and the alveolar surface.
55 olution from immune cell infiltration of the bronchioles and vessels at day 14, consistent with acute
56 a cells of wild-type and COX-1(-/-) terminal bronchioles and was strongly induced 24 hours after V(2)
57 ized network of conducting airways (bronchi, bronchioles) and gas-exchanging units (alveoli).
58          The conducting airways (bronchi and bronchioles) and peripheral gas exchange (alveolar) regi
59 erminal bronchioles, 29% and 34% of terminal bronchioles, and 33% and 21% of transitional bronchioles
60 mmunostaining, in the epithelium of bronchi, bronchioles, and alveolar walls.
61 ted in the epithelial cells of nasal mucosa, bronchioles, and alveoli for up to 4 days postinfection.
62 ells were present in the conducting airways, bronchioles, and alveoli.
63 gmented in the pulmonary arteries and veins, bronchioles, and developing saccules.
64 o detected in the gastrointestinal tract, in bronchioles, and in aortic and lung endothelial cells.
65 astin, increased muscularization of terminal bronchioles, and inflammation and edema.
66 responses to bradykinin (BK) in isolated rat bronchioles, and inhibitors of RhoGEFs (Y16) and Rho-kin
67 neutrophils were observed in the alveoli and bronchioles, and lymphocytes were observed in the septa,
68 ell infiltrates in the lungs around bronchi, bronchioles, and pulmonary arteries and veins; lung remo
69 s type II cells, Clara cells in the terminal bronchioles, and putative bronchoalveolar stem cells as
70  changes observed in DKO lung blood vessels, bronchioles, and saccules.
71 s made it possible to show that the terminal bronchioles are narrowed and destroyed before the onset
72 at the smallest conducting airways, terminal bronchioles, are the early site of tissue destruction in
73 lized in epithelial cells of the alveoli and bronchioles, as well as in adjoining capillary endotheli
74 s cells are detected in clumps in the distal bronchioles at the time when cell proliferation is maxim
75                                              Bronchioles became smaller in their cross-sectional area
76  rings, neuroepithelial bodies, and terminal bronchioles/bronchoalveolar duct junctions.
77 ng of epithelial cell differentiation in the bronchioles, causing squamous and goblet cell metaplasia
78          Here we show that human respiratory bronchioles contain a unique secretory cell population t
79 une cell localizations, suggesting asthmatic bronchioles contain cellular niches which perpetuate T2-
80 bronchioles, and 33% and 21% of transitional bronchioles contained mucus plugs, with a high coefficie
81 ed to approximate the structure of the human bronchiole, containing airway, vascular, and extracellul
82                                              Bronchiole count and small airway stereology metrics wer
83 ]) was enriched in the biological process of bronchiole development and smooth muscle proliferation a
84 une cell distributions surrounding asthmatic bronchioles differed from controls but did not correlate
85       Furthermore, ABX mice exhibited severe bronchiole epithelial degeneration and increased host mo
86 f airway epithelial cells that led to severe bronchiole epithelial degeneration, despite control of v
87                                    Asthmatic bronchioles exhibit a T2-driven proximalization associat
88           Test the hypothesis that asthmatic bronchioles exhibit disturbances in epithelial biology t
89  a microscale organotypic model of the human bronchiole for studying pulmonary infection.
90 aser capture microdissection (LCM) of distal bronchioles in a murine asbestos inhalation model, we sh
91 nd Main Results: Compared with the number of bronchioles in control subjects (mean = 11.2/cm(3); SD =
92            The single-cell atlas of terminal bronchioles in COPD demonstrated M1-like macrophages and
93  structures with concurrent loss of terminal bronchioles in regions of minimal fibrosis.
94 molecular mechanisms that govern respiratory bronchioles in the human lung remain uncharacterized.
95 through calcineurin within club cells of the bronchioles, inciting inflammation.
96  Large airway diseases that commonly involve bronchioles include bronchiectasis, asthma, and chronic
97 ine-positive proliferating cells in the same bronchiole indicates that EGFR is up-regulated within th
98 atous tissue destruction, number of terminal bronchioles, infiltrating inflammatory cells, and host g
99 e lungs as well as greater thickening of the bronchiole linings, increased numbers of eosinophils and
100 lular matrix alterations underlying terminal bronchiole loss in COPD.
101 ked cellular infiltration around vessels and bronchiole of lung by day 15, followed by epithelial hyp
102 s) was significantly greater in the terminal bronchioles of CYP2A13/2F1-humanized mice than in Cyp2ab
103  The coincident localization within terminal bronchioles of EGFR, EGF, and TGF-alpha to groups of squ
104 liated cells did not occur in the peripheral bronchioles of either Stat3(Delta/Delta) or Gp130(Delta/
105 f neutrophils into the pulmonary bronchi and bronchioles of lungs infected with P. haemolytica, three
106 ytokine levels, and mucus production in lung bronchioles of mice, whereas increasing local and system
107 pes and structures that resemble the bronchi/bronchioles of the developing human airway surrounded by
108 ber and cross-sectional area of the terminal bronchioles or in alveolar dimensions (mean linear inter
109  samples (in epithelium of small bronchi and bronchioles or lymphoid aggregates).
110 y airway tree: upper airways, small airways (bronchioles), or the most distal alveoli.
111 tal asthma, and 67% extended over 80% of the bronchiole pathlength.
112                                     Terminal bronchiole pathology was associated with the upregulatio
113                                           In bronchioles, PD-L1 levels were strongly directly correla
114 ers of transitional bronchioles and terminal bronchioles per milliliter of lung were significantly lo
115  airways, including preterminal and terminal bronchioles (pre-TBs/TBs), underlie progressive airflow
116 and Main Results: The lumen area of terminal bronchioles progressively narrows with COPD severity as
117 piratory airways or terminal and respiratory bronchioles (RA/TRBs) that accumulate in persons with lu
118 11.2/cm(3); SD = 6.2), there was significant bronchiole reduction in subjects with IPF (42% loss; mea
119 ll atlas, and genes associated with terminal bronchiole reduction using stereology, micro-computed to
120 chanisms contributing to renewal of terminal bronchioles remain poorly defined.
121 specific epithelial differentiation in these bronchioles, represents the cellular manifestation and l
122                 This indicates heterogeneous bronchiole sampling due to the harvesting location in th
123 e around small arteries (SMart) and terminal bronchioles (SMtb).
124 llations, but this is disrupted in mice with bronchiole-specific ablation of Bmal1, leading to enhanc
125  obstructions and numbers up to the terminal bronchioles (TBs) in smokers with limited emphysema and
126 nchioalveolar stem cells (BASCs) in terminal bronchioles (TBs).
127 the inflammatory response of the organotypic bronchiole to infection.
128 ways, including the terminal and respiratory bronchioles (TRBs), which are implicated in respiratory
129 i tumor formation, while conversely promotes bronchiole tumor formation in mice.
130       Absence of mucus deposition inside the bronchiole wall and low collagen around the lung bronchi
131 s, and B cells) are associated with terminal bronchiole wall remodeling.
132 of the transitional bronchioles and terminal bronchioles was also lower in pre-COPD and all COPD grou
133 -CT showed that the total number of terminal bronchioles was decreased (2.9/ml [2.6-4.4] vs. 5.3/ml [
134 he cross-sectional area of the open terminal bronchioles was reduced (0.093 mm(2) [0.084-0.123] vs. 0
135 r duct bifurcations and in adjacent terminal bronchioles was significantly reduced in the 129 strain
136 matogonias; (iv) The epithelium of the fetal bronchioles was very faint for CR1 and strongly positive
137 mplement direct infection of the organotypic bronchiole, we present a clickable extension that facili
138 nuclear cell infiltration around vessels and bronchioles were observed only in mice receiving allogen
139            More than 30% of both bronchi and bronchioles were obstructed by cast formation after smok
140 irway regions (mouth, trachea, bronchus, and bronchiole) were similar.
141 m of the nasal cavity, trachea, bronchi, and bronchioles with accompanying inflammation.
142 cellular deposition of these crystals in the bronchioles with associated destruction of airway epithe
143 llular infiltrates (median number of LVs per bronchiole: with infiltrates, 5.00 (BOS), 9.00 (RAS), 4.

 
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