ライフサイエンスコーパス: bronchiole

1 ble to airway obstruction (nose < bronchi << bronchioles).

2 d primary human cultures from trachea versus bronchioles.

3 dysplastic and sloughed cells in respiratory bronchioles.

4 o widespread papillary adenocarcinoma in the bronchioles.

5 10+ papillary adenocarcinomas throughout the bronchioles.

6 ited transgene expression to the respiratory bronchioles.

7 n as stem/progenitor cells for repair in the bronchioles.

8 carcinomas restricted to proximal and distal bronchioles.

9 and likely interacts with the Clara cells of bronchioles.

10 .4 +/- 1.6% of the epithelial cells in large bronchioles.

11 hils into the walls and lumen of bronchi and bronchioles.

12 sive extracellular matrix of the bronchi and bronchioles.

13 endocrine cells involving distal bronchi and bronchioles.

14 lial cells of the injury target zone, distal bronchioles.

15 pithelial cells of the trachea, bronchi, and bronchioles.

16 nodules with adjoining thickened and dilated bronchioles.

17 n control subjects (median number of LVs per bronchiole: 4.75 (BOS), 6.47 (RAS), 4.25 (control), P =

18 centrilobular region, and small bronchi and bronchioles), abnormal findings (reticulation, tiny nodu

19 enlargement of airspaces distal to terminal bronchioles accompanied by destruction of alveolar walls

20 s distinct from those of peripheral airways (bronchioles, acini, and alveoli), were established well

21 of cells contributing to renewal of terminal bronchioles after Clara cell depletion.

22 chiole wall and low collagen around the lung bronchioles after Ova-allergen challenge further confirm

23 y response that promotes airway fibrosis via bronchiole airway epithelial damage and obliteration.

24 f the alpha(4)beta(1) ligand, VCAM-1, on the bronchioles, allowing direct access of the leukocytes to

25 docrine cells, make up the epithelium of the bronchioles along the conducting airways.

26 However, no tumors develop in the bronchioles, although recombination occurs throughout th

27 ng in vivo, human lung stem cells form human bronchioles, alveoli, and pulmonary vessels integrated s

28 diated communication between the organotypic bronchiole and cultures of Aspergillus fumigatus and Pse

29 P)-2 in epithelial cells lining the terminal bronchioles and alveolar ducts as well as macrophages an

30 reactivity in epithelial cells lining distal bronchioles and alveolar ducts, sites of initial lung de

31 infection, P. aeruginosa enters the terminal bronchioles and alveoli and comes into contact with alve

32 t lungs resulted in the expression of GFP in bronchioles and alveoli within 5 days.

33 losis is initially deposited in the terminal bronchioles and alveoli, as well as following release fr

34 ted the lumen, epithelium, and adventitia of bronchioles and bronchi in lungs of calves with BLAD com

35 enchymal cells and acinar buds and decreased bronchioles and dilated airspaces in SPC-PDGFA transgeni

36 DNA synthesis in the epithelium of terminal bronchioles and more proximal airways.

37 by contraction of the smooth muscle walls in bronchioles and pulmonary arteries and aggregation of pl

38 s to humans, with well developed respiratory bronchioles and submucosal glands.

39 -expressing stem cell population in terminal bronchioles and support the notion that regiospecific st

40 e sparing larger airways as well as terminal bronchioles and the alveolar surface.

41 olution from immune cell infiltration of the bronchioles and vessels at day 14, consistent with acute

42 a cells of wild-type and COX-1(-/-) terminal bronchioles and was strongly induced 24 hours after V(2)

43 The conducting airways (bronchi and bronchioles) and peripheral gas exchange (alveolar) regi

44 mmunostaining, in the epithelium of bronchi, bronchioles, and alveolar walls.

45 ted in the epithelial cells of nasal mucosa, bronchioles, and alveoli for up to 4 days postinfection.

46 ells were present in the conducting airways, bronchioles, and alveoli.

47 o detected in the gastrointestinal tract, in bronchioles, and in aortic and lung endothelial cells.

48 astin, increased muscularization of terminal bronchioles, and inflammation and edema.

49 responses to bradykinin (BK) in isolated rat bronchioles, and inhibitors of RhoGEFs (Y16) and Rho-kin

50 neutrophils were observed in the alveoli and bronchioles, and lymphocytes were observed in the septa,

51 ell infiltrates in the lungs around bronchi, bronchioles, and pulmonary arteries and veins; lung remo

52 s type II cells, Clara cells in the terminal bronchioles, and putative bronchoalveolar stem cells as

53 s made it possible to show that the terminal bronchioles are narrowed and destroyed before the onset

54 lized in epithelial cells of the alveoli and bronchioles, as well as in adjoining capillary endotheli

55 s cells are detected in clumps in the distal bronchioles at the time when cell proliferation is maxim

56 rings, neuroepithelial bodies, and terminal bronchioles/bronchoalveolar duct junctions.

57 ng of epithelial cell differentiation in the bronchioles, causing squamous and goblet cell metaplasia

58 ed to approximate the structure of the human bronchiole, containing airway, vascular, and extracellul

59 Furthermore, ABX mice exhibited severe bronchiole epithelial degeneration and increased host mo

60 f airway epithelial cells that led to severe bronchiole epithelial degeneration, despite control of v

61 a microscale organotypic model of the human bronchiole for studying pulmonary infection.

62 aser capture microdissection (LCM) of distal bronchioles in a murine asbestos inhalation model, we sh

63 Large airway diseases that commonly involve bronchioles include bronchiectasis, asthma, and chronic

64 ine-positive proliferating cells in the same bronchiole indicates that EGFR is up-regulated within th

65 atous tissue destruction, number of terminal bronchioles, infiltrating inflammatory cells, and host g

66 e lungs as well as greater thickening of the bronchiole linings, increased numbers of eosinophils and

67 ked cellular infiltration around vessels and bronchiole of lung by day 15, followed by epithelial hyp

68 s) was significantly greater in the terminal bronchioles of CYP2A13/2F1-humanized mice than in Cyp2ab

69 The coincident localization within terminal bronchioles of EGFR, EGF, and TGF-alpha to groups of squ

70 liated cells did not occur in the peripheral bronchioles of either Stat3(Delta/Delta) or Gp130(Delta/

71 f neutrophils into the pulmonary bronchi and bronchioles of lungs infected with P. haemolytica, three

72 ytokine levels, and mucus production in lung bronchioles of mice, whereas increasing local and system

73 ber and cross-sectional area of the terminal bronchioles or in alveolar dimensions (mean linear inter

74 samples (in epithelium of small bronchi and bronchioles or lymphoid aggregates).

75 y airway tree: upper airways, small airways (bronchioles), or the most distal alveoli.

76 chanisms contributing to renewal of terminal bronchioles remain poorly defined.

77 This indicates heterogeneous bronchiole sampling due to the harvesting location in th

78 e around small arteries (SMart) and terminal bronchioles (SMtb).

79 llations, but this is disrupted in mice with bronchiole-specific ablation of Bmal1, leading to enhanc

80 nchioalveolar stem cells (BASCs) in terminal bronchioles (TBs).

81 the inflammatory response of the organotypic bronchiole to infection.

82 i tumor formation, while conversely promotes bronchiole tumor formation in mice.

83 Absence of mucus deposition inside the bronchiole wall and low collagen around the lung bronchi

84 -CT showed that the total number of terminal bronchioles was decreased (2.9/ml [2.6-4.4] vs. 5.3/ml [

85 he cross-sectional area of the open terminal bronchioles was reduced (0.093 mm(2) [0.084-0.123] vs. 0

86 r duct bifurcations and in adjacent terminal bronchioles was significantly reduced in the 129 strain

87 mplement direct infection of the organotypic bronchiole, we present a clickable extension that facili

88 nuclear cell infiltration around vessels and bronchioles were observed only in mice receiving allogen

89 More than 30% of both bronchi and bronchioles were obstructed by cast formation after smok

90 irway regions (mouth, trachea, bronchus, and bronchiole) were similar.

91 m of the nasal cavity, trachea, bronchi, and bronchioles with accompanying inflammation.

92 cellular deposition of these crystals in the bronchioles with associated destruction of airway epithe

93 llular infiltrates (median number of LVs per bronchiole: with infiltrates, 5.00 (BOS), 9.00 (RAS), 4.