ライフサイエンスコーパス: type II pneumocyte

1 IH292 lung cells, middle ear cells, and A549 type II pneumocytes.

2 ecipients, and accounted for 0% to 0.553% of type II pneumocytes.

3 tion to evaluate for Y-chromosome-containing type II pneumocytes.

4 re undifferentiated, with some maturation of type II pneumocytes.

5 vasculature, bronchial epithelial cells, and type II pneumocytes.

6 EBPalpha is expressed in bronchial cells and type II pneumocytes.

7 injection, did we detect any engraftment as type II pneumocytes.

8 4b(G12D) under the control of doxycycline in type II pneumocytes.

9 ng between conidia and A549 cells, a line of type II pneumocytes.

10 A damage and is associated with apoptosis of type II pneumocytes.

11 e growth factor (KGF) is a growth factor for type II pneumocytes.

12 10% of cells) and predominantly localized in type II pneumocytes.

13 s in SCLC lines, as compared to normal human type-II pneumocytes.

14 Marked apoptosis of CD68-negative type II pneumocytes (30 to 80%) was detected in four of

15 his model incorporates human lung epithelial type II pneumocyte (A549) (upper chamber) and endothelia

16 he early growth mechanics of fetal lungs and type II pneumocytes after tracheal ligation (TL).

17 erentially active in cell lines derived from type II pneumocytes and Clara cells (MLE-15 and mtCC1-2

18 agious lung cancer of sheep that arises from type II pneumocytes and Clara cells of the lung epitheli

19 gious lung cancer of sheep, originating from type II pneumocytes and Clara cells.

20 CXCR3 was expressed by type II pneumocytes and fibroblasts in fibrotic areas in

21 portant in determining the susceptibility of type II pneumocytes and interstitial cells to apoptosis.

22 ion of ENA-78 demonstrated that hyperplastic Type II pneumocytes and macrophages were the predominant

23 n more-efficient infection of human alveolar type II pneumocytes and thus more-severe lung damage.

24 ecific capacity to productively replicate in type II pneumocytes and to cope with the induced cytokin

25 ession of CYP1A1 in airway epithelial cells, type II pneumocytes, and endothelial cells.

26 Type II pneumocyte apoptosis was confirmed by electron m

27 erived pedigrees differentiate to type I and type II pneumocytes as well as bronchiolar secretory cel

28 MUC1 immunoreactivity was present in normal type II pneumocytes as well as in a range of atypical le

29 otein (mean 0.95+/-1.18 Sp-C+ cells per 1000 type II pneumocytes by confocal microscopy).

30 e that MUC1 is a powerful new marker for the type II pneumocyte cell lineage that allows us to follow

31 tly endocytosed and degraded by cultured pre-type II pneumocyte cells, and both processes could be bl

32 d SFTPC), which are expressed exclusively in type II pneumocytes, cells that proliferate in ventilato

33 CXCL12 was expressed in type II pneumocytes covering LAM nodules and caused AML

34 n maintaining differentiation of human fetal type II pneumocyte culture.

35 ular endothelial cells, and primary alveolar type II pneumocytes, demonstrating a much broader tissue

36 igation-mediated PCR was performed in murine type II pneumocyte-derived MLE-15 cells infected with a

37 miRNAs in mid-gestation HFL explants during type II pneumocyte differentiation in culture, we perfor

38 ve expression of neuroendocrine genes and of type II pneumocyte genes, respectively.

39 Apoptosis of type II pneumocytes has been identified in diffuse alveo

40 Proliferation of type II pneumocytes has been linked to a repair process

41 Histopathology showed abundant type II pneumocyte hyperplasia in the lungs of animals p

42 Type II pneumocyte hyperplasia, a common reaction to lun

43 sms of this protection are likely related to type II pneumocyte hyperplasia, but remain to be specifi

44 ly associated with death on a ventilator and type II pneumocyte hyperplasia.

45 n-binding growth factor that causes alveolar type II pneumocyte hyperplasia.

46 alveolar septal thickening and intermittent type II pneumocyte hyperplasia.

47 e EGF-receptor inactivation also resulted in type II pneumocyte immaturity, which was apparent from t

48 istochemistry studies localized MMP-1 to the Type II pneumocyte in patients with emphysema and not no

49 esized that up-regulation of p53 and WAF1 in type II pneumocytes in DAD is associated with underlying

50 uenza viruses preferentially infect alveolar type II pneumocytes in human lung.

51 lial cell types, including distal type I and type II pneumocytes in the late term.

52 The authors investigated whether type II pneumocytes in the lungs of cross-gender lung tr

53 accumulation of lipid-laden macrophages and type II pneumocytes in the lungs.

54 ained evidence suggesting the involvement of type II pneumocytes in the replication of PRRSV.

55 ritical role of the epithelium, particularly type II pneumocytes, in the initiation and perpetuation

56 of acute lung injury, extensive apoptosis of type II pneumocytes is largely responsible for the disap

57 te cell lineage that allows us to follow the type II pneumocyte lineage during the process of lung ca

58 lineages for the peripheral lung, i.e., the type II pneumocyte lineage markers MUC1 and surfactant p

59 In chronic interstitial pneumonia, only rare type II pneumocytes (< 5%) exhibited apoptosis, and they

60 enitor epithelial cells expressed type I and type II pneumocyte markers.

61 the expression of these marker genes during type II pneumocyte maturation.

62 gnate ligand have long been known to promote type II pneumocyte maturation; prenatal administration o

63 We conclude that proliferation of type II pneumocytes occurs during the early phase of acu

64 The number of type II pneumocytes of male karyotype showed a statistic

65 SPARKY exhibited a Type II pneumocyte phenotype characterized by surfactant

66 In chronic interstitial pneumonia, type II pneumocytes proliferate continuously, although t

67 suggesting a protective role for KGF-induced type II pneumocyte proliferation in lung injury.

68 These cells contribute minimally to the type II pneumocyte proliferation that is often present i

69 xhibited enhanced bronchiolar epithelial and type II pneumocyte proliferation.

70 Type II pneumocytes respond to influenza A infection by

71 e lung is altered in emphysema such that the Type II pneumocyte secretes MMP-1 and suggests that MMP-

72 induction of a proteolytic enzyme within the Type II pneumocyte suggests that the cells within the lu

73 Gene expression analysis of isolated type II pneumocytes suggests potential explanations for

74 olar lung carcinoma (BAC), a neoplasm of the Type II pneumocyte that affects humans, sheep, and small

75 and a similar reduction in DNMT activity in type II pneumocytes that give rise to the tumors.

76 Notably, the H5N1 virus targeted type II pneumocytes throughout the 7-day infection, and

77 -S752)) or the L858R mutant (EGFR(L858R)) in type II pneumocytes under the control of doxycycline.

78 Y-chromosome-containing type II pneumocytes were found in 9 of 25 biopsy specime

79 Rat type II pneumocytes were incubated with [3H]choline, pur

80 Alveolar epithelial type II pneumocytes were isolated and purified from adul

81 Focal proliferative lesions of alveolar type II pneumocytes were observed as early as seven days

82 in the acute/proliferative phase, apoptotic type II pneumocytes were rare whereas PCNA expression wa

83 Alveolar lining cells, including type I and type II pneumocytes, were the primary infected cells.

84 nd specific proteins synthesized in alveolar type II pneumocytes, where it is assembled and stored in

85 2D, in human lung tissue, including alveolar type II pneumocytes, which express avian-type receptors.

86 rates localization of LCAD to human alveolar type II pneumocytes, which synthesize and secrete pulmon

87 examined were detected almost exclusively in type II pneumocytes, with a minor involvement of alveola