ライフサイエンスコーパス: bronchial biopsy

1 T helper (TH )17 chemokine overexpression in bronchial biopsies.

2 thickness, and epithelial detachment (ED) in bronchial biopsies.

3 ergy skin prick tests, and bronchoscopy with bronchial biopsies.

4 esses and biomarkers using induced sputum or bronchial biopsies.

5 sm was detected in bronchoalveolar lavage or bronchial biopsies.

6 Bronchial biopsies also were examined for intracellular

7 t variation analysis signatures expressed in bronchial biopsies and airway epithelial brushings disti

8 Bronchial biopsies and bronchoalveolar lavage provide va

9 ADAM33 mRNA splice variants were detected in bronchial biopsies and embryonic lung; however, the beta

10 The transcriptome derived from bronchial biopsies and epithelial brushings of 107 subje

11 edict the subtypes of gene expression within bronchial biopsies and epithelial cells with good sensit

12 ntially by asthmatic airway smooth muscle in bronchial biopsies and ex vivo cells compared with those

13 IL-17A(+), IL-17F(+), and IL-21(+) cells in bronchial biopsies and higher numbers (P < .01) of IL-17

14 Bronchial biopsies and induced sputum were taken from 14

15 ive stress burden of airway smooth muscle in bronchial biopsies and primary cells from subjects with

16 ile in asthma and control subjects utilizing bronchial biopsies and serum, and to relate uPAR express

17 ded inflammatory cells in induced sputum and bronchial biopsies, and methacholine responsiveness.

18 Western blotting of bronchial biopsies confirmed the presence of multiple is

19 sputum total leukocyte values (P = .06), and bronchial biopsy eosinophil values (per square millimete

20 ampling, we analyzed epithelial integrity in bronchial biopsies from 14 subjects with mild and modera

21 Using bronchial biopsies from 14 subjects with mild to moderat

22 Bronchial biopsies from 15 AA patients and four controls

23 of their receptors CCR4, CCR8, and CXCR3 in bronchial biopsies from 20 asthmatics and 15 normal cont

24 Immunohistochemical analysis of bronchial biopsies from asthmatic patients demonstrated

25 RELM-beta expression was investigated in bronchial biopsies from asthmatic patients.

26 d, we measured the expression of 75 genes in bronchial biopsies from asthmatic versus healthy subject

27 d CD31(+) (endothelial) cells in sections of bronchial biopsies from asthmatics and controls were det

28 Of 372 bronchial biopsies from chronic smokers, 86 biopsies (23

29 To study IL-17-related cytokines in nasal/bronchial biopsies from controls and mild asthmatics (MA

30 Although studies of bronchial biopsies from human asthmatics also demonstrat

31 expression and activity of HATs and HDACs in bronchial biopsies from normal subjects and subjects wit

32 und in the bronchoalveolar lavage fluids and bronchial biopsies from patients with allergic asthma af

33 Bronchial biopsies from patients with mild asthma displa

34 ution of E-cadherin and p120 was observed in bronchial biopsies from severe asthmatic airways.

35 Bronchial biopsies from subjects (n = 20 in each group)

36 cells in the airway smooth muscle bundle in bronchial biopsies from subjects with asthma using immun

37 MAIT cells were reduced in bronchial biopsies from subjects with COPD treated with

38 Bronchial biopsy immunofluorescence studies showed that

39 Studies on cilomilast in COPD based on bronchial biopsy material have shown a broad range of an

40 In asthmatic bronchial biopsies, mCD48 was expressed predominantly by

41 The bronchial biopsies obtained 6 h after DE exposure showed

42 hromatic staining cells, and neutrophils) in bronchial biopsies obtained after challenge when compare

43 Cryostat sections of nasal/bronchial biopsies obtained from 14 SA and 14 mild asthm

44 is, we determined the expression of Ets-1 in bronchial biopsies obtained from asthmatic subjects and

45 els of IL-17 are found in induced sputum and bronchial biopsies obtained from patients with severe as

46 Bronchial biopsies of asthmatic patients show a negative

47 lial immunostaining for CCR3 was stronger in bronchial biopsies of asthmatics displaying marked infla

48 Airway smooth muscle cells grown from bronchial biopsies of healthy and asthmatic individuals

49 lls (BEC) were isolated by bronchoscopy from bronchial biopsies of healthy donors and patients with m

50 e expression and functional role of IL-33 in bronchial biopsies of patients with and without asthma,

51 Higher MAGI2 expression in bronchial biopsies of patients with chronic obstructive

52 tory and structural pathological features in bronchial biopsies of severe asthmatics that could be re

53 bserved with immunohistochemical analysis of bronchial biopsies of smokers compared with nonsmokers.

54 Using microarray analysis of bronchial biopsy samples from patients with COPD and con

55 Analysis of bronchial biopsy samples showed a very strong correlatio

56 Bronchial biopsy sections from control subjects, patient

57 istry and laser confocal microscopy of adult bronchial biopsies showed that alpha-smooth muscle actin

58 Bronchial biopsy specimens (n = 300) were collected from

59 Bronchial biopsy specimens and bronchial brushings were

60 Bronchial biopsy specimens and epithelial cells were obt

61 ultured cells by using flow cytometry and in bronchial biopsy specimens by using immunohistochemistry

62 Immunohistochemistry analyses of bronchial biopsy specimens confirmed increased levels of

63 with mild-to-severe asthma, we immunostained bronchial biopsy specimens for TSLP, OX40, OX40L, T(H)2

64 Bronchial biopsy specimens from 12 control subjects, 24

65 om 87 patients with stage I NSCLC and in 372 bronchial biopsy specimens from 86 chronic smokers witho

66 DP2 protein expression was assessed in bronchial biopsy specimens from asthmatic patients (n =

67 Human ASM cells were isolated from bronchial biopsy specimens from healthy subjects, smoker

68 ceptors E-prostanoid 1 to 4 (EP(1)-EP(4)) in bronchial biopsy specimens from patients with ASA, patie

69 genesis of asthma, but its expression within bronchial biopsy specimens is unknown.

70 Bronchial biopsy specimens obtained from healthy volunte

71 ASMCs cultured from bronchial biopsy specimens of nonasthmatic control subje

72 oalveolar lavage cell samples and in 5 of 18 bronchial biopsy specimens taken 4 days after virus inoc

73 RNA of laser-dissected ASM from 96 bronchial biopsy specimens was sequenced with Roche GS F

74 Bronchial biopsy specimens were processed for immunohist

75 ssed SOCS1 mRNA and protein levels in vitro, bronchial biopsy specimens, and mice.

76 f CCL26 and major basic protein were done on bronchial biopsy specimens.

77 valuated by means of immunohistochemistry in bronchial biopsy specimens.

78 signature, and eosinophilic inflammation in bronchial biopsy specimens.

79 hoalveolar-lavage fluid, induced sputum, and bronchial-biopsy specimens obtained from subjects with m

80 A nuclear role of SOCS1 was shown by using bronchial biopsy staining, overexpression of mutant SOCS

81 ion of CEACAM6 using immunohistochemistry on bronchial biopsy tissue obtained from patients with mild

82 ed in control (n = 9) and asthmatic (n = 27) bronchial biopsies using immunohistochemistry, with a se

83 l cell lung carcinoma (NSCLC) cell lines and bronchial biopsies using the reverse transcription-polym

84 The number of eosinophils in bronchial biopsies was increased by glucocorticoid withd

85 CEACAM6 protein expression in bronchial biopsies was increased in airway epithelial ce

86 Bronchial biopsies were collected from 7 subjects with C

87 Nasal and bronchial brushings and bronchial biopsies were evaluated from patients with cys

88 Asthmatic bronchial biopsies were immunostained for CD48.

89 Bronchial biopsies were obtained from 49 asbestos worker

90 and EG2(+)) on immunohistochemical stains of bronchial biopsies were quantified by computerized image

91 Bronchial biopsies were taken before and after 8 wk trea

92 In each subject, 4 to 8 bronchial biopsies were taken from large airways during