ライフサイエンスコーパス: fibrotic lesion

1 tic lesions, without anchoring to a specific fibrotic lesion.

2 for PGE2 deficiency in the evolution of the fibrotic lesion.

3 advanced disease, there is less Slit2 in the fibrotic lesions.

4 mine reduced matrix expression and mitigated fibrotic lesions.

5 of the cellular origin of the characteristic fibrotic lesions.

6 molecules into fibrils, a main component of fibrotic lesions.

7 gical by activating apoptosis selectively in fibrotic lesions.

8 f epithelial hyperplasia in association with fibrotic lesions.

9 se have pronounced lumican expression in the fibrotic lesions.

10 -alpha actin and are associated with various fibrotic lesions.

11 there are high levels of CTGF expression in fibrotic lesions.

12 ize of the fibroblast population in existing fibrotic lesions.

13 e fibroblast population size within existing fibrotic lesions.

14 the time period necessary for development of fibrotic lesions.

15 Growing evidence suggests that in fibrotic lesions, a subset of blood monocytes enters the

16 nary epithelial cells at sites of developing fibrotic lesions after 14 and 30 days of inhalation.

17 n a mouse genetic model dramatically reduces fibrotic lesions after obstructive injury, underscoring

18 o prevents this regeneration, leading to pre-fibrotic lesions and deficient oxygen exchange.

19 heterogeneity of cell types proliferating in fibrotic lesions and exclude pericytes and two epithelia

20 Rapamycin also exacerbated cystic and fibrotic lesions and impaired kidney function in these m

21 s of isoniazid in individuals with pulmonary fibrotic lesions and LTBI (n = 27830) found a reduction

22 However, fibrotic lesions and lymphocytic infiltration were obser

23 mice developed periductular onion-skin type fibrotic lesions and pronounced ductular reaction starti

24 first time sustained Egr-1 up-regulation in fibrotic lesions and suggests that Egr-1 has a role in t

25 hrombin are upregulated in wound healing and fibrotic lesions, and inhibition of these proteases atte

26 GF gene therapy markedly ameliorated hepatic fibrotic lesions, as demonstrated by reduced alpha-smoot

27 thway in the development of inflammation and fibrotic lesions associated with BOOP and ARDS.

28 ced BOOP, but still develop inflammation and fibrotic lesions associated with reovirus 1/L-induced AR

29 l, do not develop pulmonary inflammation and fibrotic lesions associated with reovirus 1/L-induced BO

30 lent deposition of interstitial collagen and fibrotic lesions at days 7 and 14 after administration.

31 ytes have been implicated as contributors to fibrotic lesions because of the transdifferentiation pot

32 he fibroconnective tissues of these advanced fibrotic lesions consistently revealed dense staining fo

33 Myc, and that lung fibroblasts isolated from fibrotic lesions constitutively express growth-promoting

34 f connective tissue growth factor present in fibrotic lesions contributes to the phenotype of sclerod

35 -fmk, inhibited apoptosis, inflammation, and fibrotic lesion development in reovirus 1/L-induced BOOP

36 especially IFN-gamma, may play a key role in fibrotic lesion development.

37 before reovirus 1/L infection also inhibited fibrotic lesion development.

38 BAL fluid, and myofibroblasts present in the fibrotic lesions expressed FOXF1 by in situ hybridizatio

39 In healing wounds and fibrotic lesions, fibroblasts and monocyte-derived fibro

40 this process with regard to wound repair and fibrotic lesion formation that is likely applicable to o

41 y events during both normal wound repair and fibrotic lesion formation.

42 In particular, stiffened matrix in fibrotic lesions has been shown to promote pathogenic my

43 at PPAR-gamma agonists also ameliorate renal fibrotic lesions in both diabetic nephropathy and nondia

44 the development of reovirus 1/L-induced BOOP fibrotic lesions in CBA/J mice and suggests that T(H)1-d

45 In fibrotic lesions in human and mouse lungs, we found exte

46 h type 2 cytokines (IL-4 and IL-13), whereas fibrotic lesions in IL-5(-/-) animals were accompanied b

47 llin was prominently expressed in subretinal fibrotic lesions in mice.

48 gene expression profile, and ability to form fibrotic lesions in model organisms.

49 Fibrotic lesions in models were represented with combina

50 ation of ICG-001 also effectively attenuated fibrotic lesions in obstructive nephropathy.

51 blation of tPA attenuated renal interstitial fibrotic lesions in obstructive nephropathy.

52 le role for CTGF in promoting development of fibrotic lesions in phenytoin-induced gingival overgrowt

53 Histopathological examination revealed fibrotic lesions in the hearts of the older D166V mice.

54 AFSC were observed to localize within fibrotic lesions in the lung, showing preferential targe

55 mitochondrial defects, reduced occurrence of fibrotic lesions in the myocardium, prevention of cardia

56 IPF hallmarks, including the ability to form fibrotic lesions in zebrafish embryos and mouse lungs, a

57 overexpressed by fibroblasts present in skin fibrotic lesions, including scleroderma.

58 elimination of fibroblasts actively forming fibrotic lesions is an effective therapeutic strategy fo

59 tabolism of collagen, the major component of fibrotic lesions, is, in part, regulated by integrins.

60 In wounds and fibrotic lesions, mast cells degranulate to release tryp

61 ontribute to the progression of inflammatory-fibrotic lesions of atherosclerosis.

62 ronchitis, to subepithelial and intraluminal fibrotic lesions of bronchiolitis obliterans by day 28.

63 Advanced fibrotic lesions of eosinophilic granuloma, containing m

64 non-invasive imaging of active cathepsins in fibrotic lesions of patients with IPF.

65 Parenchymal and bronchial inflammatory and fibrotic lesions other than acute cellular rejection (AC

66 TGF)-beta1 in the tumor microenvironment and fibrotic lesions plays a critical role in tumor progress

67 Prematurely dying animals had focal fibrotic lesions predominantly present in the left ventr

68 velopment of epithelial cell hyperplasia and fibrotic lesions, respectively.

69 In healing wounds and fibrotic lesions, some of the monocytes differentiate in

70 Hyperplastic, fibrotic lesions subsequently developed in the same regi

71 fic features of the myofibroblast in diverse fibrotic lesions, such as systemic sclerosis; kidney, li

72 cytokine pathway, exhibited more pronounced fibrotic lesions than did wild-type animals.

73 and the subsequent conduction slowing in the fibrotic lesions was a necessary but not sufficient cond

74 Importantly, the number of WT1(+) cells in fibrotic lesions was correlated with severity of lung di

75 al effect on neighboring myocytes within the fibrotic lesions was the sufficient condition necessary

76 ed throughout the lung, but inflammation and fibrotic lesions were usually confined to focal areas.

77 ected mice both inhibited the development of fibrotic lesions when administered early in the time-cou

78 e time-course and promoted the resolution of fibrotic lesions when corticosteroid administration was

79 numbers of GFP(+) cells to appear in active fibrotic lesions, while only a few GFP(+) cells could be

80 nti-TGF-beta Ab selectively inhibits chronic fibrotic lesions without affecting autoantibody producti

81 circuits formed throughout the noncontiguous fibrotic lesions, without anchoring to a specific fibrot

82 ssue growth factor by fibroblasts present in fibrotic lesions would be expected to contribute directl