ライフサイエンスコーパス: balloon-injured

1 ter 1 week of diet, both iliac arteries were balloon injured.

2 ontralateral iliac artery of each rabbit was balloon injured and stented but not transfected.

3 In the surviving animals, balloon-injured and irradiated vessels showed a trend to

4 rats accelerated reendothelialization of the balloon-injured arterial segments (reendothelialized are

5 By contrast, in balloon-injured arteries 6 weeks after injury, regenerat

6 adenovirus-mediated overexpression of p27 in balloon-injured arteries attenuated neointimal lesion fo

7 s been reduced in vivo in nonatherosclerotic balloon-injured arteries by transfer of genes that inhib

8 tein phosphorylation were observed in 1-week balloon-injured arteries compared with uninjured arterie

9 was identified in the proliferating VSMCs of balloon-injured arteries during cell migration from medi

10 Indeed, delivery of Ad-p27-126TS to balloon-injured arteries in rats not only induced faster

11 e data demonstrate that delivery of CMMCs to balloon-injured arteries is associated with accelerated

12 upregulation of tissue factor in the wall of balloon-injured arteries may result in prolonged activat

13 Finally, restoration of miR-145 in balloon-injured arteries via Ad-miR-145 inhibits neointi

14 s that have been implicated in remodeling of balloon-injured arteries, markedly upregulated TnC mRNA.

15 ed inhibition of neointimal proliferation in balloon-injured arteries.

16 livery to attenuate intimal hyperplasia in a balloon-injured artery was determined.

17 In balloon-injured, atherosclerosis-free porcine arteries,

18 rabbits, adenoviral gene transfer of TFPI to balloon-injured atherosclerotic arteries reduced the ext

19 lar proliferation limits the intimal area in balloon-injured atherosclerotic arteries.

20 n situ hybridization of aortic sections from balloon-injured baboons demonstrated increased VEGF expr

21 e cells (SMCs) and reduce neointimal mass in balloon-injured blood vessels.

22 Transplantation of these cells into balloon-injured carotid arteries and into bioprosthetic

23 Local NO-ELIP administration to balloon-injured carotid arteries attenuated the developm

24 s of S6RP, in rat embryonic aortas and adult balloon-injured carotid arteries compared with quiescent

25 ased the abundance of activated NF-kappaB in balloon-injured carotid arteries of diabetic rats.

26 Lesion formation was evaluated in balloon-injured carotid arteries of naive and adenovirus

27 reased SMC growth and intimal hyperplasia in balloon-injured carotid arteries of streptozotocin-treat

28 elial growth factor (VEGF) expression in the balloon-injured carotid artery of female Zucker fatty ra

29 stimulated smooth muscle replication in the balloon-injured carotid artery, intact carotid artery, a

30 ation was inhibited by warfarin treatment in balloon-injured carotids.

31 In balloon-injured coronary arteries, adventitial vasa vaso

32 10 cross-sectional images (40 normal and 32 balloon injured cross-sections) were captured from each

33 Expression of tk in balloon-injured hyperlipidemic rabbit arteries followed

34 ex (A-I[Milano]/PC) on neointimal lesions in balloon-injured iliofemoral arteries of hypercholesterol

35 The right common carotid artery (CCA) was balloon-injured in 21 New Zealand White male rabbits.

36 In balloon-injured nonirradiated vessels, there was complet

37 Furthermore, rET in the contralateral, balloon-injured, nontransfected limb of the VEGF group w

38 benefit was observed for the contralateral, balloon-injured, nontransfected limb.

39 ation did not inhibit neointima formation in balloon-injured normal pig coronary arteries 6 months af

40 The left carotid artery of all animals was balloon-injured on day 4 of the treatment, and all group

41 nsfer of p21 using an adenoviral vector into balloon injured porcine arteries inhibited the developme

42 atial patterns of vasa vasorum in normal and balloon injured porcine coronary arteries.

43 of TFPI gene transfer on thrombus formation, balloon-injured porcine carotid arteries were treated lo

44 micromol/L FPTIII locally for 15 minutes to balloon-injured porcine coronary arteries in vivo preven

45 more relevant model, AV-W9 was delivered to balloon-injured porcine coronary arteries in vivo using

46 In balloon-injured rabbit arteries, cell proliferation (51%

47 orospatial expression of tenascin-C (TnC) in balloon-injured rat and porcine arteries.

48 captopril on PAI-1 expression in control and balloon-injured rat aorta.

49 nal obliteration developed in saline-treated balloon-injured rat aortas (20.3+/-8.0%), and psiepsilon

50 levels and attenuated neointima formation in balloon-injured rat arteries in vivo.

51 ury-inducible TN-C protein expression in the balloon-injured rat artery wall.

52 s NF-kappa B activation during restenosis of balloon-injured rat carotid arteries as well as VSMC pro

53 for neointimal smooth muscle cells (SMCs) in balloon-injured rat carotid arteries between 7 and 30 da

54 We also examine uninjured and balloon-injured rat carotid arteries for CCN5 expression

55 , both in cultured rat VSMCs in vitro and in balloon-injured rat carotid arteries in vivo, we demonst

56 livery of Id3a inhibited lesion formation in balloon-injured rat carotid arteries in vivo.

57 CNSN SMCs seeded onto the luminal surface of balloon-injured rat carotid arteries inhibited neointima

58 characterized in vitro and then seeded into balloon-injured rat carotid arteries to determine the ef

59 Moreover, a PCL sheath deployed around balloon-injured rat carotid arteries was associated with

60 e first time that neointimal formation using balloon-injured rat carotid arteries was associated with

61 When introduced locally to balloon-injured rat carotid arteries, a well characteriz

62 administration of AdSM22-lacZ to control and balloon-injured rat carotid arteries, beta-galactosidase

63 riggers apoptosis of VSMCs in culture and in balloon-injured rat carotid arteries, thus contributing

64 ar effects were further confirmed in vivo in balloon-injured rat carotid arteries.

65 A and protein expression in the neointima of balloon-injured rat carotid arteries.

66 ease in PGC-1beta expression was observed in balloon-injured rat carotid arteries.

67 e and in VSMCs of the media and neointima of balloon-injured rat carotid arteries.

68 a steady rate to the adventitial surface of balloon-injured rat carotid arteries.

69 sing inflammation and neointima formation in balloon-injured rat carotid arteries.

70 protein of rno-miR-31 is verified in vivo in balloon-injured rat carotid arteries.

71 trogen restores endothelial cell function in balloon-injured rat carotid arteries.

72 xperimentally induced neointima formation in balloon-injured rat carotid arteries.

73 ntisense cyclin G1 vector supernatant to the balloon-injured rat carotid artery in vivo resulted in a

74 on of TIMP-1 using LTSN cells implanted onto balloon-injured rat carotid artery inhibited intimal hyp

75 that the vasoprotective effect of E2 in the balloon-injured rat carotid artery model is mediated by

76 Immunohistochemical and Western analyses of balloon-injured rat carotid artery tissues showed a tran

77 the VEGFR2-positive regenerating EC layer in balloon-injured rat carotid artery.

78 ization and inhibit neointimal thickening in balloon-injured rat carotid artery.

79 ession would parallel neointima formation in balloon-injured rat carotid, and that Axl expression wou

80 Axl expression increases in the neointima of balloon-injured rat carotids.

81 Two weeks after perivascular application to balloon-injured rat common carotid arteries, halofuginon

82 en protects against neointimal injury in the balloon-injured rat, at least in part, by facilitating t

83 Balloon-injured segments secreted significantly more 72-

84 ssing rat SMCs onto the luminal surface of a balloon-injured syngeneic rat carotid artery.

85 e importance of this observation in vivo, we balloon-injured the carotid arteries of adult and old ra

86 the molecular mechanism of PESDA binding to balloon-injured vasculature.

87 en for differentially expressed sequences in balloon-injured versus normal arteries.

88 In vivo transfection of the balloon-injured vessel with AA-Akt reduced SMC prolifera

89 educed apoptosis in the fortilin-transfected balloon-injured vessels compared with Ad-luc injured con

90 h D-EXO would inhibit neointima formation in balloon-injured vessels in vivo.

91 In balloon-injured vessels, endogenous kallistatin mRNA and

92 In balloon-injured vessels, tranilast was associated with a

93 Homer1 expression levels are upregulated in balloon-injured vs. uninjured VSMCs.