ライフサイエンスコーパス: neointimal proliferation

1 processes initiating excessive and prolonged neointimal proliferation.

2 g enough to explain persistent inhibition of neointimal proliferation.

3 ssociated with stent thrombosis or increased neointimal proliferation.

4 thrombotic occlusions, and thereby inhibited neointimal proliferation.

5 ial hypertrophy, adventitial thickening, and neointimal proliferation.

6 The risk of neointimal proliferation (1.8%) and restenosis (2%) is l

7 There was a low incidence of neointimal proliferation (1.8%) and restenosis (2%).

8 nd repeat revascularization due to excessive neointimal proliferation, a process that may be blunted

9 effect of IPC instillation of paclitaxel on neointimal proliferation after balloon overstretch of po

10 ted the hypothesis that CaMKIIdelta mediates neointimal proliferation after carotid artery ligation b

11 arrest in the synthetic state with excessive neointimal proliferation after carotid injury, as well a

12 actors for the development of restenosis and neointimal proliferation after endovascular stent implan

13 ed Z2D3 F(ab')2 in a swine model of coronary neointimal proliferation after overexpansion coronary st

14 a beta-particle-emitting stent would inhibit neointimal proliferation after placement in porcine ilia

15 ortic adventitia, coincident with prominent, neointimal proliferation among cholesterol-fed, atherosc

16 (fluoropolymer-based versus polymer-free) on neointimal proliferation and healing response in the fam

17 uting stents (DES) are effective in reducing neointimal proliferation and in-stent restenosis.

18 Neointimal proliferation and intima to media ratios in M

19 sential to the development of the concentric neointimal proliferation and luminal narrowing character

20 ly that simvastatin attenuates smooth muscle neointimal proliferation and pulmonary hypertension in p

21 PB-PES, PF-PES was associated with increased neointimal proliferation and subsequent clinical resteno

22 ion of an FP-PES resulted in lower levels of neointimal proliferation and sustained biological effect

23 Nogo-A/B-deficient mice promotes exaggerated neointimal proliferation, and adenoviral-mediated gene t

24 ilator actions, inhibition of thrombosis and neointimal proliferation, and both pro- and antiinflamma

25 ts of stents coated with agents that inhibit neointimal proliferation are extremely promising.

26 actors for the development of restenosis and neointimal proliferation are poorly understood.

27 This was accompanied by reduced neointimal proliferation, as monitored by intimal thickn

28 16 or 24 Gy exhibited marked suppression of neointimal proliferation at 28-day follow-up, with quant

29 (68)Ga positron radiation suppresses neointimal proliferation at doses of 16 and 24 Gy.

30 ISR mainly results from aggressive neointimal proliferation, but recent data also suggest t

31 t coronary angioplasty sites caused enhanced neointimal proliferation by 8 weeks.

32 but have retained the capability to inhibit neointimal proliferation by eluting immunosuppressive dr

33 he ACHIEVE paclitaxel-coated stent decreased neointimal proliferation compared with the bare-metal PE

34 ve demonstrated that ISR is mainly caused by neointimal proliferation; consequently, this pathologic

35 However, few animal models of pulmonary neointimal proliferation exist, thereby limiting a compl

36 coronary stents are effective at preventing neointimal proliferation in a porcine model of restenosi

37 Drug elution by BVS prevents neointimal proliferation in a similar fashion to drug-el

38 or produces a marked localized inhibition of neointimal proliferation in balloon-injured arteries.

39 loading technique have been shown to inhibit neointimal proliferation in experimental models of reste

40 ted vascular disease and in the treatment of neointimal proliferation in other settings.

41 g ISR lesions is counteracted by exaggerated neointimal proliferation in placebo patients.

42 Neointimal proliferation in response to arterial injury

43 hy analysis showed significantly more global neointimal proliferation in the BMS+DEB group (15.7+/-7.

44 ic approaches for limiting atherogenesis and neointimal proliferation in the future.

45 sirolimus-coated balloons effectively reduce neointimal proliferation in the porcine coronary model b

46 ug-delivery stent showed a minimal amount of neointimal proliferation in the stented segment.

47 supplemented females correlated with reduced neointimal proliferation in this group.

48 Neointimal proliferation in vivo and platelet-derived gr

49 of peri-stent remodeling is less, intrastent neointimal proliferation is greater and accompanied by m

50 vasculopathy is characterized by progressive neointimal proliferation, leading to ischemic failure of

51 The mechanisms underlying the reduced neointimal proliferation (NP) by intracoronary brachythe

52 Neointimal proliferation occurring after vascular or end

53 In this randomized trial, strut coverage and neointimal proliferation of a therapy of bare metal sten

54 et-derived growth factors help stimulate the neointimal proliferation of restenosis after coronary in

55 serial dilation (n = 27) and development of neointimal proliferation or restenosis, or both (n = 9).

56 evious studies established that stents cause neointimal proliferation proportional to injury.

57 cross-sectional area of stenosis comprising neointimal proliferation ranged from 8% to 95%, with a m

58 es (intimal hyperplasia, atherosclerosis and neointimal proliferation, sclerosis of arterialized saph

59 is corresponds to a significant reduction in neointimal proliferation seen at 4 weeks without a signi

60 drug-eluting stents has reduced the in-stent neointimal proliferation that causes restenosis and redu

61 consistent with chronic rejection, including neointimal proliferation, transplant vasculopathy, vesse

62 Neointimal proliferation was similar between PP and non-

63 The inhibitory effects on neointimal proliferation were localized to the site of a

64 balloon injury, there is marked reduction of neointimal proliferation when the injured vessel is irra

65 eptors and humoral antibody showed almost no neointimal proliferation, whereas those grafted into mic

66 In contrast, CsA therapy resulted in marked neointimal proliferation, without evidence of vascular a