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1 (3)-integrins correlated with a reduction in neointimal formation.
2 ion minimizes stent-induced inflammation and neointimal formation.
3 hronic graft vascular disease, in particular neointimal formation.
4 lar hypertrophy (RVH) and pulmonary arterial neointimal formation.
5 chimeric antibody will modulate flow-induced neointimal formation.
6 nd promotes regression of pulmonary arterial neointimal formation.
7 imal models results in discordant effects on neointimal formation.
8 month later was assessed and correlated with neointimal formation.
9 spatial growth of vasa vasorum in regions of neointimal formation.
10 relation between inflammation and subsequent neointimal formation.
11 icular weights correlated with the extent of neointimal formation.
12 s for evaluation of reendothelialization and neointimal formation.
13 media of newly placed SVGs, contributing to neointimal formation.
14 ession and the contribution of PDGFR-beta in neointimal formation.
15 of either of these two elements can suppress neointimal formation.
16 orated dexamethasone significantly decreased neointimal formation.
17 s play an active role in the pathogenesis of neointimal formation.
18 nderlying the stent determines the degree of neointimal formation.
19 me of the coronary injury with a decrease in neointimal formation.
20 oliferation and migration as well as in vivo neointimal formation.
21 attenuates VSM proliferation and consequent neointimal formation.
22 down FSP-1 expression in BM cells prevented neointimal formation.
23 cell migration, resulting in lower levels of neointimal formation.
24 ell-induced but not interferon-gamma-induced neointimal formation.
25 le cell (VSMC) migration, a key component of neointimal formation.
26 that is required for effective inhibition of neointimal formation.
27 essed re-endothelialization and HHcy-induced neointimal formation.
28 llular matrix proteins, thus contributing to neointimal formation.
29 e, which can bind GDP but not GTP, increased neointimal formation.
30 durable gradient reduction, and appropriate neointimal formation.
31 phometric analysis of endothelialization and neointimal formation.
32 pression paralleled that of RCMV-accelerated neointimal formation.
33 in reducing monocyte levels did not inhibit neointimal formation.
34 helium-dependent vasoreactivity, and reduced neointimal formation.
35 sphosphonates inhibits experimental in-stent neointimal formation.
36 njured vessels in vivo significantly reduces neointimal formation.
37 hypertensive pulmonary vascular disease with neointimal formation.
38 that otherwise could proliferate to produce neointimal formation.
40 ary hypertension (PH) and pulmonary vascular neointimal formation 4 wk after monocrotaline (MCT) admi
41 The 1.0-microCi stents, however, had greater neointimal formation (4.67 +/- 1.50 mm2) and more lumina
42 and elevation of cyclic nucleotides reduces neointimal formation after angioplasty in animal models.
47 ndicates that thrombin plays a major role in neointimal formation after balloon-induced arterial inju
48 demonstrate that inhaling 80 ppm NO inhibits neointimal formation after balloon-induced carotid arter
49 We studied the effects of NO inhalation on neointimal formation after balloon-induced injury of the
51 equally important role as arterial injury in neointimal formation after coronary stenting, and that a
52 s to examine the hypothesis that atRA limits neointimal formation after experimental vascular injury.
54 livered via a stent has been shown to reduce neointimal formation after placement in porcine and rabb
56 cal intravascular NO administration inhibits neointimal formation after vascular injury in animal mod
57 crease in medial thickness, medial area, and neointimal formation after vascular injury in both apoE
58 RAGE/ligand interaction plays a key role in neointimal formation after vascular injury irrespective
59 than Notch3, mediates SMC proliferation and neointimal formation after vascular injury through CHF1/
60 uscle cell (SMC) proliferation and attenuate neointimal formation after vascular injury, presumably t
63 ion concurrent with injury, reduces in-stent neointimal formation and arterial stenosis in hyperchole
64 d on the other hand, PDGF signaling mediates neointimal formation and exacerbates chronic rejection i
65 d proliferating VSMC in vivo, and suppressed neointimal formation and increased luminal area in both
66 inhibition of chronic rejection, absence of neointimal formation and induction of vascular accommoda
67 e factor pathway inhibitor (TFPI) attenuates neointimal formation and luminal stenosis after balloon-
68 Using this model, we found that increased neointimal formation and macrophage recruitment occurs i
71 chytherapy with this device causes increased neointimal formation and prominent, dose-dependent lack
72 deling in response to injury with pronounced neointimal formation and reduced vascular compliance.
74 r prothrombin activation by factor Xa limits neointimal formation and stenosis after arterial injury.
76 ese results implicate thrombin generation in neointimal formation and suggest that administration of
77 SMCs following vascular insult is central to neointimal formation and the development of vascular pat
78 eatment rescued Ang II-mediated increases in neointimal formation and vascular remodeling in a vein g
82 ly with arterial vascular injury facilitates neointimal formation, and conditions associated with inc
83 impacts collagen type I and III deposition, neointimal formation, and dedifferentiation of smooth mu
84 es that regulates vascular calcification and neointimal formation, and inhibits inflammation in diffe
85 ay be of relevance to in vivo events such as neointimal formation, angiogenesis, and vasculogenesis.
86 onstrated that 32P radioactive stents reduce neointimal formation at 28 days in porcine iliac and cor
87 IIa), and leukocytes have been implicated in neointimal formation, based in part on the results obtai
88 and (c) type 2 cells may be responsible for neointimal formation because they proliferate and acquir
89 eletion of the Klf4 gene in mice accelerated neointimal formation but delayed down-regulation of smoo
90 hrombin has been implicated as a mediator of neointimal formation, but adjunctive administration of a
91 lloon-injured rat carotid arteries inhibited neointimal formation by 37% and induced marked dilatatio
95 wire injury, PRCP(gt/gt) mice had increased neointimal formation, CD45 staining, and Ki-67 expressio
99 potential of the system in the prevention of neointimal formation, dexamethasone was incorporated int
100 C/R247C) mice showed significantly increased neointimal formation due to increased SMC proliferation
104 veral diverse approaches aimed at preventing neointimal formation have been devised which have yielde
105 h an inhibitory action of cortistatin on the neointimal formation in 2 models of carotid arterial lig
106 ts c-myc expression and dramatically reduces neointimal formation in a dose dependent fashion in a po
107 cetyl-salicylic acid; ASA), and sulindac, on neointimal formation in a mouse femoral arterial injury
109 tions of inflammation and arterial injury to neointimal formation in a porcine coronary overstretch r
110 itutively active I-1 gene transfer decreased neointimal formation in an angioplasty rat model by prev
112 sfer significantly reduced proliferation and neointimal formation in balloon angioplasty-injured rat
113 These results demonstrate sulindac reduces neointimal formation in both normolipidemic and hyperlip
114 role of differentiated vascular myocytes are neointimal formation in canine carotid artery was invest
115 ese phenotypic changes culminated in reduced neointimal formation in cultured human saphenous vein.
116 MC) proliferation is a critical component of neointimal formation in many models of vascular injury a
122 n vivo when administered orally, we examined neointimal formation in rat carotid arteries after ballo
125 o profound changes in their phenotype during neointimal formation in response to vessel injury or wit
126 increased re-endothelialization and reduced neointimal formation in samples at 4 weeks after implant
128 ter injury revealed significantly diminished neointimal formation in the Ad-Rad-treated carotid arter
132 helial cell function, resulting in decreased neointimal formation in the porcine coronary injury mode
134 in grafting to investigate the mechanisms of neointimal formation in the setting of type 2 diabetes.
135 ion in proinflammatory genes and progressive neointimal formation in the venous vasculature in an AV
138 ut affecting mitotic progression, suppressed neointimal formation in wire-injured mouse femoral arter
140 decreased the SMC proliferative activity and neointimal formation induced by balloon dilation injury.
147 sed a small, albeit significant, increase in neointimal formation; preservation injury of allografts
148 lmonary vascular injury by toxins can induce neointimal formation, pulmonary arterial hypertension (P
149 e-induced pulmonary vascular remodeling with neointimal formation, pulmonary arterial hypertension, a
151 arterial injury, with VSMC proliferation and neointimal formation serving as the final outcomes of th
152 y of rFGF2-SAP in an in vivo model to reduce neointimal formation, Sprague-Dawley rats underwent caro
154 rtocaval fistula had less pulmonary arterial neointimal formation than matched animals without an aor
155 ater RVH, and more severe pulmonary arterial neointimal formation than rats that received triptolide
156 on by intracoronary beta-radiotherapy of the neointimal formation that is known to be present at 1 mo
157 es acute rejection but paradoxically reduces neointimal formation, the hallmark of chronic rejection.
158 VSMC synthetic phenotype in vivo and reduce neointimal formation, thereby implicating miRNAs as exci
161 ults at 8 months demonstrated the absence of neointimal formation, vessel enlargement was present.
163 cessation caused by carotid artery ligation, neointimal formation was attenuated in induced EC-Akt Tg
165 Similarly, 1 week after carotid injury, neointimal formation was less in rats breathing 80 ppm N
166 teries were fixed and paraffin-embedded, and neointimal formation was measured by analyzing the ratio
173 determine whether these actions might affect neointimal formation, we investigated the effect of simv
174 leukocyte recruitment is causally related to neointimal formation, we subjected mice lacking Mac-1 to
175 or-specific mRNA, vascular inflammation, and neointimal formation were assessed 14 days after gene tr
176 y were found to have significantly increased neointimal formation, which was correlated with increase
177 Tissue factor pathway inhibitor reduced neointimal formation with mean intimal area of 1.2+/-0.3
179 onizing radiation has been shown to decrease neointimal formation within stents in animal models and
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