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1  can enhance endothelial recovery and reduce neointimal thickening.
2 njury also significantly reduced the area of neointimal thickening.
3 erial injury and stent design determine late neointimal thickening.
4 or contraction), independent or dependent of neointimal thickening.
5   (6) Local delivery of fluid may exacerbate neointimal thickening.
6 tasis, and endothelial denudation results in neointimal thickening.
7 or 14, 60, and 90 days and then assessed for neointimal thickening.
8  by inhibition of cellular proliferation and neointimal thickening.
9 to intima is critical for the development of neointimal thickening after balloon catheter injury of t
10          In vivo, estradiol-17 beta prevents neointimal thickening after balloon injury and in rabbit
11 elator tetrathiomolybdate was able to reduce neointimal thickening after balloon injury in the rat.
12 either inhibitor was effective in preventing neointimal thickening after mechanical injury when admin
13 f Mac-1 reduces vessel wall inflammation and neointimal thickening after murine carotid artery injury
14  delivery on amount, rate and composition of neointimal thickening after stent implantation.
15 mulation was accompanied by markedly reduced neointimal thickening after vascular injury.
16  maximal collateral flow, but it exacerbated neointimal thickening after vascular injury.
17 iferation and migration in vitro and reduces neointimal thickening and macrophage and lipid accumulat
18 se data establish a role for inflammation in neointimal thickening and suggest that leukocyte recruit
19 stenosis resulting from artery size changes, neointimal thickening and their impact on lumen size.
20           AOIs were categorized based on CAV neointimal thickening and underwent whole transcriptome
21 signed to facilitate EC regeneration, reduce neointimal thickening, and promote recovery of EC dysfun
22 8 SMCs per x600 field [control], P=.6) or on neointimal thickening at 14 days (I/M area ratio, 0.664+
23 (0.2 or 1 mg/kg IP) significant reduction in neointimal thickening at 2, 3, and 4 weeks compared with
24 robe, there was no significant difference in neointimal thickening between beta3-/- and beta3+/+ mice
25  injured artery induced a marked increase in neointimal thickening beyond that seen with injury alone
26 nd fluid shear stress may induce accelerated neointimal thickening by a PDGF-A-mediated mechanism, si
27 uire further investigation, the reduction in neointimal thickenings demonstrated that local delivery
28 lity of animal models of atherosclerosis and neointimal thickening for investigating the role of angi
29 hether rapamycin administration could reduce neointimal thickening in a porcine model of restenosis p
30  facilitate reendothelialization and inhibit neointimal thickening in balloon-injured rat carotid art
31 without medial disruption, there was reduced neointimal thickening in beta3-/- mice compared with bet
32                      Twenty-eight days later neointimal thickening in CRPtg/Fc gamma RI(-/-) and CRPt
33 that endothelin receptor blockade can reduce neointimal thickening in injured porcine coronary arteri
34 utes to atherosclerotic plaque formation and neointimal thickening in other occlusive vascular diseas
35 ned the ability of Cu2+ chelation to repress neointimal thickening in response to injury.
36 ury or tumor implantation showed exaggerated neointimal thickening in response to the injury and incr
37 intimal SMC accumulation that contributes to neointimal thickening in the setting of arterial ligatio
38 ted whether 12-LO activation plays a role in neointimal thickening in this rat model by using a speci
39 postdeployment luminal geometry affects late neointimal thickening independently of the extent of str
40 ce were protected from wire injury with less neointimal thickening, leukocyte infiltration, and cellu
41                           Significantly less neointimal thickening occurred in the rTAP-treated anima
42            Intravascular ultrasound detected neointimal thickening of < or =0.2 mm in 5 of 16 stents.
43     These fibroproliferative lesions lead to neointimal thickening of arteries in all transplanted al
44 l and remote sites, leading to inhibition of neointimal thickening, reduction in thrombogenicity, and
45          Mac-1 blockade reduces experimental neointimal thickening, suggesting that leukocyte recruit
46 young recipients consistently developed less neointimal thickening than when transplanted into old re
47 h-old) donor aortas were injured to initiate neointimal thickening, then transplanted into age-mismat
48                                              Neointimal thickening was also shown inhibited.
49                                              Neointimal thickening was also shown to be inhibited in
50                                              Neointimal thickening was correspondingly attenuated to
51                                        While neointimal thickening was initially considered the major
52                                              Neointimal thickening was significantly reduced in the G