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1 essed re-endothelialization and HHcy-induced neointimal formation.
2  that otherwise could proliferate to produce neointimal formation.
3 (3)-integrins correlated with a reduction in neointimal formation.
4 ion minimizes stent-induced inflammation and neointimal formation.
5 hronic graft vascular disease, in particular neointimal formation.
6 lar hypertrophy (RVH) and pulmonary arterial neointimal formation.
7 chimeric antibody will modulate flow-induced neointimal formation.
8 nd promotes regression of pulmonary arterial neointimal formation.
9 imal models results in discordant effects on neointimal formation.
10 month later was assessed and correlated with neointimal formation.
11 spatial growth of vasa vasorum in regions of neointimal formation.
12 relation between inflammation and subsequent neointimal formation.
13 icular weights correlated with the extent of neointimal formation.
14 s for evaluation of reendothelialization and neointimal formation.
15  media of newly placed SVGs, contributing to neointimal formation.
16 ession and the contribution of PDGFR-beta in neointimal formation.
17 of either of these two elements can suppress neointimal formation.
18 orated dexamethasone significantly decreased neointimal formation.
19 s play an active role in the pathogenesis of neointimal formation.
20 nderlying the stent determines the degree of neointimal formation.
21 me of the coronary injury with a decrease in neointimal formation.
22 oliferation and migration as well as in vivo neointimal formation.
23 sion and function in ligation injury-induced neointimal formation.
24 asia, while CCN5 gain-of-function alleviated neointimal formation.
25 ntimal hyperplasia with a 62.1% reduction in neointimal formation.
26  attenuates VSM proliferation and consequent neointimal formation.
27  down FSP-1 expression in BM cells prevented neointimal formation.
28 cell migration, resulting in lower levels of neointimal formation.
29 ell-induced but not interferon-gamma-induced neointimal formation.
30 le cell (VSMC) migration, a key component of neointimal formation.
31 that is required for effective inhibition of neointimal formation.
32 llular matrix proteins, thus contributing to neointimal formation.
33 e, which can bind GDP but not GTP, increased neointimal formation.
34  durable gradient reduction, and appropriate neointimal formation.
35 phometric analysis of endothelialization and neointimal formation.
36 pression paralleled that of RCMV-accelerated neointimal formation.
37  in reducing monocyte levels did not inhibit neointimal formation.
38 helium-dependent vasoreactivity, and reduced neointimal formation.
39 sphosphonates inhibits experimental in-stent neointimal formation.
40 njured vessels in vivo significantly reduces neointimal formation.
41 hypertensive pulmonary vascular disease with neointimal formation.
42          Coronary arteries were analyzed for neointimal formation 4 weeks after PTCA.
43 ary hypertension (PH) and pulmonary vascular neointimal formation 4 wk after monocrotaline (MCT) admi
44 The 1.0-microCi stents, however, had greater neointimal formation (4.67 +/- 1.50 mm2) and more lumina
45  and elevation of cyclic nucleotides reduces neointimal formation after angioplasty in animal models.
46 cular derived growth factors, have a role in neointimal formation after arterial injury.
47  migration and replication are important for neointimal formation after arterial injury.
48  smooth muscle cell (VSMC) proliferation and neointimal formation after arterial injury.
49                       This lack of effect on neointimal formation after balloon and stent arterial in
50 ndicates that thrombin plays a major role in neointimal formation after balloon-induced arterial inju
51 demonstrate that inhaling 80 ppm NO inhibits neointimal formation after balloon-induced carotid arter
52   We studied the effects of NO inhalation on neointimal formation after balloon-induced injury of the
53 /- and smN1+/- mice showed a 70% decrease in neointimal formation after carotid artery ligation.
54 equally important role as arterial injury in neointimal formation after coronary stenting, and that a
55 s to examine the hypothesis that atRA limits neointimal formation after experimental vascular injury.
56    Adamts7 knockout mice also showed reduced neointimal formation after femoral wire injury.
57 livered via a stent has been shown to reduce neointimal formation after placement in porcine and rabb
58                         Immune modulation of neointimal formation after vascular injury has been inve
59 cal intravascular NO administration inhibits neointimal formation after vascular injury in animal mod
60 crease in medial thickness, medial area, and neointimal formation after vascular injury in both apoE
61  RAGE/ligand interaction plays a key role in neointimal formation after vascular injury irrespective
62  than Notch3, mediates SMC proliferation and neointimal formation after vascular injury through CHF1/
63 uscle cell (SMC) proliferation and attenuate neointimal formation after vascular injury, presumably t
64                       This may contribute to neointimal formation after vascular injury.
65 smooth muscle cells (SMCs) may contribute to neointimal formation after vascular injury.
66 ion concurrent with injury, reduces in-stent neointimal formation and arterial stenosis in hyperchole
67 eceptor antagonism prevented the exacerbated neointimal formation and ECM synthesis conferred by loss
68 d on the other hand, PDGF signaling mediates neointimal formation and exacerbates chronic rejection i
69 d proliferating VSMC in vivo, and suppressed neointimal formation and increased luminal area in both
70  inhibition of chronic rejection, absence of neointimal formation and induction of vascular accommoda
71 ze vascular cell-specific effects of CCN5 on neointimal formation and its role in preventing in-stent
72 e factor pathway inhibitor (TFPI) attenuates neointimal formation and luminal stenosis after balloon-
73    Using this model, we found that increased neointimal formation and macrophage recruitment occurs i
74 ties of SMCs to migrate in vitro and inhibit neointimal formation and MMP9 expression in vivo.
75      Simvastatin reverses pulmonary arterial neointimal formation and PAH after toxic injury.
76 chytherapy with this device causes increased neointimal formation and prominent, dose-dependent lack
77 deling in response to injury with pronounced neointimal formation and reduced vascular compliance.
78                          Sunitinib decreased neointimal formation and smooth muscle cell proliferatio
79 r prothrombin activation by factor Xa limits neointimal formation and stenosis after arterial injury.
80 cularly effective for attenuating subsequent neointimal formation and stenosis.
81 ese results implicate thrombin generation in neointimal formation and suggest that administration of
82 SMCs following vascular insult is central to neointimal formation and the development of vascular pat
83 nt strut coverage with ECs, which suppressed neointimal formation and ultimately alleviated ISR.
84 eatment rescued Ang II-mediated increases in neointimal formation and vascular remodeling in a vein g
85 s to myofibroblasts, which may contribute to neointimal formation and vascular remodeling.
86 le cells into the arterial lumen, leading to neointimal formation and vascular stenosis.
87 h muscle cell (SMC) proliferation leading to neointimal formation and vessel reocclusion.
88 ly with arterial vascular injury facilitates neointimal formation, and conditions associated with inc
89  impacts collagen type I and III deposition, neointimal formation, and dedifferentiation of smooth mu
90 es that regulates vascular calcification and neointimal formation, and inhibits inflammation in diffe
91 ay be of relevance to in vivo events such as neointimal formation, angiogenesis, and vasculogenesis.
92 onstrated that 32P radioactive stents reduce neointimal formation at 28 days in porcine iliac and cor
93                                              Neointimal formation at IEL disruptions in the ascending
94 IIa), and leukocytes have been implicated in neointimal formation, based in part on the results obtai
95  and (c) type 2 cells may be responsible for neointimal formation because they proliferate and acquir
96 eletion of the Klf4 gene in mice accelerated neointimal formation but delayed down-regulation of smoo
97 hrombin has been implicated as a mediator of neointimal formation, but adjunctive administration of a
98 lloon-injured rat carotid arteries inhibited neointimal formation by 37% and induced marked dilatatio
99              Finally, CMMC treatment reduced neointimal formation by 55% at 4 weeks (P<0.05).
100 ia of injured carotid arteries and decreased neointimal formation by 80% and 60%, respectively.
101                                              Neointimal formation causes restenosis after intracorona
102  wire injury, PRCP(gt/gt) mice had increased neointimal formation, CD45 staining, and Ki-67 expressio
103 te accumulation, cellular proliferation, and neointimal formation compared with wild-type mice.
104           Pulmonary vascular remodeling with neointimal formation consisting of vascular smooth muscl
105                                 Furthermore, neointimal formation correlated precisely with PDGFR-bet
106 potential of the system in the prevention of neointimal formation, dexamethasone was incorporated int
107 C/R247C) mice showed significantly increased neointimal formation due to increased SMC proliferation
108                    Further, visfatin-induced neointimal formation, endothelial inflammasome formation
109 (rFGF2-SAP) on vascular SMC cytotoxicity and neointimal formation following arterial injury.
110             Acta2(-/-) mice showed increased neointimal formation following vascular injury in vivo,
111 veral diverse approaches aimed at preventing neointimal formation have been devised which have yielde
112                 High rates of restenosis and neointimal formation have driven increasing interest in
113 h an inhibitory action of cortistatin on the neointimal formation in 2 models of carotid arterial lig
114 ts c-myc expression and dramatically reduces neointimal formation in a dose dependent fashion in a po
115 cetyl-salicylic acid; ASA), and sulindac, on neointimal formation in a mouse femoral arterial injury
116        We further tested the role of HO-1 on neointimal formation in a mouse model of vein graft sten
117 tions of inflammation and arterial injury to neointimal formation in a porcine coronary overstretch r
118 itutively active I-1 gene transfer decreased neointimal formation in an angioplasty rat model by prev
119          Neovascularization is a hallmark of neointimal formation in atherosclerotic plaques and rest
120 ries and exacerbates ligation injury-induced neointimal formation in bacterial artificial chromosome
121 sfer significantly reduced proliferation and neointimal formation in balloon angioplasty-injured rat
122   These results demonstrate sulindac reduces neointimal formation in both normolipidemic and hyperlip
123 role of differentiated vascular myocytes are neointimal formation in canine carotid artery was invest
124 ese phenotypic changes culminated in reduced neointimal formation in cultured human saphenous vein.
125 MC) proliferation is a critical component of neointimal formation in many models of vascular injury a
126 inhibit platelet aggregation, did not affect neointimal formation in mice of either genotype.
127  ablation of the miR-21 stem loop attenuated neointimal formation in mice post-stenting.
128 leading to augmented vascular remodeling and neointimal formation in mice.
129  via a beta-particle-emitting stent inhibits neointimal formation in porcine arteries.
130     PDGFR-beta is necessary for flow-induced neointimal formation in prosthetic grafts.
131 nesis of vascular remodeling associated with neointimal formation in pulmonary arteries.
132 n vivo when administered orally, we examined neointimal formation in rat carotid arteries after ballo
133                      By 11 wk, the extent of neointimal formation in rats treated with ACE inhibition
134          Klf4 mutant mice exhibited enhanced neointimal formation in response to vascular injury caus
135 o profound changes in their phenotype during neointimal formation in response to vessel injury or wit
136  increased re-endothelialization and reduced neointimal formation in samples at 4 weeks after implant
137 x, attenuating VSMC synthetic phenotypes and neointimal formation in Senp1-deficient mice.
138 d investigator quantified pulmonary arterial neointimal formation in small pulmonary arteries.
139 ter injury revealed significantly diminished neointimal formation in the Ad-Rad-treated carotid arter
140                  Importantly, suppression of neointimal formation in the apoE transgenic mice also ab
141         Interruptions in the IEL resulted in neointimal formation in the ascending aorta but not in m
142                        Erlotinib ameliorated neointimal formation in the dose response study.
143 l narrowing was a consequence of significant neointimal formation in the injured areas.
144 naling lipid phosphatidic acid (PA), reduced neointimal formation in the mouse carotid artery ligatio
145 helial cell function, resulting in decreased neointimal formation in the porcine coronary injury mode
146 cellular and molecular pathways of increased neointimal formation in the setting of diabetes.
147 in grafting to investigate the mechanisms of neointimal formation in the setting of type 2 diabetes.
148 ion in proinflammatory genes and progressive neointimal formation in the venous vasculature in an AV
149  disease) may need to be present to increase neointimal formation in this model.
150 age accumulation in a model of lipid-induced neointimal formation in vivo.
151 ut affecting mitotic progression, suppressed neointimal formation in wire-injured mouse femoral arter
152                   The lack of an increase in neointimal formation indicates that additional diabetes
153 decreased the SMC proliferative activity and neointimal formation induced by balloon dilation injury.
154                                              Neointimal formation induced by carotid artery ligation
155                             However, because neointimal formation is only observed in patients with p
156 ed by air alone for 1 week did not attenuate neointimal formation measured at 14 days.
157 tion for preventing thrombotic occlusion and neointimal formation of synthetic vascular grafts.
158 ictable progressive vascular stenosis due to neointimal formation or complete occlusion from acute th
159 ial responses were associated with increased neointimal formation (P < .01).
160             Overexpression of TFPI inhibited neointimal formation (P=0.038), resulting in enhanced lu
161 sed a small, albeit significant, increase in neointimal formation; preservation injury of allografts
162 lmonary vascular injury by toxins can induce neointimal formation, pulmonary arterial hypertension (P
163 e-induced pulmonary vascular remodeling with neointimal formation, pulmonary arterial hypertension, a
164                           Pulmonary arterial neointimal formation (quantified by a vascular occlusion
165 arterial injury, with VSMC proliferation and neointimal formation serving as the final outcomes of th
166 y of rFGF2-SAP in an in vivo model to reduce neointimal formation, Sprague-Dawley rats underwent caro
167 lobal or SMC-specific LMO7 deletion enhanced neointimal formation, TGF-beta signaling, ECM deposition
168 ries had significantly less inflammation and neointimal formation than FG-AduPA arteries.
169 rtocaval fistula had less pulmonary arterial neointimal formation than matched animals without an aor
170 ater RVH, and more severe pulmonary arterial neointimal formation than rats that received triptolide
171 on by intracoronary beta-radiotherapy of the neointimal formation that is known to be present at 1 mo
172 es acute rejection but paradoxically reduces neointimal formation, the hallmark of chronic rejection.
173  VSMC synthetic phenotype in vivo and reduce neointimal formation, thereby implicating miRNAs as exci
174 lular matrix proteins and MMPs contribute to neointimal formation upon vascular injury.
175        We documented for the first time that neointimal formation using balloon-injured rat carotid a
176 ults at 8 months demonstrated the absence of neointimal formation, vessel enlargement was present.
177                                 Reduction in neointimal formation was associated with reduced arteria
178 cessation caused by carotid artery ligation, neointimal formation was attenuated in induced EC-Akt Tg
179                                              Neointimal formation was attenuated to a lesser extent i
180      Similarly, 1 week after carotid injury, neointimal formation was less in rats breathing 80 ppm N
181 teries were fixed and paraffin-embedded, and neointimal formation was measured by analyzing the ratio
182                    A significant increase in neointimal formation was noted in lepr(db/db) mice (139+
183             More importantly, injury-induced neointimal formation was significantly attenuated by PDE
184                                              Neointimal formation was significantly less at the flow
185                                              Neointimal formation was significantly suppressed at 5 w
186                                     However, neointimal formation was similar between wild-type and N
187                     Vascular remodeling with neointimal formation was studied in normal C57Bl/J6 and
188 determine whether these actions might affect neointimal formation, we investigated the effect of simv
189 leukocyte recruitment is causally related to neointimal formation, we subjected mice lacking Mac-1 to
190 or-specific mRNA, vascular inflammation, and neointimal formation were assessed 14 days after gene tr
191 y were found to have significantly increased neointimal formation, which was correlated with increase
192      Tissue factor pathway inhibitor reduced neointimal formation with mean intimal area of 1.2+/-0.3
193 nd Acta2(-/-) SMC proliferation in vitro and neointimal formation with vascular injury in vivo.
194 onizing radiation has been shown to decrease neointimal formation within stents in animal models and
195  recurrent in-stent restenosis by inhibiting neointimal formation within the stent.

 
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