戻る
「早戻しボタン」を押すと検索画面に戻ります。 [閉じる]

コーパス検索結果 (１語後でソート)

通し番号をクリックするとPubMedの該当ページを表示します
1 whether estrogen was capable of accelerating reendothelialization.
2 therapy in managing restenosis and improving reendothelialization.
3 rable polymers can delay healing and inhibit reendothelialization.
4 ion after wire injury and allowed for vessel reendothelialization.
5  wild-type mice has no effect, apoE4 impairs reendothelialization.
6 -specific gene transfer of Prkcd accelerated reendothelialization.
7 eading to stent malapposition and incomplete reendothelialization.
8  oxide synthase and repressed carotid artery reendothelialization.
9 e impaired in diabetes, resulting in delayed reendothelialization.
10 apolipoprotein A-I expression rescues normal reendothelialization.
11  while accelerating, rather than inhibiting, reendothelialization.
12 arly growth response factor-1 (Egr-1) during reendothelialization.
13 in endothelial cells (ECs), thereby delaying reendothelialization.
14 me the adverse effects of Prkcd knockdown on reendothelialization.
15 nificant difference in the degree of luminal reendothelialization.
16 dothelial cell (EC) migration contributes to reendothelialization after angioplasty or rupture of ath
17 d whether statin therapy may also accelerate reendothelialization after carotid balloon injury.
18 t, in contrast to E2, it fails to accelerate reendothelialization after carotid electric injury.
19                                 Importantly, reendothelialization after focal carotid endothelial inj
20 ols with CRP of <1 microg/mL, carotid artery reendothelialization after perivascular electric injury
21 leling the in vitro findings, carotid artery reendothelialization after perivascular electric injury
22                                              Reendothelialization after VBT is not completed at 6 mon
23 ated MAPK pathways, possibly contributing to reendothelialization and angiogenesis after vascular inj
24 roliferation and migration are important for reendothelialization and angiogenesis.
25                        Estradiol accelerates reendothelialization and attenuates medial thickening af
26 utoregulation in vascular ECs, L5 may impair reendothelialization and collateralization in diabetes.
27                        In summary, decreased reendothelialization and enhanced endothelial apoptosis,
28 verexpression of endostatin led to decreased reendothelialization and increased apoptosis of luminal
29              VEGF overexpression accelerated reendothelialization and increased luminal endothelial c
30 ation of anti-TSP1 antibody could facilitate reendothelialization and inhibit neointimal thickening i
31 s repair of injured arteries by facilitating reendothelialization and inhibiting neointima developmen
32 d the effect of endostatin overexpression on reendothelialization and neointima formation in a mouse
33  blue staining) or 2 weeks for evaluation of reendothelialization and neointimal formation.
34 ting restenosis, while selectively promoting reendothelialization and preserving EC function.
35  insights and therapeutic targets to improve reendothelialization and reduce restenosis in diabetes.
36    Pro-healing stent coatings may facilitate reendothelialization and reduce the risk of neoatheroscl
37 elivery of antibody against TSP1 facilitated reendothelialization and reduced neointimal lesion forma
38 uced diabetic mice, 1,25-VitD3 also promoted reendothelialization and restored the impaired angiogene
39  and/or endogenous VEGF by VEGF-trap delayed reendothelialization and significantly increased neointi
40 er coronary interventions may reflect plaque reendothelialization and stabilization.
41           This lack of discrimination delays reendothelialization and vascular healing, increasing th
42 g in the labyrinth, failed SA remodeling and reendothelialization, and markedly reduced numbers of ma
43                                Unexpectedly, reendothelialization (assessed by resistance to Evans bl
44 ed nonirradiated vessels, there was complete reendothelialization at 1 month, and platelet recruitmen
45 anning electron microscopy showed incomplete reendothelialization at 1 month, and these areas demonst
46  as well as stimulating a 2-fold increase in reendothelialization at 14 days after injury.
47 rap overexpression alone also led to delayed reendothelialization at 2 weeks (P<0.01) and increased n
48 ithout a significant change in the degree of reendothelialization at 2 weeks.
49 on at the time of balloon injury accelerated reendothelialization at 4 weeks compared with saline (P<
50 ypically fully mature neointima and complete reendothelialization at all sites.
51 ble receptor molecule results in accelerated reendothelialization at sites of balloon angioplasty, su
52  mice to evaluate how cholesterol influences reendothelialization, atherosclerosis, and EPC function
53 ts not only induced faster and more complete reendothelialization, but also effectively improved neoi
54                         We hypothesized that reendothelialization by cell therapy would modulate aort
55 marrow-derived EPC incorporation at sites of reendothelialization, carotid injury was established in
56     Tissue factor overexpression accelerated reendothelialization compared with controls at 2 weeks a
57                                      Delayed reendothelialization contributes to restenosis after ang
58 dostatin serum levels, whereas the degree of reendothelialization correlated negatively with endostat
59                            Furthermore, poor reendothelialization correlated with increased neointima
60 ured arteries is associated with accelerated reendothelialization, enhanced endothelium-dependent vas
61  euthanatized after 1 week for evaluation of reendothelialization (Evans blue staining) or 2 weeks fo
62 ion of a neutralizing VEGF antibody impaired reendothelialization following balloon injury performed
63 leling the in vitro findings, carotid artery reendothelialization following perivascular electric inj
64                         The effects of CO on reendothelialization have not been evaluated.
65                                 SMCs promote reendothelialization in a PKCdelta-dependent paracrine m
66 ol and EDC equally stimulated carotid artery reendothelialization in an ERalpha- and G protein-depend
67 ter injury disclosed significantly increased reendothelialization in arteries treated with C6.7 antib
68 damage and vascular dysfunction by improving reendothelialization in mice.
69 ber of angiogenic myeloid cells and promoted reendothelialization in the carotid artery injury model.
70                    ID significantly enhanced reendothelialization in the injured carotid arteries as
71 ce rescued diabetes-associated impairment of reendothelialization in the murine carotid-injury model.
72 helial and macrophage apoptosis and impaired reendothelialization in vitro.
73  Thus, CRP downregulates eNOS and attenuates reendothelialization in vivo in mice, and this action of
74 ell migration and proliferation in vitro and reendothelialization in vivo.
75 ic denudation of the endothelium accelerated reendothelialization in vivo.
76 cell proliferation, but that did not prevent reendothelialization in vivo.
77                                              Reendothelialization involves endothelial progenitor cel
78                                  The rate of reendothelialization is critical in neointima formation
79                               Carotid artery reendothelialization is decreased in ApoER2(-/-) mice, a
80                                              Reendothelialization is impaired by malfunctioning EPCs
81                                 Furthermore, reendothelialization is impaired in SR-BI(-/-) mice.
82  the hypothesis that the EPC contribution to reendothelialization may be impaired in diabetes, result
83 esized that estrogen-induced acceleration of reendothelialization might be mediated in part by effect
84 y of proangiogenic miR-126 was tested in the reendothelialization model.
85                               Relaxation and reendothelialization of carotid arteries and circulating
86                   It has been suggested that reendothelialization of damaged blood vessels protects a
87  represent a promising cell source for rapid reendothelialization of damaged vasculature after expans
88 stradiol treatment significantly accelerated reendothelialization of injured arterial segments within
89 ilability in the carotid artery and improved reendothelialization of injured carotid arteries in vivo
90 t in 34 male Sprague-Dawley rats accelerated reendothelialization of the balloon-injured arterial seg
91 ion formation were related to the functional reendothelialization of the damaged vessel, endothelium-
92 d rat, at least in part, by facilitating the reendothelialization of the damaged vessel.
93 us air controls, and in vivo, it accelerates reendothelialization of the denuded artery by day 4 afte
94 n endothelial proliferation as determined by reendothelialization of the denuded rat aorta.
95 e-1, showed rapid and nearly complete (>90%) reendothelialization of the denuded vessels in the G-CSF
96 upts endothelial cell (EC) proliferation and reendothelialization of the injured vessel.
97 ssion of E2F1 at the site of injury improves reendothelialization of the injured vessel.
98 ll (EC) proliferation and negatively affects reendothelialization of the injured vessel.
99 elial precursors showed defective homing and reendothelialization of the retinal vasculature compared
100 ment in endothelium-dependent relaxation and reendothelialization of their injured carotid arteries.
101    In contrast, estradiol did not accelerate reendothelialization or augment EPC mobilization into th
102 eloping strategies aimed at accelerating the reendothelialization process.
103 imals exhibited reduced restenosis, complete reendothelialization, reduced hypercoagulability, and re
104      SMC-specific knockout of Prkcd impaired reendothelialization, reflected by a smaller Evans blue-
105                                   Delinquent reendothelialization (rET) has been shown to have a perm
106             We investigated whether improved reendothelialization using RGD-coated stents results in
107 ce, LXR activation stimulated carotid artery reendothelialization via LXRbeta- and ERalpha-dependent
108 ascular injury by promoting EPC function and reendothelialization via upregulation of heme oxygenase-
109                              Acceleration of reendothelialization via VEGF-2 gene-eluting stents prov
110 lanted into nondiabetic mice, revealing that reendothelialization was impaired in the recipients of d
111  that was survived to 2 weeks (n=5), luminal reendothelialization was measured via CD-31 staining.
112                                              Reendothelialization was nearly complete in the VEGF ste
113                      A similar impediment to reendothelialization was observed in rats with SMC-speci
114                                              Reendothelialization was paralleled by a decrease in inf
115                                              Reendothelialization was significantly reduced in diabet
116                                      Delayed reendothelialization was suggested as a pivotal cause, b
117  levels and improvements of EPC function and reendothelialization were all abrogated by pharmacologic
118 nical consequence of these stents is delayed reendothelialization, which may increase the risk of lat
119 stradiol caused a dose-dependent increase in reendothelialization, which was measured as absolute are
120                                 The impaired reendothelialization with CRP was mimicked by NOS antago

 
Page Top