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1 ponse is necessary for EC regeneration after carotid artery injury.
2  an occlusive thrombus after FeCl(3)-induced carotid artery injury.
3 well as neointima formation, after ZO common carotid artery injury.
4 lets, formed unstable thrombi in response to carotid artery injury.
5 ically upregulated following balloon-induced carotid artery injury.
6 ation and neointimal thickening after murine carotid artery injury.
7 hrombus formation on ferric chloride-induced carotid artery injury.
8 tiplatelet agent developed stroke related to carotid artery injuries.
9        One hundred fourteen patients had 157 carotid artery injuries (43 bilateral), and 79 patients
10 d with permanent cranial nerve morbidity nor carotid artery injury, although 4 patients (all Knosp 3-
11 2) (PAMAM G-3) prevents thrombosis following carotid artery injury and pulmonary thromboembolism in m
12 ng from murine liver wounds, swine liver and carotid artery injuries, and the human radial artery pun
13 endothelial matrix, mice were subjected to a carotid artery injury assay in which ferric chloride adm
14 d with higher risk of stroke due to internal carotid artery injuries, but monitoring was not useful f
15  FVIII had no effect after longer (3-minute) carotid artery injury, but it shortened the TTO after sh
16                    One patient with grade II carotid artery injuries (by CTA and DSA) on antiplatelet
17      Angiography identified 24 patients with carotid artery injuries (CAI) and 43 patients with verte
18         Whole-blood clotting times and FeCl3 carotid artery injury correction demonstrated that plate
19 hrombosis was measured in vivo after FeCl(3) carotid artery injury, endothelial COX1 deletion acceler
20           Among those with isolated internal carotid artery injuries, five of nine with delayed strok
21 g for ipsilateral and contralateral internal carotid artery injury grade (adjusted risk ratio, 2.91;
22           Ferric chloride was used to induce carotid artery injury in 97 wild-type (WT), 84 PAI-1-/-,
23                                        After carotid artery injury in CD40 ligand knockout (CD40L(-/-
24                       Following wire-induced carotid artery injury in mice, the majority of circulati
25 s neointimal formation after balloon-induced carotid artery injury in rats.
26                                 After common carotid artery injury, knockdown of Nox4 by adenoviral N
27 red with wild-type (WT) in a FeCl(3)-induced carotid artery injury model.
28 ibitor significantly reduced thrombosis in a carotid artery injury model.
29 r wild-type (WT) littermates using the mouse carotid artery injury model.
30 lls and promoted reendothelialization in the carotid artery injury model.
31                                         In 2 carotid artery injury models (FeCl(3) and Rose Bengal/la
32 DO-1 inhibitors, an adenine-induced CKD, and carotid artery injury models were used.
33                                        After carotid artery injury, Nf1(+/-) mice demonstrated increa
34                                              Carotid artery injury of Acta2(SMC-R179C/+) mice leads t
35 d markedly impaired thrombus formation after carotid artery injury or inferior vena cava ligation.
36 ient mice have reduced thrombus growth after carotid artery injury relative to conventionally raised
37 e found that after mesenteric arteriolar and carotid artery injury, Slit2 delayed vessel occlusion ti
38   By using a ferric chloride (FeCl3)-induced carotid artery injury thrombosis model, we found time to
39      Thrombus generation after photochemical carotid artery injury was accelerated in iron-loaded mic
40 cordingly, neointimal lesion formation after carotid artery injury was attenuated in these mice.
41  The time to occlusion after FeCl(3)-induced carotid artery injury was delayed (11.8 +/- 3.6 minutes,
42                                  Left common carotid artery injury was induced with a guidewire in ap
43        Using 3 complementary mouse models of carotid artery injury, we demonstrated that both tamoxif
44 able occlusive thrombi after ferric chloride carotid artery injury, whereas the majority of wild-type
45  Recognition of brain injury in asymptomatic carotid artery injuries with conventional methods can be
46     Among patients who sustained an internal carotid artery injury with or without additional vessel