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1 aque in rats feeding with high fat diet plus balloon injury.
2 f rat decorin expression up to 8 weeks after balloon injury.
3 ima formation and adventitial reaction after balloon injury.
4 t carotid arteries of rats immediately after balloon injury.
5 imal formation in rat carotid arteries after balloon injury.
6 in the development of stenotic lesions after balloon injury.
7 worsens atherosclerosis and restenosis after balloon injury.
8 are downregulated in rat carotid arteries on balloon injury.
9 RNA was found to be expressed markedly after balloon injury.
10 proliferation and neointima formation after balloon injury.
11 ns play a role in SMC growth responses after balloon injury.
12 fed New Zealand White rabbits 6 months after balloon injury.
13 Adventitial neovascularization occurs after balloon injury.
14 le cells of the arterial wall in response to balloon injury.
15 could reduce intimal hyperplasia induced by balloon injury.
16 , was examined in rat carotid arteries after balloon injury.
17 -selectin and L-selectin are expressed after balloon injury.
18 nous arteries and from arteries subjected to balloon injury.
19 for both gelatinases were upregulated after balloon injury.
20 arteries but declined again by 21 days after balloon injury.
21 tinases from pig carotid artery tissue after balloon injury.
22 and promote recovery of EC dysfunction after balloon injury.
23 iac artery of each animal was subjected to a balloon injury.
24 reduce neointimal hyperplasia after arterial balloon injury.
25 rantly expressed in the vascular walls after balloon injury.
26 ects on preventing intimal hyperplasia after balloon injury.
27 the neointima of rat carotid arteries after balloon injury.
28 uired to reduce neointimal hyperplasia after balloon injury.
29 n vascular smooth muscle cells (VSMCs) after balloon injury.
30 d vascular smooth muscles in the media after balloon injury.
31 ccelerate reendothelialization after carotid balloon injury.
32 Tenascin-C is expressed in response to balloon injury.
33 is expressed locally in arteries at sites of balloon injury.
34 artery wall promotes neointima growth after balloon injury.
35 gnificantly increased in the neointima after balloon injury.
36 by treatment with M1/70 (intimal area after balloon injury, 0.12 +/- 0.09 mm2, compared with 0.32 +/
37 inflammation (-0.82 versus -0.24, P = 0.03), ballooning injury (-1.27 versus -0.53, P = 0.03) and NAS
41 Zealand White rabbits (n = 7) by a repeated balloon injury (4 wk apart) and 4 mo of hyperlipemic die
43 , and in neointimal cells 3 and 7 days after balloon injury; 72-kD gelatinase mRNA persisted after 21
44 Local CMMC administration at the time of balloon injury accelerated reendothelialization at 4 wee
45 show that Ad-E2F1 overexpression at sites of balloon injury accelerates functional endothelial recove
48 abbits (n = 37) by the combination of double-balloon injury and a nine-month high-cholesterol (HC) di
49 duced experimental atheroma in 33 rabbits by balloon injury and an atherogenic diet (0.3% cholesterol
50 n of intimal SMCs in 33 rabbits subjected to balloon injury and cholesterol feeding (0.3%) for 4 mont
51 ty, we produced atheroma in rabbit aortas by balloon injury and cholesterol feeding for 4 months (Bas
53 g(-1) x d(-1) beginning 2 days before aortic balloon injury and continued for the total 8 weeks of th
54 his trend was also observed at 28 days after balloon injury and gene transfer during which AV-W9-trea
55 Zealand White rabbits underwent simultaneous balloon injury and gene transfer of one femoral artery w
59 retrieved 3, 7, 14, 28, 42, or 56 days after balloon injury and immunostained as well for proliferati
60 17 beta prevents neointimal thickening after balloon injury and in rabbit cardiac transplant allograf
61 in rat neointima at 7 days and 14 days after balloon injury and is also present in early human athero
62 gelatinase production occurs in response to balloon injury and may play a role in permitting migrati
64 proliferation and neointima formation after balloon injury and suggest that LXR ligands may constitu
65 Rat carotid arteries that were subjected to balloon injury and transduced with Ad-15-LOX1 upon expos
66 rea of the AV-W9-treated group 10 days after balloon injury and treatment was 0.42+/-0.36 mm(2), wher
67 the neointima reached a maximum 7 days after balloon injury and was associated with the presence of p
68 imals were killed at days 4, 8, and 14 after balloon injury, and coronary artery segments were studie
69 Four pigs were killed 28 d after coronary balloon injury, and four pigs with uninjured coronary ar
70 efore injury, 4 days after, or 12 days after balloon injury, and maintained under circumferential ten
72 otid artery in a time-dependent manner after balloon injury as compared with its levels in uninjured
73 ed intravenously beginning 15 minutes before balloon injury as either a high dose (0.5 mg/kg bolus an
74 timal hyperplasia was assessed after carotid balloon injury at 21 days by computerized morphometry.
75 was 7.6-fold elevated 3 hours (P<.05) after balloon injury, back to baseline at 2 days, increased ag
76 d Results- Rabbits subjected to iliac artery balloon injury (balloon denudation with or without stent
79 vided into 3 groups of 10 each: control (C), balloon injury (BI), and BI followed by ICBT (16 Gy at 0
83 24 hours, 3 days, 7 days, and 14 days after balloon injury by in situ hybridization, immunohistochem
84 g decreases neointimal hyperplasia following balloon injury, by inhibiting the inflammatory and throm
86 increased at 72 h, 1 week, and 2 weeks after balloon injury compared with its levels in uninjured lef
87 uli present at the site of coronary arterial balloon injury contribute to the progression and develop
88 nant genes in atherosclerotic arteries after balloon injury could inhibit intimal cell proliferation.
89 Tissue sections from arteries 3 days after balloon injury demonstrated rFGF2-SAP binding to medial
92 t New Zealand White rabbits underwent aortic balloon injury followed by a 1% cholesterol diet for 8 w
94 nary arteries) were subjected to overstretch balloon injury followed by IR with doses of 0 to 18 Gy o
97 ation promotes medial cell replication after balloon injury; however, signaling of intimal cell repli
99 iven locally in vivo at the site of coronary balloon injury in a porcine model, it can inhibit neoint
100 this hypothesis, we examined the response to balloon injury in atherosclerotic rabbit arteries after
101 of RAGE and S100/calgranulins in response to balloon injury in diabetic compared with nondiabetic rat
102 ons in vascular function and structure after balloon injury in hypercholesterolemic rabbits could be
121 ignaling by recombinant hirudin also blocked balloon injury-induced EGFR tyrosine phosphorylation and
122 d 15-HETE as a major eicosanoid and enhanced balloon injury-induced expression of MCP-1 in smooth mus
126 nduced VSMC growth and motility in vitro and balloon injury-induced neointima formation in vivo.
128 p27-p16 fusion protein, named W9, inhibited balloon injury-induced neointimal hyperplasia in rabbit
129 Furthermore, CsA and GFPVIVIT attenuated balloon injury-induced neointimal smooth muscle cell pro
131 ation of its levels substantially suppressed balloon injury-induced smooth muscle cell migration and
132 duction of Ad-15-LOX1 into arteries enhanced balloon injury-induced smooth muscle cell migration from
133 -mediated expression of dnSTAT-5B attenuated balloon injury-induced smooth muscle cell migration from
134 expression of dngp130 or dnSTAT-3 attenuated balloon injury-induced STAT-3 phosphorylation and cyclin
135 ome the blockade effect of NFATs by VIVIT on balloon injury-induced vascular wall remodeling events,
138 trated that endothelial recovery at sites of balloon injury is a critical determinant of consequent i
141 e similarly regulated in vivo in a rat aorta balloon injury model and found that p47(phox) protein wa
142 intimal hyperplasia in this porcine arterial balloon injury model compared with untreated or control
143 was evaluated in vitro and in a rat arterial balloon injury model following transduction with Ad-p27-
147 nsic pathway of coagulation, in a sequential balloon injury model of the rabbit abdominal aorta.
150 development of neointimal hyperplasia in the balloon injury model, this strategy has not been tested
154 e in vitro findings, the in vivo rat carotid balloon-injury model of restenosis evidenced that AC8 de
157 e role of Orai1 in neointima formation after balloon injury of rat carotid arteries and its potential
162 ) less neointima/media area ratio 14 d after balloon injury of the aorta compared with injured rats t
163 male, and the responsiveness of this gene to balloon injury of the artery is more rapid and more robu
164 the expression of RAGE and its ligands after balloon injury of the carotid artery in both Zucker diab
165 nts the neointimal proliferative response to balloon injury of the carotid artery in intact female ra
168 ns were administered 7 days before oversized balloon injury of the left anterior descending coronary
169 evelopment of myointimal proliferation after balloon injury of the rat carotid artery in vivo, (2) wh
170 he rapid SMC proliferation that occurs after balloon injury of the rat carotid artery using en face c
171 approach to test the hypothesis that, after balloon injury of the rat carotid artery, adventitial fi
172 or their effect on neointima formation after balloon injury of the rat carotid artery, both full-leng
179 neously [S.C.]) or vehicle, beginning before balloon injury of the right common carotid artery and co
180 17 beta-estradiol + MPA, or (4) vehicle, and balloon injury of the right common carotid artery was ca
184 raft survival, intimal hyperplasia following balloon injury or as seen in chronic graft rejection and
186 ant improvements in steatosis (P = .006) and ballooning injury (P = .005), with a reduction of mean N
187 ATA-6 gene transfer to the vessel wall after balloon injury partially restored the levels of GATA-6 p
194 -activated receptor gamma (PPAR gamma) after balloon injury significantly inhibits VSMC proliferation
196 rotid arteries were harvested at the time of balloon injury (T = 0) and at 0.5, 1, 2, and 4 hours aft
197 reater increase in neointima formation after balloon injury than that observed in intact females (P <
198 tallic stents had been placed at the site of balloon injury; the contralateral iliac artery of each r
200 at carotid arteries in the early hours after balloon injury, thus attenuating the stimulus for leukoc
204 creen of 11 rat strains by use of a standard balloon injury to the left iliac artery to observe wheth
207 creased again at 4 days, and by 7 days after balloon injury was 3.2-fold elevated (P<.05) when compar
209 e production of O2- by vessels 14 days after balloon injury was determined and correlated with circul
215 a formation in a model of rat carotid artery balloon injury was significantly attenuated after treatm
216 d rats, the induction of PAI-1 expression by balloon injury was significantly suppressed by 44% (P<.0
218 antibody to alphavbeta3, on the responses to balloon injury were tested in hyperlipidemic rabbits.
219 d wall, measured at both 4 and 29 days after balloon injury, were similar in the control and antibody
220 tory and thrombotic responses at the site of balloon injury, which appears to play a pivotal role in
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