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1 s on pulsatile blood flow through the dorsal aortae.
2 uptake of the tracer in AAA than nondilated aortae.
3 elium-dependent relaxation in isolated mouse aortae.
4 ed specifically for formation of the lateral aortae.
5 tion in the atheroprotected section of mouse aortae.
6 n atherosclerotic lesions of ApoE(-/-) mouse aortae.
7 s, or increase MAPK activation in p47phox-/- aortae.
8 igh levels in LDLR knockout/IL-1ra transgene aortae.
9 on area was found by en face analysis of the aortae.
10 ra was present in C57BL/6J and LDLR knockout aortae, absent in IL-1ra knockout aortae, and present at
11 n microscopy techniques, we examined valves, aortae and coronary arteries from patients with and with
16 red endothelium-dependent relaxations of rat aortae and led to ER stress in endothelial cells, which
17 gain-of-function Notch alleles show enlarged aortae and underdeveloped cardinal veins, whereas those
18 or its receptor EphB4 also leads to enlarged aortae and underdeveloped cardinal veins; however, endot
19 ions in renal arteries, carotid arteries and aortae, and flow-mediated dilatations in third-order mes
20 expressed in endoderm underlying the lateral aortae, and loss of cxcl12b phenocopies cxcr4a deficienc
21 R knockout aortae, absent in IL-1ra knockout aortae, and present at high levels in LDLR knockout/IL-1
24 of two vascular beds are specified, but the aortae are distended and lack contact with the surroundi
25 tly upregulated in the medial layer of db/db aortae, as well as in thoracic aortic samples from patie
27 reased poly(ADP-ribosyl)ation of GAPDH in WT aortae, but not in the aortae from PARP-1-deficient mice
28 e also showed dilated thoracic and abdominal aortae compared with control ApoE-/- mice, although athe
29 layer of cells surrounding the paired dorsal aortae concomitant with its expression in the primitive
30 Analysis of smooth muscle cells from mouse aortae demonstrated that MIF deficiency reduced smooth m
33 kewise, although the primordia of the dorsal aortae formed normally, anomalies were observed in these
35 down-regulation of Hcy metabolic enzymes in aortae from Ang II-infused rats were prevented by BT tre
42 ibutes to activation of Vav-1, -2, and -3 in aortae from hyperlipidemic mice and that oxidatively mod
47 Furthermore, 1-hour in vitro incubation of aortae from streptozotocin-diabetic mice with various PA
48 milarly, vascular smooth muscle cells in the aortae from the LKLF-/- animals displayed a cuboidal mor
50 endothelium- and NO-dependent relaxation in aortae from wild-type mice, but not in aortae from homoz
51 um- and nitric-oxide-dependent relaxation in aortae from wild-type mice, but not in aortae from homoz
55 s a key factor that shapes the paired dorsal aortae in mouse, as sema3E(-/-) embryos develop an abnor
56 olesterol and surgically transplanting these aortae into recipient Apoe-deficient mice that were trea
58 VCAM-1 protein expression was increased in aortae obtained from hypercholesterolemic, oophorectomiz
59 ough the original bilaterality of the dorsal aortae occurs as the result of inhibitory factors (antag
60 size and complexity was observed within the aortae of age- and gender-matched apo E-/- and apo E-/-/
65 vessels from the aortic wall by loading the aortae of donor atherosclerotic Apoe-deficient mice with
67 eroprotective cytokine IL-10 were reduced in aortae of IRF5-deficient mice, and in vitro studies demo
69 erotic plaques, are also up-regulated in the aortae of mice with uPA-overexpressing macrophages, and
70 Endovascular stents were expanded in the aortae of obese insulin-resistant and type 2 diabetic Zu
71 nhanced phospho-Ser536 RelA formation in the aortae of rats chronically infused with Ang II was obser
74 cent cells was similarly observed in vivo in aortae of young Zucker diabetic rats, compared with lean
76 g by vasculogenesis (particularly the dorsal aortae) or angiogenesis, but low in vessels forming by c
79 the groups, whereas en face analysis of the aortae revealed a dose-dependent effect of macrophage LP
80 abeling of organ cultures of embryonic chick aortae revealed rapid formation of disulfide-cross-linke
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