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1 elium-dependent relaxation in isolated mouse aortae.
2 ed specifically for formation of the lateral aortae.
3 tion in the atheroprotected section of mouse aortae.
4 n atherosclerotic lesions of ApoE(-/-) mouse aortae.
5 s, or increase MAPK activation in p47phox-/- aortae.
6 s on pulsatile blood flow through the dorsal aortae.
7 igh levels in LDLR knockout/IL-1ra transgene aortae.
8  uptake of the tracer in AAA than nondilated 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
12 ty to atherosclerosis was evaluated in whole aortae and cross sections of the aortic sinus in male an
13                                          Rat aortae and cultured rat aortic endothelial cells were tr
14 ed the vasoactivity elicited by Abeta in rat aortae and in human middle cerebral arteries.
15                      In contrast, the dorsal aortae and intersegmental arteries caudal to the heart w
16 e with loss-of-function mutations show small aortae and large cardinal veins.
17 red endothelium-dependent relaxations of rat aortae and led to ER stress in endothelial cells, which
18 gain-of-function Notch alleles show enlarged aortae and underdeveloped cardinal veins, whereas those
19 or its receptor EphB4 also leads to enlarged aortae and underdeveloped cardinal veins; however, endot
20 ions in renal arteries, carotid arteries and aortae, and flow-mediated dilatations in third-order mes
21 expressed in endoderm underlying the lateral aortae, and loss of cxcl12b phenocopies cxcr4a deficienc
22 R knockout aortae, absent in IL-1ra knockout aortae, and present at high levels in LDLR knockout/IL-1
23                               Hearts, lungs, aortae, and pulmonary arteries from lipopolysaccharide-t
24 ndothelial extracellular matrix in progeroid aortae, and ultrasound assessment of live HGPS mice reve
25                                        In WT aortae, Ang II increased NADPH-dependent O2- production
26  of two vascular beds are specified, but the aortae are distended and lack contact with the surroundi
27 tly upregulated in the medial layer of db/db aortae, as well as in thoracic aortic samples from patie
28                           Autoradiography of aortae at 2 h postinjection revealed high uptake of [(99
29 ling event is the fusion of bilateral dorsal aortae at the midline to form the dorsal aorta.
30 reased poly(ADP-ribosyl)ation of GAPDH in WT aortae, but not in the aortae from PARP-1-deficient mice
31 e also showed dilated thoracic and abdominal aortae compared with control ApoE-/- mice, although athe
32 layer of cells surrounding the paired dorsal aortae concomitant with its expression in the primitive
33   Analysis of smooth muscle cells from mouse aortae demonstrated that MIF deficiency reduced smooth m
34        Dorsal and anterior to the heart, the aortae exhibited abnormally small lumens, as did the ant
35               However, in the fibulin-2 null aortae, fibulin-1 immunostaining was increased in the in
36 kewise, although the primordia of the dorsal aortae formed normally, anomalies were observed in these
37 ily associated with the endothelial layer of aortae; freshly isolated aortic ECs released >10-fold mo
38                                              Aortae from Ang II-infused ApoE-/-OPN-/- mice expressed
39  down-regulation of Hcy metabolic enzymes in aortae from Ang II-infused rats were prevented by BT tre
40                         Exposure of thoracic aortae from AT-deficient animals to ox-LDL (0-500 microg
41          Endothelial function was reduced in aortae from Bmal1-KO mice and improved by scavenging rea
42                                              Aortae from Bmal1-KO mice exhibited enhanced superoxide
43 vity and covalent modification were found in aortae from diabetic animals.
44 on in aortae from wild-type mice, but not in aortae from homozygous null SR-BI knockout mice.
45 on in aortae from wild-type mice, but not in aortae from homozygous null SR-BI knockout mice.
46 ibutes to activation of Vav-1, -2, and -3 in aortae from hyperlipidemic mice and that oxidatively mod
47 ls (BAECs) exposed to HOG-LDL or in isolated aortae from mice fed an atherogenic diet.
48                                              Aortae from mice were harvested at 4-hour intervals for
49                                              Aortae from p47phox-/- and matched wild-type (WT) mice (
50 )ation of GAPDH in WT aortae, but not in the aortae from PARP-1-deficient mice.
51   Furthermore, 1-hour in vitro incubation of aortae from streptozotocin-diabetic mice with various PA
52 milarly, vascular smooth muscle cells in the aortae from the LKLF-/- animals displayed a cuboidal mor
53                                           In aortae from TXNIP-deficient mice, TNF-induced VCAM1 expr
54  endothelium- and NO-dependent relaxation in aortae from wild-type mice, but not in aortae from homoz
55 um- and nitric-oxide-dependent relaxation in aortae from wild-type mice, but not in aortae from homoz
56                  Here, we report that dorsal aortae fusion is tightly regulated by a change in signal
57                                       During aortae fusion, the notochord ceases to exert its negativ
58 human AAA (HAAA) sections compared to normal aortae (HA).
59 ntrast, Akita-Elane(-/-) and Akita-Pad4(-/-) aortae had TXB(2) levels similar to wild type.
60 s a key factor that shapes the paired dorsal aortae in mouse, as sema3E(-/-) embryos develop an abnor
61 olesterol and surgically transplanting these aortae into recipient Apoe-deficient mice that were trea
62 nd VEGF at the midline, fusion of the dorsal aortae is signaled.
63   VCAM-1 protein expression was increased in aortae obtained from hypercholesterolemic, oophorectomiz
64 ough the original bilaterality of the dorsal aortae occurs as the result of inhibitory factors (antag
65  size and complexity was observed within the aortae of age- and gender-matched apo E-/- and apo E-/-/
66 igher in both intact and endothelium-denuded aortae of Akita mice.
67 ects in coverage and association with dorsal aortae of alpha-smooth-muscle-actin-positive cells.
68             [2H]-Cholesterol was retained in aortae of anti-VEGFR3-treated mice.
69 etermined in the ascending and the abdominal aortae of ApoE(-/-) and wild-type mice.
70                 Histological analysis of the aortae of ApoE(-/-) and WT mice showed that increased pu
71  and weaker banded structure observed in the aortae of Apoe(-/-) mice in response to AngII, were subs
72                          Histologically, the aortae of DAPT-treated Apoe(-/-) mice had significant re
73              VEZF1 expression was reduced in aortae of diabetic mice and upregulated in diabetic muri
74  vessels from the aortic wall by loading the aortae of donor atherosclerotic Apoe-deficient mice with
75 RNA and protein levels were downregulated in aortae of hypertensive rats.
76 eroprotective cytokine IL-10 were reduced in aortae of IRF5-deficient mice, and in vitro studies demo
77                                              Aortae of mice treated with Ang II antagonism had fewer
78 erotic plaques, are also up-regulated in the aortae of mice with uPA-overexpressing macrophages, and
79     Endovascular stents were expanded in the aortae of obese insulin-resistant and type 2 diabetic Zu
80 nhanced phospho-Ser536 RelA formation in the aortae of rats chronically infused with Ang II was obser
81          Immunohistochemical staining of the aortae of spontaneously hypertensive rats demonstrated s
82 xide synthase mRNA expression upregulated in aortae of these mice.
83 cent cells was similarly observed in vivo in aortae of young Zucker diabetic rats, compared with lean
84                           Exposure of rabbit aortae or ECs to normal flow (12 dyn/cm2, 24 hours) was
85 g by vasculogenesis (particularly the dorsal aortae) or angiogenesis, but low in vessels forming by c
86                    Real-time PCR analysis of aortae retrieved from apoE-/- mice demonstrated increase
87 ts in an age-dependent manner, compared with aortae retrieved from C57BL/6 control animals.
88  the groups, whereas en face analysis of the aortae revealed a dose-dependent effect of macrophage LP
89 abeling of organ cultures of embryonic chick aortae revealed rapid formation of disulfide-cross-linke
90                    By 24 weeks of age, Akita aortae showed markedly impaired relaxation in response t
91 ller fatty streaks in the cusp region of the aortae than did P-selectin-positive mice.
92                      Compared with wild-type aortae, the thromboxane metabolite TXB(2) was roughly 10
93                                Mouse C57BL/6 aortae transduced with adenoviruses containing A20 (or b
94 etic mice and upregulated in diabetic murine aortae upon systemic inhibition of mmu-483*.
95                                    Comparing aortae, vena cavae, and femoral vessel bundles, we ident
96 response were diminished in Egr-1-/-/apoE-/- aortae versus apoE-/-.
97                                          Rat aortae were banded between the origins of the left renal
98      After 19 weeks on the atherogenic diet, aortae were collected for quantitative analysis of the e
99                                     Thoracic aortae were excised from anesthetized animals and cut in
100                                          Rat aortae were isolated 4 days after balloon injury, mainta
101               VSMCs cultured from PRKO mouse aortae were markedly hyperproliferative, and their growt
102        Adult male Sprague-Dawley rats, whose aortae were studied in an in vitro preparation.

 
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