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1  by TEMRI in 22 subjects (8 normals, 14 with aortic atherosclerosis).
2 ensitivity, but also ameliorated significant aortic atherosclerosis.
3 nt (Ldlr-/-) C57BL/6 male mice had increased aortic atherosclerosis.
4 e in the elderly and in patients with severe aortic atherosclerosis.
5 ce developed significantly more diet-induced aortic atherosclerosis.
6 rol levels on a chow diet and develop severe aortic atherosclerosis.
7 <.001 for IgM) correlated with the extent of aortic atherosclerosis.
8 od pressure is independently associated with aortic atherosclerosis.
9 od may prove useful for the in vivo study of aortic atherosclerosis.
10 d for quantitative analysis of the extent of aortic atherosclerosis.
11 s noted in apoE(-/-) and LDLR(-/-) mice with aortic atherosclerosis.
12 complementary information regarding thoracic aortic atherosclerosis.
13 s recently been associated with coronary and aortic atherosclerosis.
14  paralleled the susceptibility to developing aortic atherosclerosis.
15 /PC-treated mice demonstrated no increase in aortic atherosclerosis (11 +/- 1% versus 10 +/- 4%, P=NS
16 e at 25 weeks demonstrated a 32% increase in aortic atherosclerosis (11 +/- 1% versus 15 +/- 4%, P=.0
17  FvQ/Q,ApoE-/- mice (n=8) had developed more aortic atherosclerosis (40+/-6% lesion area) compared wi
18  Predictors of type I outcomes were proximal aortic atherosclerosis, a history of neurologic disease,
19 sis and risk of being in the top quartile of aortic atherosclerosis after adjustment for the Framingh
20  deposits is an indicator of the presence of aortic atherosclerosis and an independent predictor of c
21 iation between atherosclerosis risk factors, aortic atherosclerosis and aortic valve abnormalities in
22    Early-life risk factor exposure increases aortic atherosclerosis and blood pressure in humans and
23 s used to assess independent associations of aortic atherosclerosis and cardiovascular events.
24                  An atherogenic diet induced aortic atherosclerosis and exacerbated cerebral beta-amy
25                 LCHP-fed mice developed more aortic atherosclerosis and had an impaired ability to ge
26 nant A-I(Milano)/PC prevented progression of aortic atherosclerosis and reduced lipid and macrophage
27  MaxV50 was strongly predictive of extent of aortic atherosclerosis and risk of being in the top quar
28 ivariate analysis, prior neurological event, aortic atherosclerosis, and duration of cardiopulmonary
29 oke were prior neurological event, diabetes, aortic atherosclerosis, and the combined end points of l
30 tly underestimated the severity of ascending aortic atherosclerosis, and this underestimation was mor
31    Atherosclerosis risk factors and proximal aortic atherosclerosis are independently associated with
32                       MR imaging measures of aortic atherosclerosis are predictive of future adverse
33       A direct comparison of the severity of aortic atherosclerosis between female LDLr(-/-) and LDLr
34 heart failure, left ventricular hypertrophy, aortic atherosclerosis, bicaval venous cannulation, with
35  of beta-arrestin2 in ldlr(-/-) mice reduced aortic atherosclerosis by 40% and decreased the prevalen
36 , apoA-IMilano gene therapy (n = 15) reduced aortic atherosclerosis by 65% (p < 0.001) and plaque mac
37 up to 50%, whereas HL-S145G markedly reduced aortic atherosclerosis by up to 96% (p < 0.02) in both m
38                                     Finally, aortic atherosclerosis development was significantly low
39 s on the extent and severity of coronary and aortic atherosclerosis, even in the presence of a favora
40 tension, a major risk factor for stroke, and aortic atherosclerosis has not been determined in the ge
41 ations between atherosclerosis risk factors, aortic atherosclerosis (imaged by transesophageal echoca
42 thesis that apo A-I(Milano)/PC would inhibit aortic atherosclerosis in apo E-deficient mice.
43  CRP transgene expression causes accelerated aortic atherosclerosis in apoE-/- mice.
44 non-HDL-C, or on the development of proximal aortic atherosclerosis in C57Bl/6, apoE-KO, or LDLr-KO m
45 pid profile led to significantly lower (65%) aortic atherosclerosis in hABCA1-Tg mice.
46  associated with the presence or severity of aortic atherosclerosis in the general population.
47 E-/- mice developed considerably accelerated aortic atherosclerosis in the presence of a similar seru
48 OUTCOME MEASURES: Prevalence of coronary and aortic atherosclerosis in the US armed forces and by age
49 es the severity of asymptomatic coronary and aortic atherosclerosis in young people.
50        In control mice, from 20 to 25 weeks, aortic atherosclerosis increased by 59% (11 +/- 1% versu
51                                The extent of aortic atherosclerosis increased from 2 to 3 mo and from
52    Quantitative morphometric analysis of the aortic atherosclerosis indicated that the transgenic ani
53 inical and pathologic evidence that thoracic aortic atherosclerosis is an important embolic source, d
54 his study was to investigate whether complex aortic atherosclerosis is associated with increased risk
55              In selected high-risk patients, aortic atherosclerosis is associated with increased risk
56                                              Aortic atherosclerosis may not be an independent risk fa
57                                  Measures of aortic atherosclerosis may provide heritable quantitativ
58 g history were independently associated with aortic atherosclerosis of any degree (P:</=0.001) and wi
59 d pressure variables associated with complex aortic atherosclerosis (protruding plaques >/=4 mm thick
60 presence of intracranial but not coronary or aortic atherosclerosis significantly increased the odds
61 serum lipoprotein levels and the presence of aortic atherosclerosis suggested that intrinsic alterati
62 an the unstable group and significantly less aortic atherosclerosis than each of the other 2 groups.
63 so lacked TLR4 or MyD88 demonstrated reduced aortic atherosclerosis that was associated with reductio
64 ible to identify perioperatively significant aortic atherosclerosis (using transesophageal echocardio
65 igh-fat feeding, pneumonitis was absent, but aortic atherosclerosis was 2- to 6-fold greater in beta3
66                                              Aortic atherosclerosis was almost completely prevented i
67                                              Aortic atherosclerosis was analyzed in low-density lipop
68   After 22 weeks of treatment, rank order of aortic atherosclerosis was control>vitamin E (with or wi
69 transplantation, at which time the extent of aortic atherosclerosis was determined.
70 ciation between blood pressure variables and aortic atherosclerosis was evaluated by multiple logisti
71         The association between genotype and aortic atherosclerosis was examined in 145 human aortas.
72                                              Aortic atherosclerosis was identified with Sudan IV stai
73 om the pro-atherogenic plasma lipid profile, aortic atherosclerosis was increased 10-fold in ABCA1-Tg
74                                     Advanced aortic atherosclerosis was induced in 18 rabbits by athe
75                                The extent of aortic atherosclerosis was measured by planimetry of the
76                                              Aortic atherosclerosis was measured by quantifying mean
77                                              Aortic atherosclerosis was present in all mice on the hi
78                       Despite decreased HDL, aortic atherosclerosis was significantly reduced (-35% t
79 edicting the top quartile of gender-specific aortic atherosclerosis were 0.57, 0.60, and 0.75 for mod
80 , however, SCD1 inhibition strongly promoted aortic atherosclerosis, which could not be reversed by d

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