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1 himeric recipient origin in association with arteriosclerotic alterations.
2 d aortic aneurysms was compared with that of arteriosclerotic aneurysms.
3 Disruption of CXCR3+ Th1 cell trafficking to arteriosclerotic arteries may contribute to the therapeu
4  and had lower ejection fraction and greater arteriosclerotic burden but less severe AS.
5 [95% CI, 3.2-22]) and variables representing arteriosclerotic burden.
6 sclerosis, diabetes, and uremia that promote arteriosclerotic calcification-elicit the ectopic vascul
7  obesity, hyperlipidemia, hyperglycemia, and arteriosclerotic calcification.
8  is an early key event in the development of arteriosclerotic cardiovascular disease (ASCVD), thus an
9 y-lowering B-vitamin intervention may reduce arteriosclerotic cardiovascular disease event rates in p
10                                              Arteriosclerotic cardiovascular disease is the leading c
11 ns reduced the rate of the primary composite arteriosclerotic cardiovascular disease outcome (myocard
12 w therapeutic strategy for the prevention of arteriosclerotic cardiovascular disease.
13 onvenient assessment method to contribute to arteriosclerotic cardiovascular screening.
14                       Several differences in arteriosclerotic changes in both the grey and white matt
15  mice, and we show that IFN-gamma can induce arteriosclerotic changes in the absence of detectable im
16                   It was of interest that no arteriosclerotic changes were observed for the duration
17 cipients shows that IFN-gamma contributes to arteriosclerotic development following transplantation.
18 drome are affected by accelerated, premature arteriosclerotic disease that leads to heart attacks and
19 S activity as a result of ischemia or native arteriosclerotic disease, iNOS gene therapy may serve to
20 tonomous influence in experimental models of arteriosclerotic disease, which may have implications wi
21  littermate control WT mice developed robust arteriosclerotic disease.
22 es <50% narrowing, and controls were free of arteriosclerotic disease.
23  phenotypic response that promotes occlusive arteriosclerotic disease.
24 , a cytokine characteristically expressed in arteriosclerotic diseases, acts directly on vascular smo
25 edial immunoprivilege, are typically seen in arteriosclerotic diseases, such as atherosclerosis and t
26 lls that may contribute to the chronicity of arteriosclerotic diseases.
27 ies have identified increased mortality from arteriosclerotic heart disease among black men working i
28 T cells are essential in the early stages of arteriosclerotic lesion development after cardiac transp
29 ients underwent allograft biopsies to assess arteriosclerotic lesions and endothelial activation, end
30 ciated with cell growth and is active within arteriosclerotic lesions but is not known to be triggere
31 coronary artery, which naturally accumulates arteriosclerotic lesions in migrating salmon, we partial
32 s of heme oxygenase action on heme, prevents arteriosclerotic lesions that occur following aorta tran
33 ions or cell death have been detected within arteriosclerotic lesions, and it is known that microbial
34 othelial dysfunction, systemic inflammation, arteriosclerotic lesions, and left ventricle remodeling,
35 ved myocardial architecture and were free of arteriosclerotic lesions.
36 ells may help prevent their proliferation in arteriosclerotic lesions.
37                         A total of 492 total arteriosclerotic outcomes (primary outcome) and 317 CHF
38 he independent relationship between tHcy and arteriosclerotic outcomes and congestive heart failure (
39 nd may contribute to the excess incidence of arteriosclerotic outcomes experienced by both patient gr
40              No association between tHcy and arteriosclerotic outcomes was observed in a univariate m
41 rhomocysteinemia, a putative risk factor for arteriosclerotic outcomes, is seen in >85% of hemodialys
42 otal homocysteine levels are associated with arteriosclerotic outcomes.
43 ts provide a link between HCMV infection and arteriosclerotic plaque formation.
44 ll-surface molecules that cause the observed arteriosclerotic responses.
45 se because of significant atherosclerotic or arteriosclerotic risk factors, high-risk conditions that
46 temic neutralization of IL-6R did not reduce arteriosclerotic thickening but reduced endothelial inte
47 ed the development of vascular rejection and arteriosclerotic thickening.
48 o the benefit of our patients afflicted with arteriosclerotic valvular and vascular diseases.
49 NO) bioavailability has been demonstrated in arteriosclerotic vascular disease, the integrity of this
50 e of the underlying disease and/or unrelated arteriosclerotic vascular events.
51 r smooth muscle cell PTH1R activity inhibits arteriosclerotic Wnt/beta-catenin signaling and reduces
52 of vascular PTH receptor (PTH1R) activity on arteriosclerotic Wnt/beta-catenin signaling in vitro and