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1 and uptake into macrophage foam cells in the arterial intima.
2 tion of lipoproteins on proteoglycans in the arterial intima.
3 accumulation of modified lipoproteins in the arterial intima.
4 proliferation of smooth muscle cells in the arterial intima.
5 l (SMC) proliferation and migration into the arterial intima.
6 s of platelet-derived growth factor-B in the arterial intima, a factor known to suppress smooth muscl
8 d may explain why graft rejection within the arterial intima, an anatomic compartment in which EC may
9 raft that accumulated in the endocardium and arterial intima and adventitia near draining lymphatics.
15 s are both characterized by expansion of the arterial intima as a result of the infiltration of monon
16 L), one of the main LDL modifications in the arterial intima, contributes to massive intracellular ch
17 trating CD8+ T cells, such as within a graft arterial intima, CTL subsets may emerge that display EC
19 Secretory phospholipase A2 activity in the arterial intima has the potential to amplify atherogenic
21 The accumulation of myeloid cells in the arterial intima, including macrophages and dendritic cel
22 e trapping of lipid-laden macrophages in the arterial intima is a critical but reversible step in ath
26 erial far wall intima-media complex (carotid arterial intima-media thickness) at baseline and every 6
27 or each 0.03-mm increase per year in carotid arterial intima-media thickness, the relative risk for n
30 can occur at various sites (cardiac valves, arterial intima or media, capillaries), involve localize
31 ecules (eg, low-density lipoproteins) in the arterial intima, which is bordered by endothelial cells
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