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1 accumulation of modified lipoproteins in the arterial intima.
2  proliferation of smooth muscle cells in the arterial intima.
3 l (SMC) proliferation and migration into the arterial intima.
4 and uptake into macrophage foam cells in the arterial intima.
5 tion of lipoproteins on proteoglycans in the arterial intima.
6 s of platelet-derived growth factor-B in the arterial intima, a factor known to suppress smooth muscl
7 actors in the induction of thickening of the arterial intima after balloon angioplasty injury.
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.
10       The majority of cells infiltrating the arterial intima and myocardium were T cells and macropha
11             Human Bruch's membrane ages like arterial intima and other connective tissues for which p
12 trating macrophages, specifically within the arterial intima and perivascular areas.
13 is may induce trapping of macrophages in the arterial intima and promote atherosclerosis.
14             Blood-derived macrophages in the arterial intima are a characteristic feature of active a
15 s are both characterized by expansion of the arterial intima as a result of the infiltration of monon
16    While excessive atherogenic lipids in the arterial intima can trigger endothelial dysfunction in a
17 L), one of the main LDL modifications in the arterial intima, contributes to massive intracellular ch
18 trating CD8+ T cells, such as within a graft arterial intima, CTL subsets may emerge that display EC
19 on of each pair component, and also in mouse arterial intima during flow-induced remodeling.
20   Secretory phospholipase A2 activity in the arterial intima has the potential to amplify atherogenic
21 cells (VSMC) are associated with accelerated arterial intima hyperplasia and restenosis after angiopl
22 ositively correlated with the progression of arterial intima hyperplasia.
23 s a lipid-driven inflammatory disease of the arterial intima in which the balance of pro-inflammatory
24     The accumulation of myeloid cells in the arterial intima, including macrophages and dendritic cel
25 e trapping of lipid-laden macrophages in the arterial intima is a critical but reversible step in ath
26                                       In the arterial intima, lipoprotein components that are generat
27         The annual rate of change in carotid arterial intima-media thickness differed significantly b
28                                      Carotid arterial intima-media thickness is used as a noninvasive
29 erial far wall intima-media complex (carotid arterial intima-media thickness) at baseline and every 6
30 or each 0.03-mm increase per year in carotid arterial intima-media thickness, the relative risk for n
31                         Once resident in the arterial intima, monocytes accumulate lipid, via increas
32         Mononuclear cell infiltration of the arterial intima occurs in the absence of C6, but C6 defi
33 d to be elevated in diseased lower-extremity arterial intima of individuals with peripheral arterial
34  can occur at various sites (cardiac valves, arterial intima or media, capillaries), involve localize
35 and remodeling, leading to thickening of the arterial intima termed transplant vasculopathy or cardia
36 er segmental glomerulosclerosis and vascular arterial intima-to-lumen ratio.
37 ccumulation of oxidized phospholipids in the arterial intima, which are crucial for initiating plaque
38 ecules (eg, low-density lipoproteins) in the arterial intima, which is bordered by endothelial cells