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1 geneous, composed of particles with variable atherogenicity.
2 me B cytotoxins in promoting CD4(+) NKT cell atherogenicity.
3  APOE posttranslational modification to L5's atherogenicity.
4  cell recruitment that may contribute to its atherogenicity.
5 ortant in determining the relative degree of atherogenicity.
6  nitration, additionally contributing to its atherogenicity.
7 profiles that often correlate with increased atherogenicity.
8 f its biochemistry, genetics, metabolism and atherogenicity.
9 l, and 3) explaining the mechanisms of lipid atherogenicity.
10 e may be a feature that contributes to their atherogenicity.
11 ion of LDL, particularly with respect to its atherogenicity.
12 prothrombotic mechanisms contributing to its atherogenicity.
13 tion, but this did not explain their greater atherogenicity.
14 EDAS were related to measures of lipoprotein atherogenicity and diabetes risk using multivariable-adj
15  polyunsaturated fatty acids, displaying low atherogenicity and thrombogenicity indexes (0.10 and 0.1
16 RS analysis allowed direct prediction of the Atherogenicity and Thrombogenicity indexes, which are us
17 utritional standpoint, displaying the lowest atherogenicity and thrombogenicity indices (0.02 and 0.1
18  lowest peroxide value, free fatty acid, and atherogenicity and thrombogenicity indices.
19                               The indices of atherogenicity and thrombogenicity were also within the
20                  In addition, the indices of atherogenicity and thrombogenicity were significantly re
21 ypes had statistically the lowest indices of atherogenicity and thrombogenicity.
22  Oxidative modification of LDL increases its atherogenicity, and 15-lipoxygenase (15-LO) has been imp
23 holesterol lowering, anti-inflammatory, anti-atherogenicity, and anti-cancer potential.
24 ay contribute to decreased oxidative damage, atherogenicity, and cardiovascular disease.
25 pathophysiology of atherosclerosis and Lp(a) atherogenicity, and the use of OxPL-apoB measurement for
26                Second, several mechanisms of atherogenicity are known to varying extent, but the rela
27 epatic ACAT2 could account for the increased atherogenicity associated with cholesteryl ester-enriche
28 tios, and the indices of thrombogenicity and atherogenicity depended on specific omega-3 PUFAs-rich o
29                       The mechanism of Lp(a) atherogenicity has not been elucidated, but likely invol
30     To evaluate lipid quality the indices of atherogenicity (IA) and thrombogenicity (IT) were calcul
31 , these results indicate that CAPN6 promotes atherogenicity in inflamed macrophages by disturbing CWC
32 itor several key determinants of lipoprotein atherogenicity including particle abundance, size, and l
33 7% - 32%, Polyunsaturated (EPUFA) 23% - 22%, Atherogenicity Index (AI) 0.64 - 0.75, Thrombogenicity I
34 holesterolemic acid ratios (HH) (0.87-2.43), atherogenicity index (IA) (0.26-0.60), and thrombogenici
35                                              Atherogenicity index and desaturase activity indices wer
36                                          The atherogenicity index was 0.29 and the thrombogenicity in
37 olyunsaturated to saturated fatty acids, the atherogenicity index, the thrombogenicity index, the hyp
38 72.3-77.1), thrombogenicity (1.22-1.45), and atherogenicity indices (0.53-0.58) did not differ betwee
39  sought to estimate TRL/remnant per-particle atherogenicity, investigate causal relationships with in
40                Although the mechanism of its atherogenicity is unknown, Lp(a) has been implicated in
41                                         This atherogenicity may be a reflection of the association of
42 wed us to address the question of the direct atherogenicity of chylomicrons and large VLDL.
43                   Research investigating the atherogenicity of diet-induced Lp(a) changes is needed t
44     APOE glycosylation may contribute to the atherogenicity of L5 and be a useful biomarker for rapid
45 ans-11 18:1) on the blood lipid profile, the atherogenicity of LDL, and markers of inflammation and i
46 sease (CAD) may enhance understanding of the atherogenicity of lipid fractions.
47 size reveals important information about the atherogenicity of lipoprotein profile.
48 s such as apolipoprotein B-100 increases the atherogenicity of low-density lipoproteins (LDL).
49                         We conclude that the atherogenicity of Lp(a) (CHD risk quotient per unit incr
50   However, the underlying mechanisms for the atherogenicity of Lp(a) are not completely understood.
51        From these data, we estimate that the atherogenicity of Lp(a) is approximately 6-fold (point e
52                  These data suggest that the atherogenicity of Lp(a) lipoprotein may be mediated in p
53 s and chronically elevated Lp(a) levels, the atherogenicity of Lp(a) may stem from its capacity as a
54 emotaxis, providing novel mechanisms for the atherogenicity of Lp(a).
55 sights into plaque rupture and the potential atherogenicity of Lp(a).
56 O-glycans that is potentially related to the atherogenicity of Lp(a).
57 pertriglyceridemia and may contribute to the atherogenicity of nephrotic dyslipidemia.
58 s, LPL in the artery wall might increase the atherogenicity of oxidized LDL, since it enables its bin
59  composition and structure and to reduce the atherogenicity of OxLDL by decreasing its lysoPC content
60                                 The relative atherogenicity of TGRL positively correlated with partic
61 se cholesterol transport) determine the anti-atherogenicity of the HDL fraction.
62  allow us to examine experimentally the anti-atherogenicity of the HDL subclasses.
63 e of RLP by the liver as well as the general atherogenicity of these particles.
64 plasma residence time, thereby elevating the atherogenicity of these particles.
65 obesity, and type 2 diabetes, and the marked atherogenicity of this condition.
66 rticles, and (v) exploration of the relative atherogenicity of TRL and remnants compared to LDL.
67                  To examine the per-particle atherogenicity of TRL/remnants and LDL, SNPs were catego
68 on, and determine whether differences in the atherogenicity of TRL/remnants and low-density lipoprote
69 gh less abundant, have substantially greater atherogenicity per particle than LDL.
70  TRL/remnants having a substantially greater atherogenicity per particle than LDL.
71 tor for coronary heart disease (CHD) but its atherogenicity relative to that of low-density lipoprote
72 of LDL forms small, dense LDL with increased atherogenicity that provides a new route to atherogenic
73                                    ApoCIII's atherogenicity was traditionally attributed to hypertrig