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Atherosclerotic progression

Blake, 1989 Winyard et al., 1989). We suggest that within the inflamed rheumatoid joint (or the artery wall in atherogenesis), the production of ROM and proteases by endothelial cells and/or macrophages may cause the release of copper ions from Cp (see Section 2.2.3.2). It has been reported that Cp is cleaved faster in serum from patients with inflammatory diseases when compared to normal serum (Laurell, 1985). The oxidative modification of LDL by Cp-derived copper ions may explain the observation that increased serum cholesterol values are associated with accelerated atherosclerotic progression in men with high serum copper concentrations (Salonen et al., 1991). [Pg.107]

Treating mice with 23 led to the inhibition of atherosclerotic progression, whereas macrophage-specific knockout of LXR exacerbates atherosclerosis [111]. In vivo activation of LXR leads to increased fatty acid synthesis, accumulation of TG and the development of hepatic steatosis [109]. Successful LXR agonists will show desirable HDL elevation without these side effects [112]. [Pg.187]

ASAP 6 yr 520 M-F Supplementation with combination of vitamin and slow release vitamin C slow down atherosclerotic progression in hypercholesterolemic persons (214)... [Pg.231]

Salonen RM, Nyyssonen K, Kaikkonen J, et al. Six-years effect of combined vitamin C and E supplementation on atherosclerotic progression. The Antioxidant Supplementation on Atherosclerotic Progression. Circulation 2003 107 947-953. [Pg.239]

Salonen, J.T. and Salonen, R. (1993) Ultrasound B-mode imaging in observational studies of atherosclerotic progression. Circulation. 87(suppl II) 56—65. [Pg.237]

Ge is suggested to possess antioxidative properties, but this did not lead to any attenuation of atherosclerotic progression in Kurosawa hypercholsterolemic (KHC) rabbits (Wakabayshi 2001). Furthermore, the excessive intake of Ge-containing supplements induced acute renal failure or renal (Schauss 1991) and multi-organ (Luck et al. 1999) dysfunction in humans. [Pg.790]

Wellenius GA, Mukamal KJ, Kulshreshtha A, et al. Depressive symptoms and the risk of atherosclerotic progression among patients with coronary artery bypass grafts. Circulation 2008 117 2313-2319. [Pg.346]

Atherosclerotic lesion l Monocyte recruitment l Progression of atherosclerosis... [Pg.942]

PPARa Liver, heart, skeletal muscle, atherosclerotic lesions TG- and LDL-C-lowering and HDL-C-raising re-directs excess cholesterol from the peripheral tissues to the liver for excretion into the bile via HDL-C slowed progression of atherosclerosis Fatty acids, eico-sanoids (fatty acids derived from FAS ) Fibrates fenofibrate (Tricor ), genfibrozil (Lopid ) Dyslipidemia... [Pg.945]

PPARy White adipose tissue, atherosclerotic lesions Insulin-sensitizing and glucoselowering re-directs TG from non-adipose tissues and visceral adipose depots for storage in subcutaneous adipose tissue slowed progression of atherosclerosis Fatty acids, eico-sanoids Th iazolid i ned iones pioglitazone (Actos ), rosiglita-zone (Avandia ) Type 2 diabetes, (insulin resistance, metabolic syndrome)... [Pg.945]

Reducing LDL cholesterol while substantially raising HDL cholesterol (statin + niacin) appears to reduce the risk of atherosclerotic disease progression to a greater degree than statin monotherapy. [Pg.175]

The primary goal of lipid-lowering therapies in CKD is to decrease the risk for progressive atherosclerotic cardiovascular disease (Table 76-1). [Pg.875]

Atherosclerosis, a disease of the vascular wall, is the substrate for the arterial forms of CVD. Atherosclerotic plaques exhibit a focal distribution along the arterial tree as a consequence of local conditions that favor their initiation and progression. Low or reversed shear stress, for example, contributes to plaque development, a process in which the regulation of several genes may be involved (Resnick and Gimbrone 1995). [Pg.217]

Atherosclerosis is a progressive vascular fibroproliferative-inflammatory disease. It is triggered, maintained, and driven by risk factors such as hypercholesterolemia, hyperlipidemia, and hypertonus [28]. The characteristic clinical manifestation of atherosclerosis is the atherosclerotic lesion, developing in the vessel wall (atherosclerotic plaque). [Pg.91]


See other pages where Atherosclerotic progression is mentioned: [Pg.176]    [Pg.187]    [Pg.387]    [Pg.376]    [Pg.345]    [Pg.140]    [Pg.664]    [Pg.176]    [Pg.187]    [Pg.387]    [Pg.376]    [Pg.345]    [Pg.140]    [Pg.664]    [Pg.130]    [Pg.225]    [Pg.226]    [Pg.443]    [Pg.127]    [Pg.24]    [Pg.46]    [Pg.49]    [Pg.49]    [Pg.192]    [Pg.67]    [Pg.72]    [Pg.191]    [Pg.200]    [Pg.207]    [Pg.208]    [Pg.209]    [Pg.221]    [Pg.222]    [Pg.74]    [Pg.791]    [Pg.919]    [Pg.220]    [Pg.178]    [Pg.608]    [Pg.140]    [Pg.270]   
See also in sourсe #XX -- [ Pg.790 ]




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