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Atherosclerosis development

Kleemann R, Princen HM, Emeis JJ, et al. Rosuvastatin reduces atherosclerosis development beyond and independent of its plasma cholesterol-lowering effect in APOE 3-Leiden transgenic mice Evidence for anti-inflammatory effects of rosuvastatin. Circulation 2003 108 1368-1374. [Pg.103]

Fuhrman, B. et al., Grape powder polyphenols attenuate atherosclerosis development in apolipoprotein E-deficient (E°) mice and reduce macrophage atherogenicity, J. Nutr., 135, 722, 2005. [Pg.152]

Rosenblat M., Volkova N., Coleman R., and Aviram M., Pomegranate by-product administration to apolipoprotein E-deficient mice attenuates atherosclerosis development as a result of decreased macrophage oxidative stress and reduced cellular uptake of oxidized low-density lipoprotein, J. Agric. Food. Chem., 54, 1928, 2006. [Pg.154]

Like any muscle, the heart requires a constant supply of oxygen and nutrients, which are carried to it by the blood in the coronary arteries. In CHD, plaques or fatty substances build up inside the walls of the arteries. The plaques also attract blood components (e.g., platelets) that stick to the artery wall lining. This process, called atherosclerosis, develops gradually, over many years. It often begins early in life, even in childhood. The fatty accumulation can break open and lead to the formation of a blood clot that seals the break. The presence of the blood clot occludes the vessel and reduces blood flow. [Pg.241]

Bell TA, III Brown JM, Graham MJ, Lemonidis KM, Crooke RM, Rudel LL. Liver-specific inhibition of acyl-coenzyme axholesterol acyltransferase 2 with antisense oligonucleotides limits atherosclerosis development in apolipoprotein BlOO-only low-density lipoprotein receptor-/- mice. Arterioscler Thromb. Vase. Biol. 2006 26 1814-1820. [Pg.1673]

This disorder has a late onset it rarely manifests itself in childhood. The most distinctive clinical presentation of dysiipoproteinemia is the presence of palmar xanthomas, the yellow deposits that occur in the creases of the palms. Tuberous and tuberoeruptive xanthomas also occur but are not unique to this syndrome. Premature atherosclerosis develops in 30% to more than 50% of these patients, particularly in the lower extremities. ... [Pg.930]

In brief, these findings shed light on the atheroprotective effects of captopril, which remained poorly understood over a long period of time. Specifically, captopril appears to limit atherosclerosis development by preventing EC dysfunction and inhibiting pro-inflammatory cell recruitment into the intima. [Pg.281]

Shen J, Herderick E, Comhill JF, Zsigmond E, Kim H-S, Kuhn H, Guevara NV, Chan L Macrophage-mediated 15-lipoxygenase expression protects against atherosclerosis development. [Pg.141]

HIO. Hulthe, J., and Fagerberg, B., Circulating oxidized LDL is associated with subclinical atherosclerosis development and inflammatory cytokines (AIR Study). Arterioscler. Thromb. Vase. Biol. 22, 1162-1167 (2002). [Pg.30]

Asset, G., Bauge, E., Wolff, R.L., Fruchart, J.C., and Dallongeville, J., Effects of dietary maritime pine seed oil on lipoprotein metabolism and atherosclerosis development in mice expressing human apolipoprotein B, Eur. J. Nutr., 40, 268-274, 2001. [Pg.293]

Magnolol, SM, or EGb Treatment Inhibited the Formation of Atherosclerotic Lesions. The atherosclerotic lesions (su-danophihc areas) in the thoracic aortas were prominent under enface observation in cholesterol-fed rabbits. The formation of the atherosclerotic lesions, as expressed by the ratio of atheroma area/total surface area of thoracic aorta, was significantly reduced with magnolol, SM, or EGb treatment compared with the control (C) group. These results indicated that treatment with magnolol or SM or EGb inhibited atherosclerosis development (36-38). [Pg.278]

It is well accepted that innate and adaptive immune mechanisms modnlate atherosclerosis [1,2] and immune responses to OSEs, such as OxPLs, play a central role in the development of atherosclerosis. [3] Following lipid accnmnlation in the vessel wall, atherosclerosis develops when the net balance between snbsets of immune cells and their products, such as proinflammatory and anti-inflammatory subsets of macrophages, B-1 cells and B-2 cells and their respective IgM and IgG antibodies, T effector cells and Tregs and co-stimulatory and co-inhibitory molecules tilts toward a pro-inflammatory phenotype [4]. [Pg.282]

Aviram, M., and Rosenblat, M. Paraoxonases 1, 2, and 3, oxidative stress, and macrophage foam cell formation during atherosclerosis development. Free Radic. Biol. Med. 2004 37(9) 1304-16. [Pg.379]

This result could be explained on the basis of the elevated PAF-acetylhydrolase activity in the plasma of rabbits of group B. This study shows that polar hpids of cultured gilthead sea bream (Sparns auratd) contain bioactive micro-constituents, PAF inhibitors, that inhibit PAF activity both in vitro and in vivo, consequently inhibiting early atherosclerosis development. The above data reinforce the beneficial effect of cultured gilthead sea bream polar lipids against atherosclerosis development (Nasopoulou et al., 2010). [Pg.299]

Although the in vitro and in vivo evidences indicate that berberine possesses cholesterol-lowering potential, a recent work suggested that promotion of foam cell formation by berberine could counterbalance its beneficial effects [38]. By using the model of atherosclerosis in apolipoprotein E-deficient mice, they showed that berberine induced in vivo foam cell formation and promoted atherosclerosis development. Thus, this effect could counterbalance the beneficial effect of this cholesterol-lowering compound on atherosclerosis. [Pg.4477]

Protective effects of low-dose suppemental vitamin C (1.0 g/kg diet) observed for only eight weeks after this time atherosclerosis developed. Protective effect of high-dose vitamin C (4.0 g/kg diet persisted for up to ten weeks). [Pg.337]

There are three levels of occlusive disease in the lower limb arteries aortoiliac, femoropopliteal, and infrapopliteal disease. Disease confined to one level may be asymptomatic or it can present with intermittent claudication. The presence of two or three levels of disease are symptomatic, and patients usually present with severe claudication or rest pain. Three levels of disease are often seen in patients with skin damage and critical limb ischemia. Without an intervention most limbs with critical ischemia will be amputated within 1 year. In patients with diabetes mellitus the disease is usually confined in the infrapopliteal vessels. Such patients may develop critical limb ischemia with one level of disease because this is the most distal of the three. Usually, multiple stenoses and/or occlusions are found in at least two of the run-off arteries. Although it is known that atherosclerosis develops most often in bifurcations, in the lower extremities the most frequently involved site is the superficial femoral artery. Other common sites are the aortoiliac, iliac, femoral popliteal, and tibioperoneal trunk bifurcations. [Pg.24]

Indicates the strongest correlation with atherosclerosis development. [Pg.102]


See other pages where Atherosclerosis development is mentioned: [Pg.124]    [Pg.918]    [Pg.236]    [Pg.56]    [Pg.919]    [Pg.827]    [Pg.285]    [Pg.136]    [Pg.145]    [Pg.147]    [Pg.148]    [Pg.289]    [Pg.106]    [Pg.45]    [Pg.369]    [Pg.218]    [Pg.1950]    [Pg.262]    [Pg.263]    [Pg.274]    [Pg.275]    [Pg.93]    [Pg.827]    [Pg.542]    [Pg.242]    [Pg.243]    [Pg.243]    [Pg.244]    [Pg.244]    [Pg.109]    [Pg.3624]    [Pg.127]   
See also in sourсe #XX -- [ Pg.44 , Pg.136 , Pg.145 , Pg.148 ]

See also in sourсe #XX -- [ Pg.123 ]

See also in sourсe #XX -- [ Pg.23 , Pg.766 ]

See also in sourсe #XX -- [ Pg.766 ]




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Atherosclerosis

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