CD36在冠状动脉成形术后再狭窄中的临床意义(3)
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[9] Glagov S. Intimal hyperplasia, vascular modeling, and the restenosis problem. Circulation, 1994, 89: 2888-2991.
[10] Welt FGP, Edelman ER, Simon DI, et al. Neutrophil, not macrophage, infiltration precedes neointimal thicking in balloon-injured arteries. Arterioscler Thromb Vasc Biol, 2000, 20: 2553-2258.
[11] Miller DD, Karim MA, Edwards WD, et al. Relationship of vascular thrombosis and inflammatory leukocyte infiltration to neointimal growth following porcine coronary artery stent placement. Atherosclerosis, 1996, 124: 145-155.
[12] Rahaman SO, Lennon DJ, Febbraio M, et al. A CD36-dependent signaling cascade is necessary for macrophage foam cell formation. Cell Metab, 2006, 4(3): 211- 221.
[13] Handberg A, Skjelland M, Michelsen AE, et al. Soluble CD36 inp lasma is increased in patients with symptomatic atheroscleroticca rotid plaques and is related to plaque instability. Stroke, 2008, 39 (11):3092-3095.
[14] Ferreira V, vanDijk KW, Groen AK, et al. Macrophage-specific inhibition of NF-kappaB activation reduces foam-cell formation. Atherosclerosis, 2006, 32: 83-97.
[15] Inoue T, Sakai Y, Fujito T, et al. Clinical significance of neutrophil adhesion molecules expression after coronary angioplasty on the development of restenosis. Thromb Haemost, 1998, 79: 54-58.
[16] Avanzas P, Arroyo-Espliguero R, Cosin-Sales J, et al. Markers of inflammation and multiple complex stenoses (pancoronary plaque vulnerability) in patients with non-ST segment elevation acute coronary syndromes. Heart, 2004, 90: 847-852.
[17] Abdullah U, Recep D, Remzi Y, et al. The relationship between plasma C-reactive protein levels and presence and severity of coronary stenosis in patients with stable angina. Angiology, 2008, 58(6): 657-662.
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