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The same LASSS treatment also conferred nitration resistance with a greater effect for Y198 than Y250, indicating a novel mechanism independent of an anti-oxidative function of LASSS
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126 It is generally thought that the disease initiation involves activation of endothelial cells to express chemotactic factors and cell adhesion molecules that mediate recruitment of blood monocytes into the arterial intima, where they differentiate into macrophages and, following uptake of LDL particles, eventually become lipid-laden foam cells involved in atherosclerotic plaque formation
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