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A case of lipid core plaque progression and rupture at the edge of a coronary stent: elucidating the mechanisms of drug-eluting stent failure.
In the case of a vessel model with a fibrotic core plaque, the lumen healthy areas that suffer a contact pressure higher than 0.25 MPa are reduced from 36.86% to 22.38% for the left healthy area (LHA), and from 40.13% to 21.36% in the right healthy area (RHA).
The lipid core plaque (LC) is responsible for stenosis of the aorta (AO).
Substitution of these histidine residues or agents that would mask these histidine residues may have therapeutic potential for preventing neuronal uptake and subsequent accumulation in neurons and ultimately the destruction of the neuron and drive the protein to the protective pathway involving diffuse/compact/dense core plaque accumulation.
These include a thin fibrous cap overlying a large lipid core, plaque inflammation and the presence of microchannels [ 2, 4, 5].
Carotid bifurcation, which is situated in a transitional zone between elastic and muscular artery types, also develops foam-cell lesions and lipid core plaque at an early age.
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In the sonicated volume, Trypan blue (red) co-localized with FITC-3d6 signal (green) and stained dense core plaques.
These data were confirmed by analysis of Thioflavin S-positive core plaques measured in the brains of experimental and control mice (Figure 5B).
Vaccination significantly reduced Aβ burden (both diffuse and core plaques) in several areas of the brains of immune mice versus control animals at age 18±0.5 mo (Figure 5A).
Collectively, these results suggest that the DNA epitope vaccine is effective in reducing amyloid burden (diffuse and core plaques) in the brains of 3xTg-AD mice, which at the start of immunization did not possess Aβ pathology (protective vaccination).
Substitution of the histidine residues, therefore, is hypothesized to drive Aβ along a protective pathway that will ultimately result in the increased accumulation of diffuse/compact/dense core plaques (modeled in Figure 6).
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