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Other researchers have used 3D US to monitor ulcerated plaques prospectively for more than a year, reporting that the vast majority of plaques (76.5%) remained unchanged, 23.5% of ulcerations regressed while only 5.8% of ulcerations progressed [61].
In contrast, for the majority of plaques, HS-129 and HS-136 only labeled the compact cores.
In young mice (4- to 6-month old), the most abundant plaques were those less than 500 μm (70.53 ± 9.74%), whereas in older mice (18 months) the vast majority of plaques (69.41 ± 11.73%) were medium to large (>500 μm).
A β immunostaining showed that there is a variety of different types of β-amyloid plaques at early stages, although the majority of plaques were tiny and compact (phase I); and both compact and diffuse plaques were observed at later stages, as shown in the therapeutic protocol (phase II).
A comparison of all fitted curves for each individual plaque (originating from the example in Figure 1b) highlighted the fact that only a few plaques became very large whereas the majority of plaques showed much flatter curves with slower Aβ accumulation.
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In the present study adiponectin is not correlated with calcified plaques, the majority of coronary plaques in our study cohort.
Results of this study confirm that most of the calcified plaques show smooth protruding sign surrounding the coronary ostium, as the majority of calcified plaques are ostial lesions, located in the proximal regions of the coronary arteries, particularly in the LAD.
Since the majority of coronary plaques was calcified, adiponectin levels account for only 3% of the variability in total plaque number.
In multiple sclerosis, the majority of active plaques show normal or increased diffusivity, but some may show restricted diffusion, often at the margins [68].
Because amyloid deposition is a gradual process, the majority of the plaques may have been deposited before the treatment had an effect.
With the C-terminal abAβx-42 a majority of neocortical plaques in all four patients were ring-shaped, as described in the first study on patient Sw1 [ 17], i.e. the weakly stained centres of larger plaques were surrounded by distinct immunoreactive coronas.
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