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Thus, research targeting the qualitative and quantitative assessment of coronary plaques, including the assessment of plaque size, plaque composition and plaque remodelling, has become feasible.
Our results showed negative relationships between adsorption rate and plaque size, plaque productivity, and emigration rate, but only to a certain extent.
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Introduction of the GFP-Sma plasmid into sma− cells rescued the null mutant phenotype and produced normal WT size plaques on bacterial lawns, rather than the enormous plaques seen with the sma− mutant (Fig. 1I, sma−+GFP-Sma), indicating that sma gene knockout was responsible for the altered plaque size.
Both phages GFP-N-λ and GFP-C-λ formed normal size plaques as compare to the wild-type λKM10 vector phage and stably expressed GFP even after several consecutive amplification cycles.
One of these mixtures contained different sized plaques to see whether plaque size affected clonality estimation.
Furthermore, in the presence of amber codon between gpD and GFP genes this phage formed normal-size plaques and stably expressed GFP even after several cycles of phage amplification.
No obvious larger size of plaque was found.
The software was programmed to measure the number of plaques and the average size of plaques after thresholding for colour.
Univariate general linear model (GLM) analysis was used to compare sizes of plaque calcifications determined with OCT with those determined with dual-energy multidetector CT, and the significance of factors such as cardiac motion was assessed.
The same correlation was revealed for the number and average size of plaques (Fig. 2e, f).
The number and size of plaques were then analyzed and recorded.
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