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As fluoride binding to the plaque reservoirs and the release from the reservoir is rather complex, the source of the fluoride may play an important role.
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They found that some NSAIDs--naproxen and two forms of ibuprofen--blocked FDDNP from binding to the plaques, indicating that the drugs themselves had already latched on.
To some extent, gallium may also be taken up by atherosclerotic plaques due to its binding to the circulating transferrin and avidly to the transferrin receptors at the site of atherosclerotic arteries.
Articles reporting quantification with other β-amyloid compounds have been excluded when (a) there was uncertainty about the selectiveness of the binding to amyloid plaques (e.g., C BF-227) or (b) utilization of recently released compounds still needing for a systematic evaluation (e.g., F-AZ4694, namely, NAV4694).
The combined binding of scV/Tc to both macrophages and endothelial cells in plaque neoangiogenesis in theory provide two targets for scV/Tc binding to boost plaque signal [8],[8]],[8]].
As predicted by computed models, we have demonstrated using in vivo bioassays that dual-targeted MPIO markedly enhance binding to atherosclerotic plaque endothelium compared to single-ligand MPIO (7-fold increase in binding compared with P-selectin-MPIO and 6-fold increase compared with VCAM-MPIO) (Fig. 3A) [11].
Moreover, this derivative also exhibited similar binding to amyloid plaques in the AD mouse brain as Aβ40 (Figure 5).
When binding to Aβ plaques and NFTs, the asymmetric LCO HS-72 emitted light with a variation in color, although the red shift of tau was not as evident as with p-FTAA (difference between means=−0.1535±0.008382; R=0.7529; Figure 3 E, and Supporting Information, Table S1).
A newly developed calcium phosphate remineralization technology based on casein phosphopeptide-stabilized amorphous calcium phosphate (CPP-ACP) stabilizes high concentrations of calcium and phosphate ions, together with fluoride ions, in an amorphous state, at the tooth surface by binding to pellicle and plaque [5].
The authors suggested that ApoE may participate in aggregate formation in the AD brain by binding to AGE-modified plaque components, which may explain why ApoE4 is associated with increased risk of AD.
Given that initial brain influx would be expected to be the same in both mouse models, and differential retention of 18F-7B in transgenic mice could result from its binding to Aβ plaques and clearance of the unbound tracer as a function of time, we therefore used dynamic PET imaging over 1 to 75 min to interrogate regional localization of 18F-7B withen the brains of transgenic and WT mice.
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