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Increased [18F]-PBR111 binding was measured in vivo with PET which corresponds with the brain regions with increased brain inflammation identified with [125I]-CLINDE autoradiography and OX-42 immunohistochemistry (Figure 5).
Non-specific binding was measured in the presence of 100 µM Mazindol (Sigma).
Basal binding was measured in the absence of cannabinoid receptor agonists and defined as 0% in each experiment.
The binding was measured in 75 μl reactions.
Non-specific binding was measured in the presence of 20 μM cold ryanodine.
Nonspecific binding was measured in the presence of 100 μ M 5′- N-ethylcarboxamido) adenosine (NECA).
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The surface coverage by binding is measured in resonance units (RU), the signal follows the binding in real-time during the association and dissociation process.
Between groups changes were not significant (Table 2).> -wrap-foot> Platelet surface expression (% of positive cells) of P-selectin and fibrinogen binding were measured in unstimulated samples (basal activation) and after stimulation with ADP 0.1-10 μM for 20 minutes before fixing with 0.2% paraformaldehyde.
The levels of the constitutively active and total (active plus latent) NF-κB DNA-binding were measured in the presence of 0.03% and 0.6% DOC, respectively; at high concentration DOC dissociates complexes of NF-κB with the IκB inhibitory protein [24], [38], [47].
NMS binding was measured directly in saturation experiments using six concentrations (30 pM to 1000 pM) of [H]NMS for 1 h.
HCEC cells were cultured with inhibitors of glycosylation (NB-DGJ, kifunensine, benzyl-α-GalNAc, or 2F-Fuc), then CTB binding was measured by an in-cell ELISA method.
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