Sentence examples for binding in the cortex from inspiring English sources

We have previously demonstrated benzodiazepine binding in the cortex and hippocampus of mu-opioid receptor knockout (KO) mice.

Our results thus apply to AV-45 binding in the cortex only.

The TSPO binding sites were shown to be widespread and with high density in several subcortical nuclei, with more moderate binding in the cortex and dorsal striatum.

In contrast, [125I]BOP binding in the cortex was better described by a two-site model, with estimated Kd of 262 +/- 16 pM for a higher affinity site and 16.9 +/- 1.3 nM for a lower affinity site.

In the present study, we developed an optimized method to quantify AV-45 binding in the cortex only, using each subject's MRI white matter segmentation as a mask on their respective AV-45 image.

These data suggest modifying F-Aβ40 to F-Aβ40 H13,14G by substituting glycine for histidine at domains 13 and 14 significantly decreases neuronal binding in the cortex and hippocampus.

The specific-to-nonspecific binding ratios were calculated as follows: (Binding in hypothalamus − Nonspecific binding in the cerebellar cortex) / Nonspecific binding in the cerebellar cortex [34, 35].

Significantly increased binding was found in motor cortex, pons, dorsolateral prefrontal cortex, and thalamus in the ALS patients, with significant correlation between binding in the motor cortex and the burden of upper motor neuron signs clinically evident.

In this case, CTCF is bound at both sites in cerebellum and liver and occupies only one binding site in the cortex sample.

In contrast, two example peaks called by MMDiff and not by DESeq are shown in Figure 7E and F. In Figure 7E, CTCF seems to be bound at two distinct binding sites in the cortex and liver.

The receptor binding data suggest a preferential interaction with the 5-HT1A receptor subtype, because galanin did not alter 5-HT2 receptor agonist and antagonist binding in the limbic cortex (Fuxe et al. 1990).