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Nonspecific binding is determined in the presence of 10 μM triamcinolone.
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In both assays, non-specific binding was determined in the presence of haloperidol (10 μmol/L).
Nonspecific binding was determined in the presence of 10-μM DTG and 1-μM -pentazocine.
Nonspecific binding was determined in the presence of 7A (5 μM) as a competitor.
Nonspecific binding was determined in parallel experiments utilizing 7A (5 μM) as a competitor.
Nonspecific binding was determined in the presence of 10-μM -pentazocine.
Unspecific binding was determined in the presence of a high concentration (0.5 100 μM) of the non-labelled competitor substance.
Nonspecific binding was determined in parallel experiments utilizing 7A (2.5 μM) for Aβ1-42 fibrils and 7A (5 μM) for AD tissue as a competitor.
A 1.83 ± 0.10% CD-31 binding was determined in the tumor tissue from the control mice, whereas the samples from sunitinib-treated animals showed reduced binding of 0.58 ± 0.05% CD-31 (n = 8/4 - tumors from four mice; p < 0.001).
Non-specific binding was determined in the presence of 10 µM GTPγS.
Non specific binding was determined in the presence of vasopressin (1 µM).
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