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We study this trade-off in multiple experiments using different swarm sizes.
This lack of dysbindin depletion on EGF receptor stability was verified across multiple experiments using scanning densitometry (Fig 4B).
Based on findings from multiple experiments using the extinction-reinstatement model, a 'final common pathway' for drug-seeking has been proposed, as that projecting from the medial prefrontal cortex (mPFC) to the nucleus accumbens core [43].
In multiple experiments using LS174T and HepG2 cells, we consistently achieved approximately 30 40% reduction of C2-O-sLeX expression after C2GnT1 gene knock-down and a representative experiment is shown in Fig. 3D.
This decrease in BNP-Luc expression was repeated in multiple experiments using different concentrations of TrpC3 d-siRNA and different times of incubation, suggesting that TrpC3 plays an important role in activating the signaling cascades necessary for BNP production in hypertrophic cardiac myocytes.
The amount of cell death was quantitated digitally (the 'SimplePCI' software) for each condition by counting the apoptosis events in multiple random fields from images taken from multiple experiments using the formula 'number of apoptotic nuclei/total number of nuclei x 100'.
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The amount of cell death was plotted for each condition by counting the apoptosis events in random fields from multiple independent experiments using the formula 'number of apoptotic nuclei/total number of nuclei x 100'.
To test this hypothesis, we performed multiple transient transfection experiments using pER4-GFP plasmid, by which ERBB4 expression in MSCs can be reported and quantified using the population of GFP-positive MSCs in flow cytometry analysis.
This was not the case for regions 9, 10, and 14, for which multiple long PCR experiments using varying amounts of DNA template were necessary to obtain successful amplifications.
Multiple lineage tracing experiments using Cre transgenic mice and real-time imaging have demonstrated that radial glial cells likely give rise to a majority of cells in the cerebral cortex (43, 44).
Despite these findings with over-expressed POSH and Cbls, we were unable to demonstrate interaction of the endogenous proteins in multiple co-IP experiments using extracts from both neuronal and non-neuronal cells with or without use of proteasome inhibitors (data not shown).
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