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To account for such plasticity in the process of migration, we adopted a reaction norm approach.
To study the inhibitory effects of L2H17 in cell migration, we adopted a scratch wound model in the presence of mitomycin C which inhibited cell proliferation.
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To further examine whether endogenous hsa-miR-125a-3p hsa-miR-125a-3p hsa-miR-125a-3p hsa-miR-125a-3psion, we andpted hsa-miR-125a-5p hsa-miR-125a-5p hsa-miR-125a-5p hsa-miR-125a-5pnous hsa-miregulatep and hsa-migration5p using andinvasion'-O-methyl oligonucleotides [ 23- 26].
We adopted a migration matrix model allowing for asymmetric migration rates between regions and variable subpopulation sizes.
In order to solve this problem, we adopted intra-Europe migration data from the MIMOSA project (De Beer et al. 2010b; Raymer et al. 2011).
To determine whether hsa-miR-125a-3p hsa-miR-125a-3p hsa-miR-125a-3p hsa-miR-125a-3pon and hsa-miR-125a-5p hsa-miR-125a-5p hsa-miR-125a-5p hsa-miR-125a-5pproare.
We adopted the length of unrestricted gas migration (LUGM) as the main design criterion in this assessment.
For the business-as-usual scenario, we adopted the United Nations medium variant net migration assumptions (UNPD 2016).
Therefore, we adopted the event history model to analyze the migration-hazard function.
Consequently, we adopted and changed taxonomic names to match the collated information on migration to the taxonomic names of the species used in the phylogeny.
Then, we adopted invasion-associated cellular and nude mouse models to study the role of NM23-H1 iNPCPcellll migration and metastasis.
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