In our experimental conditions, M1 and M2 cell migration was similar when tested through the sole polycarbonate membrane and was statistically different only if HUVECs and astrocytes where present in the model.
These tumor epithelial cells were found to display morphological features of EMT, were found at microarray analysis to show upregulation of invasion factors, and were demonstrated to have acquired functional invasiveness when tested in an in vitro migration assay.
When tested compounds were added either at 20 hpf (when primordium migration begins; data not shown) or 36 hpf (when primordium migrated beyond the yolk extension and 2-3 neuromasts have already been deposited), we observed in all cases a disruption in the migration of the primordium compared to the DMSO control (Fig. 4).
CNS ECM scaffolds retained neurosupportive proteins and growth factors and, when tested with the PC12 cell line in vitro, were cytocompatible and stimulated proliferation, migration, and differentiation.
Thereby, when tested in vitro, the two CC-PLA2 and MVL-PLA2 impaired adhesion and migration of HBMEC (human brain microvascular endothelial cells) and HMEC-1 (human microvascular endothelial cell), respectively, by interfering with integrin function.
The resulting cerebellar scaffold retained neurosupportive proteins and growth factors and, when tested with neural stem cells (NSCs) in vitro, was found to be cytocompatible and to stimulate the proliferation and migration of these cells.
When tested on serum, OraQuick remained negative.
CLX MICs significantly decreased when tested with EPI.
Estimators of migration rates based on coalescence theory can detect asymmetries (directionality) in migration rates and differences in population sizes, a considerable advantage when testing migration rates in the context of evolutionary theory [ 91].
When testing for migration following the split between the SMO and TUX groups, migration rates were higher than 1 in the SMO-TUX direction (m = 1.416, 90% highest posterior density (HPD), 0.004-4.21) and close to 1 in the opposite direction TUX-SMO (m = 0.91, 90% HPD, 0.007-4.47), suggesthat that divergence took place in the presence of gene flow from the SMO to the Tuxtlas region.
