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Upon knock down of both tbx2a and tbx3b we observed absence of AVC constriction and looping altogether and the defects in cell proliferation were more severe, suggesting that tbx2a and tbx3b play additive roles in heart morphogenesis.
In high-glucose medium, however, the effects of NDRG2 on cell proliferation were more prominent.
While genes responsible for cardiac maldevelopment (a condition characterised by abnormal heart morphogenesis), like SNIP, A2BP1 and KIAA1437, were upregulated in the TOF group, genes involved in stress response and cell proliferation were more expressed in the RVH condition.
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Fibroblast proliferation was more pronounced onto XCAPPy than onto XCA, due to its higher hydrophobicity and surface roughness.
These results are consistent with the notion that cell proliferation is more active during embryonic development than in adult tissues.
It seems likely that NPC proliferation is more sensitive to the gene expression changes brought about by proinflammatory cytokines.
Data on a role of CTLA4 in limiting CD8+ T cell proliferation is more controversial [19], [20].
This is supported by our results showing that, although the observed increase in proliferation was more pronounced with increasing TGF-β1 concentrations, AP activity and formation of mineralized matrix was dose-dependently reduced.
This independent line of investigation suggests that the ability of CXCL10 to inhibit endothelial cell proliferation is more associated with its binding to glycosaminoglycans than its binding to CXCR3.
Proliferation was more pronounced in γδ-T cells compared to non-γδ-T cells, resulting in a relative increase in γδ-T cell frequency compared to other lymphocyte populations.
There was no evidence of impaired proliferation with the A2-BMLF-1 peptide compared to the A2-BRLF-1 peptide; indeed in some assays, A2-BMLF-1 proliferation was more pronounced despite higher expression of PD-1 on these cells (Figure 7A, chronic infection).
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