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In vitro cells do not encounter the same selective pressure as in vivo cells do, and this difference in selective pressure may provide an explanation as to why the tumor cells maintain a lower level of methylation.
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We first showed that in vitro stellate cells do indeed exhibit and abrupt transition to fast spiking.
This viewpoint is based probably on the fact that in vitro cultured cancer cells do not exert a negative effect on their normal neighbors, do not produce toxic products and, most likely, are not capable of doing them in vivo.
Since our imaging was of extracellular matrix, it would not be possible to confirm this in live cells, since in vitro cultured living cells do not organize basement membranes properly.
Although ATSC contained less CD146+ cells, exhibited better proliferation and displayed similar alkaline phosphatase activity upon osteogenic in vitro differentiation, cells did not develop into bone-depositing osteoblasts on β-TCP after 8 weeks in vivo.
Particle uptake in vitro into cells did not occur by any of the expected endocytic processes, but rather by diffusion or adhesive interactions.
With respect to glial differentiation in vitro, Dicer-null NS cells do not undergo apoptosis under those conditions, but do fail to terminally differentiate.
Moreover, in vivo and in vitro phenotype of cancer cells do not always coincide.
Indeed, it was reported that in vitro memory CD8 T cells do not require costimulatory signals (Flynn and Mullbacher, 1996).
Also, CDK6 EE did not affect the long-term proliferative output of LT-HSCs in vitro in conditions where cells do not return to G0.
Despite failing to detect MPGES1 positive B cells in the rheumatoid tissue, we showed that SF and PB B cells from RA patients are able of upregulating MPGES1 and COX-2 upon in vitro activation while unstimulated B cells do not readily express these enzymes.
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