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Both studies showed that c-Myc-deficient enterocytes could proliferate; however, our study showed that both the level of proliferation and cell size were reduced compared with wild-type intestinal enterocytes.
During the first week in culture, a lower level of proliferation was seen in the GTA matrices but over the four-week culture period, the GTA and EDAC matrices provided for the greatest cell proliferation.
As it can be seen, MSCs show their highest level of proliferation after 5 days.
The increase in FLT uptake level is caused by the upregulation of TK-1 activity without an increase in the level of proliferation markers.
Because parabasal cells express high level of proliferation marker MIB-1, they are thought to function as transient amplifying (TA) cells derived from basal cells in the larger airways[14, 15].
It has been reported that commensal bacteria-mediated TLR signaling is important for homeostatic level of proliferation of epithelial cells.
This unusual high level of proliferation indicates ongoing repair of the tissue even at this late time point.
We found that the steady-state level of proliferation is abnormally upregulated in the TAK1-deficient intestinal epithelium.
The Ki67 marker was used to show the level of proliferation in the prostatic epithelium of OHT-treated ARR2PBCreER(T2)×Ptenfl/fl mice.
The level of proliferation was quantified by the light emission detected via an Orion microplate luminometer (Berthold Detection Systems, Pforzheim, Germany).
Since the absolute level of proliferation greatly differed between the two T cell types, we also expressed the data as the percent of the maximum response (Fig. 4C).
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