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The other type of microglial cells, which were reactive for Mac-1, showed enlarged cell bodies from which processes with an enlarged and thicker appearance emanated, thus being consistent with a reactive phenotype.
However, the enlargement of the SAM is mainly due to enlarged cell areas and not increased cell number, which indicates that cell proliferation is still under control in mutant SAMs even if impairment exists in the cell cycle.
However, to obtain effectively enlarged cell coverage, performance of the initial acquisition and symbol synchronization should also be enhanced.
Our experiments show that besides p16INK4A cytoplasmic localization, the doxorubicin-induced senescent-like phenotype is characterized by a morphologically flattened and enlarged cell shape, an increase in SA-b-gal activity and the structural alteration and redistribution of F-actin.
To analyze cell types in the glial scars in the injured white matter, mature activated astrocytes density was assessed by counting GFAP-positive cells with number of processes and enlarged cell bodies in P10 rat pups (Figure. 2 A B).
At doses of 0.05, 0.1 and 0.25 µM, doxorubicin did not increase the percentage of ssDNA positive cells, while it did induce a dose-dependent increase of SA-b-gal positivity accompanied by a flattened and enlarged cell shape, thus suggesting a pro-senescent non apoptotic effect.
In this study we demonstrate that Cord Blood Endothelial Progenitor Cells (EPCs) exposed to low, sub-apoptotic doses of doxorubicin show a senescence phenotype characterized by increased SA-b-gal activity, decreased TRF2 and chromosomal abnormalities, enlarged cell shape, and disarrangement of F-actin stress fibers accompanied by impaired migratory ability.
Therefore, enlarged cell size is often associated with polyploids.
GFAP-positive cells exhibited markedly enlarged cell bodies and thickened processes, typical features of an activated phenotype.
In addition, enlarged cell size in the floor plate and hypochord is correlated with the expanded ER (Fig. 6E and F).
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At a cellular level, this suppression by stat92E heterozygosity correlates with restoration of more normal G1/S cell cycle phasing in mutant discs and a partial reversion of an ept enlarged-cell phenotype.
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