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Subsequent expression profiling of kidney SP from embryonic and adult mouse kidneys reported similar Sca-1, but not musculin, positivity [ 145, 146].
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The SP isolated from adult mouse kidneys was initially reported to be Sca-1+ with >95% of the SP expressing the basic helix loop helix transcription factor musculin, which has been linked to promoting a dedifferentiated fate [ 144].
In normal adult human and mouse kidneys, expression of c-KIT has been reported to be limited to the distal nephrons [19], [20], [22].
Some investigators use FSP1 to differentiate fibroblasts from macrophages in the fibrotic mouse kidney [41], while others have reported FSP1 expression on monocytes and macrophages [42], [43].
Previous studies have reported that mouse kidney progenitor cells accelerate renal regeneration after ischemic injury by differentiation into epithelial cells and incorporating into the renal tubule [ 9, 23– 25].
PET/CT imaging revealed non-uniform distribution of 64Cu signal in mouse kidneys.
Mice kidneys: Proteins were extracted from frozen mouse kidneys using RIPA [43] For microscopy, kidneys were fixed in 4% formaldehyde.
Taken together, 27 month old mouse kidneys represent a robust model of kidney aging.
Moreover, HNF4α inactivation induces EMT in embryonic mouse kidneys [ 43].
The C. albicans genes that were found to be regulated during these infections did not show considerable overlap with those reported previously for mouse kidney infections or human oral infections (Andes et al., 2005; Zakikhany et al., 2007).
The SCID-hu Thy/Liv mouse, first reported by Namikawa et al. in 1990 [10], is generated by coimplanting human fetal thymus and liver beneath the mouse kidney capsule.
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