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The result showed strong positive intensity within tumor grafts of all groups as well as in the locally invaded region of the mouse kidney (data not shown).
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Obvious structural changes were not observed in contralateral kidneys and sham-operated mouse kidneys (data not shown).
Comparison of the mutant mouse kidney expression data to Wilms' tumour data is consistent with a block in MET as the origin of WT1-mutant Wilms' tumours and highlights clear biological differences between these tumour types.
No expression could be seen in the adult mouse kidney sections examined (data not shown).
We then immunostained normal mouse kidney tissues with multiple markers (data not shown) and then applied the system to immunostain human renal tumors.
In contrast to human kidney, cadherin-9 was no longer present at the end of embryonic kidney development in the mouse, and was not detectable in the adult kidney (data not shown).
These models are demonstrated on data collected from a progenitor cell compartment within the developing mouse kidney, the cap mesenchyme.
Furthermore our data suggest that the C. albicans cells growing in RPMI 1640 and the mouse kidney differ with respect to their carbon metabolism.
Data were acquired over a region of 2.5 mm by 2.5 mm on the exposed mouse kidney.
In the context of our in vitro data, we were especially interested in examining the levels of KLHL3 and CUL3 in the mouse kidney (Fig 4A).
Unlike human kidney development, mouse kidney development continues postnatally.
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CEO of Professional Science Editing for Scientists @ prosciediting.com