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Panel A of Figure 1 shows large vessel signal for an adult mouse kidney in a sagittal orientation.
This difference could contribute to the absence of an induction of megalin mRNA expression by PPARα agonists in the mouse kidney in vivo and should be further explored in future studies.
In summary, we have presented a preliminary study on using UHS-OMAG to image renal microcirculation within mouse kidney in vivo.
In our previous study, we observed that xenon preconditioning significantly upregulated miR-21 expression in mouse kidney in time-dependant manner (17).
Thus, some studies of ACE2 activity in mouse kidney in which 100 μg of renal homogenates [ 29] or 100 μM substrate [ 30] were used may be confounded by the presence of tissue inhibitors or substrate inhibition.
In conclusion, data obtained from our WNK4 −/ − mice under various conditions clearly show that WNK4 is a strong positive regulator, and never a negative regulator, of NCC in the mouse kidney in vivo.
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Interestingly, it was recently reported that PknB is not only involved in regulation of the central metabolism of S. aureus [15], but also determines staphylococcal infection of mouse kidneys in an abscess model [17].
In order to see whether this phenomenon was restricted to renal epithelia of rats, we included rat livers and mouse kidneys in the study.
This antibody actually showed less glomerular binding but more tubular binding to mouse kidneys in vivo than the wild-type R4A.
Lindström et al. further investigated how this protein helps the nephron to develop by using a wide range of techniques, including growing genetically altered mouse kidneys in culture and capturing images of the developing nephrons with time-lapse microscopy.
This localization is conserved in vivo, such as in the distal tubular epithelial cells in mouse kidney and in the follicular epithelial cells in Drosophila.
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Justyna Jupowicz-Kozak
CEO of Professional Science Editing for Scientists @ prosciediting.com