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The Brazilian guidelines state treatable ROP in ROP zone I, any stage with plus disease, ROP in zone I, stage 3 with no-plus or ROP in zone II, stages 2 or 3 with plus disease or at least, at threshold ROP [ 11].
Estrogen deficiency decreased glomerular estrogen receptor expression in ROP Os/+ mice, which we had previously found to be low in the parental ROP strain.
Considerable evidences support the concept that ROP is not only a vascular disorder, but is also associated with functional visual deficits in ROP patients as well as in animal models.
Deamidation of globin chains is especially promising and may indicate underlying prenatal pathologic mechanisms in ROP.
The resulting 17-residue designed sequence is 41% identical to the relevant regions in ROP.
As our understanding of the pathologic basis for plus disease in ROP grows, objective methods of recognizing and measuring retinal vascular abnormalities are also being designed.
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The proteinuria in ROP- Os/+ mice reached a peak at 12 weeks.
We found that the urine protein to creatinine ratio was significantly higher in ROP- Os/+ mice compared to both C57- Os/+ and ROP-+/+ at all time points.
To test the involvement of TGFβ-related candidate genes in glomerular fibrogenesis, we evaluated the effect of Itch, which was upregulated in ROP- Os/+ kidneys, on TGFβ signaling.
Interestingly, a Nrf2-dependent stress response, which is the target for a new class of diabetic nephropathy drug [ 46], appears to also be activated in ROP- Os/+ kidneys.
However, on the C57Bl/6J background the mutation does not cause FSGS, although nephron number in these mice are equivalent to those in ROP- Os/+ mice.
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