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b K 1 in renal cortex determined from compartmental analysis.
The influx rate constant in renal cortex (K 1) was 2.2-fold lower in Tg mice (P = 0.027, Fig. 4b).
In renal cortex and medulla, CAT and Cu/Zn SOD activities were increased, while GPX activity was unchanged.
Iopromidum caused a significant increase in medullary R2* within the first 20 min after injection (P<0.001), whereas no relevant changes were observed in renal cortex.
We evaluated: renal parameters, NADPH-diaphorase and nitric oxide synthase activity in kidney, renal morphology and apoptotic cells in renal cortex.
The post-necrotic cellular regeneration in renal cortex was significantly lower (p<0.001) in CsA-treated rats on the high-protein than on the standard diet.
In support of this view, the pharmacokinetic analyses of 11C-metformin in renal cortex revealed a lower K 1 in Tg mice, i.e., the basolateral cellular uptake in renal cortex is slower as there is lower expression level of the basolateral uptake transporter.
The influx rate constant of 11C-metformin in renal cortex (K 1) was 2.2-fold lower in transgenic mice whereas the backflux rate constant (k 2) was similar in the two groups, consistent with protein expression.
Additionally, a significant increase in B1 receptor protein expression in renal cortex of Ang II-infused rats was observed compared to control suggesting that bradykinin receptor activation could account for the effect of enalapril to enhance the actions of tempol.
In addition, tubulointerstitial histopathologic changes were noted in renal cortex of congenics.
Retinaldehyde (RAL) was not measured in plasma and unchanged in renal cortex, but was significantly decreased in diabetic liver (0.3×control).
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