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As shown in Fig. 5A and 5B, Nrf2−/− exhibited higher basal levels of both glial cell types compared to their wild type controls.
Inhibiting the expression of p53 in MBA-15 cells resulted in elevated basal levels of both osterix and osteocalcin (Fig 3B).
Still for unclear reasons, the basal levels of both sphingomyelin and ceramide were higher in IL-6−/− mice as compared to control animals; however, when normalized to total phospholipids, the basal ceramide levels were identical in both genotypes.
In comparison Arnt silencing seemed to induce an increase in basal levels of both CXCL8 and CCL5.
Since the basal levels of both deoxynucleoside adducts are low, they should provide high sensitivity to increases triggered by oxidative damage.
Compared with neurons, astrocytes showed far higher basal levels of both NFE2L2 and GCLC, indicative of a higher basal Nrf2 activity.
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Consistent with the p38 and ERK1/2 phosphorylation, the NF-κB transcription factor was also activated [1] following PSMA stimulation and the minimal basal level of both IL-6 and CCL5 production was increased two-three fold.
The loss of SirT1 therefore increased the basal level of both IGFBP-1 and IκBα in multilineages of cells, and potentially increased thresholds for activating SirT1-modulated signaling pathways.
In accordance with previous findings, our results demonstrate that casp2−/− cells maintained significantly higher basal levels of ROS (both superoxide and peroxide) (Fig. 6A and B) as well as protein carbonylation (Fig. 6D) than the WT cells.
There were no differences in basal levels of cytokines/chemokines between both non-infected WT and KO mice (data not shown).
H2O2 stimulation resulted in an increase in Nrf2 stability (2.4 ± 0.2-fold) in random oligonucleotide (RO) transfection controls whereas HDAC2 KD showed a significant reduction of both basal levels of Nrf2 (0.5 ± 0.0-fold; p < 0.05) and H2O2 stimulated Nrf2 (1.5 ± 0.3-fold; p < 0.05) compared with RO controls (Fig. 2G).
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