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Ketorolac reversed this decrease in threshold, suggesting that the rats have inflammatory pain.
Moreover, CrHis treatment effectively reversed this decrease in the retina.
Interestingly, TETA treatment reversed this decrease in mRNA expression to levels similar to non-diabetic control values.
While treatment with IL-1β significantly decreased COL2A1 mRNA levels in both C28/I2 cells and PHCs, treatment with MATN3 at the same time reversed this decrease.
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Interestingly, anti-PD-L1 caused a greater increase in MHC II MFI compared to anti-PD-1.Macrophage MHC II MFI was also decreased in fungal sepsis and anti-PD-L1 (but not anti-PD-1) acted to reverse this decrease.
On the other hand, 3 MA by attenuating JNK activity reversed this signaling pathway and decreased the expression of FOXO3a effectors and pro-apoptotic marker Bax and, hence, decreased Bax to Bcl-2 ratio.
In MDA-MB-231 cells, silencing of Id1 reversed this and SNAI2 expression was decreased, as was cell migration.
We demonstrate that scavenging H2O2 reverses this decrease, pointing to inhibition of ROS as a novel therapeutic approach focused on restoring LES function.
We have shown by both reverse transcription PCR and real-time quantitative PCR that allicin reverses this decrease in eNOS mRNA expression, which suggests an additional mechanism that may regulate its ability to increase the release of NO and decrease the apoptosis rate.
Zn supply ameliorated GSH level and partially reversed the decrease in GSH/GSSG, but it did not ameliorate GPx activity.
Furthermore, the overexpression of HSP70 significantly reversed the decrease of mitochondrial membrane potential and the release of mitochondrial cytochrome c in IECs during hypoxia/reoxygenation.
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