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Just by drawing signaling pathways from insulin and nutrients to mTOR with feedback inhibition of insulin-signaling, we can predict that low insulin levels (by not activating mTOR) extend life span (good health), whereas low insulin responsiveness can be a feedback response to over-activated mTOR, which shortens lifespan (bad health).
Thus, the down-regulation of UVR8 measured at longer UV-B exposures (Table S7 in Additional file 2) may be a feedback response to the treatment.
In short, HF-diet attenuates the secretion of NAPE and N-acylethanolamines, which are supposed to be a feedback response to the presence of intestinal lipid.
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Whether the activation of IL-10 signaling is triggered directly by the aged RPE/choroid or is a feedback response from the increased immunological activity of the aged RPE/choroid is not known.
This suggests that the dowregulation of IRS-1 in OA Obs, the major IGF-1 signaling pathway, is a feedback response to increased exposure to elevated endogenous IGF-1 levels.
As we have previously demonstrated (Brostjan et al, 2008; Starlinger et al, 2011), total VEGF increases significantly in patient blood after neoadjuvant BV treatment, which is considered a feedback response and pharmacodynamic marker of VEGF inactivation by BV.
Furthermore, taurine slightly decreases beta-amyloid peptide aggregation 53 and the high levels observed in LCR hippocampus would be consistent with a feedback response to ongoing neurodegeneration.
Surprisingly, transcripts for multiple HSPs are transiently induced, and then down-regulated as a class after 4 h UV-B (Table S8 in Additional file 2); thus, as suggested for UVR8 in shielded leaves, the down-regulation observed at longer exposure times may be part of a feedback response to suppress physiological changes induced by initial UV-B perception.
However, when TGF-β signaling is increased, a higher level of SMAD7 expression is induced as a feedback response and this will make the amount of USP15 insufficient, thereby limiting the duration of TGF-β/SMAD signaling (Aggarwal and Massague, 2012; Eichhorn et al., 2012).
The negative relationship of PBDEs with TSH might be a normal feedback response to elevated T4 levels.
Since our analysis was performed 24 h after exposure began, the reduced transcript levels might be the result of a feedback response to the depletion of glycogen stores.
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CEO of Professional Science Editing for Scientists @ prosciediting.com