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In our model, we observe activation of the trigeminal ganglion using the inflammatory substances CFA and IS.
We did not observe activation of the UPR either in control flies or in NTE expressing flies, indicating that upregulation of NTE is a consequence rather than a cause of the MYOC-induced UPR (Figure 8).
We did neither observe activation of the auditory pathway nor the thalamus, in line with our previous work [26], [27] and data shown by Tanaka et al. in sleep stage 1 [25].
We did not observe activation of ackA in this study.
Additionally, we observe activation of AKT and mTOR that may in part explain growth inhibition of invasive prostate cancer cells in hypoxic condition.
It is noteworthy that although the translocated IGH locus is in a favorable position to do so, we did not observe activation of transcription initiated from the adjacent alternative BANK1 exon 1b promoter or from an intronic cryptic promoter.
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In accordance with those findings Darb-Esfahani et al. observed activation of mTOR in PTEN willed-type cells, in the absence of activated AKT [ 16].
These findings are consistent with experimentally observed activation of the pyramidal II <c + a> slip system in Mg-Y alloys, and provide important insight into the relationship between dislocation structure and macroscopic enhancement of plasticity.
We observed activation of the striatum and deactivation of left M1 during successful versus unsuccessful stopping.
Using Northern blots, Quinn et al. [14] observed activation of CYC6 transcription by 25 µM Ni.
We observed activation of the ventral striatum and enhanced memory formation during reward anticipation.
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