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Among other possibilities, the induction of Th1 responses can be inhibited by polyunsaturated fatty acids (PUFA), possibly by insertion in the membrane [48].
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We considered two possibilities for the induction of the UPR activity in PVD neuron.
For instance, the network suggests parallel possibilities for the induction of the gene expression of RELA by IL-1 β and TFN- α, either directly or mediated by suppression of the transcriptional repressor OSR2 (an example for a positive feed-forward network motif).
The lack of further depletion of the second administration might be due the possibility of the induction of rat anti-mouse antibodies, which were unfortunately not evaluated.
These data raised the possibility that the induction of ATL9 by chitin might be dependent on NADPH oxidase activity.
To test the possibility that the induction of CDKN1C might arise from the downregulation of DMR-LIT1, we looked at the expression of LIT1 upon above drug treatment.
To exclude the possibility that the induction of a sustained calcium signal was a particular property of ANC28.1, we repeated the experiment shown in Fig. 2A using the superagonistic CD28-specific antibody TGN1412.
This finding, considered together with the observation that ROS is augmented by TGFβ, highlights the possibility that the induction of Tregs in the periphery by TGFβ could be related to ROS.
This raised the possibility of the induction of an alternative form of programmed cell death: necroptosis.
One possibility is the induction of adhesion molecules in endothelial cells.
However, the possibility for the induction of transcription of tyrosinase gene under interferon administration should not be neglected.
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