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Our data suggest that the deficiency in vitamin B12 could have dramatic effect on the dopaminergic cells, in patients under Levodopa therapy, considering that (i) B12 deficiency decreases the cellular content in SAM, as has been showed in B12 deficient N1E-115 cells (ii) Levodopa enhances the cellular consumption of SAM, a metabolic condition that may accentuate the apoptotic effect of B12.
Copper (Cu) deficiency decreases the activity of Cu-dependent antioxidant enzymes such as Cu,zinc-superoxide dismutase (Cu,Zn-SOD) and may be associated with increased susceptibility to oxidative stress.
Rather, TLR3 deficiency decreases the production of the pro-inflammatory mediators TNF-α and CCL5 resulting in uncontrolled viral replication that outpaces the developing adaptive immune response.
Recently, it was reported that NOX2 deficiency decreases β-cell destruction and preserves islet function in STZ-induced diabetes by reducing ROS production, immune response, and β-cell apoptosis [31].
Experimental human zinc deficiency decreases Th1 but not Th2 immune response.
► DGAT1 deficiency decreases cholesterol uptake and absorption in ApoE-null mice.
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A second independent study on LGP2-deficient mice, however, reported that LGP2 deficiency decreased cytokine responses to infection with several RNA viruses [24].
The latter may be caused by Fe deficiency decreased active Fe content.
We found that LRRK2 deficiency decreased the level of phosphorylated Rip2 upon thapsigargin treatment (Fig. 7D).
berghei IgG enhanced parasite growth and C3 deficiency decreased parasite growth in mice.
Ces1g deficiency decreased PUFA release from TG, which consequently caused sustained SREBP1c activation and increased de novo lipogenesis in the liver (Quiroga et al., 2012a) (Fig. 4).
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