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These findings are consistent with our previous results in which microinjection of recombinant Rad51 protein improved the defective DNA repair capacity of freshly isolated oocytes from AKR/J mice, decreasing the amount of existent DDSBs and consequently suppressing spontaneous apoptosis [7].
In addition, Lira et al. [ 42] showed that the same chronic exercise alters the ileum contraction reactivity of young mice, decreasing the response to acetylcholine.
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As expected, the injection of antisense oligonucleotide to Ldlr-null mice decreases the hepatic Fmo3 gene expression, resulting in decreased mouse plasma TMAO thereby decreasing aortic lesion in western diet fed mice (Shih et al., 2015).
Genetic reduction of ACAT1/SOAT1 in mice decreased the concentration of cholesterol esters in the brain by 86% (Hutter-Paier et al., 2004).
Specifically, intraperitoneal propofol hemisuccinate (PHS), a water-soluble prodrug of propofol, administered 15 min prior to KCl induced CSD on the cortex of mice, decreased the number of CSD deflections at doses of 120 and 200 mg/kg without any effect on CSD amplitude [202].
Knockout of Bcl-2 and Bcl-XL in mice decreased the viability of oocytes around the time of primordial follicle formation [13], [62].
NKB treated male mice decreased the survival time in the hypoxia test at the dose 100 mg/kg.
In addition, isolated macrophages from wound of PPARγ-KO mice decreased the expression of all the detected phagocytosis-related genes.
Genetic activation of HSL in mice decreases the adipose mass and leads to triacylglycerol deposition in multiple tissues.
Trimming the whiskers of adult NgR1-deficient mice decreased the amount of surface AMPAR at spines to that of WT mice with intact whiskers.
Akt1 transgene activation in 12-month-old DTG mice decreased the expression of these genes to levels observed in the muscle of 3-month-old mice.
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