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We observed that in some 3'UTR mice, the livers were strongly adhered to the stomach (Fig 1e).
Pathway analysis, using Gene Network [ 20], confirmed that 1,396 genes with higher expression in the adult livers were strongly enriched for metabolic functions like monocarboxylic acid, steroid and bile acid metabolic processes, as well as the response to xenobiotic process (Table 2A).
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Accordingly, the populations of CD4+ CD69+ T cells in mouse spleen and liver were strongly down regulated by DEX treatment (Fig. 4C).
From 3 wk prepartum to 1 wk postpartum, mRNA abundances of PPARΑ and several PPARΑ target genes involved in fatty acid uptake, fatty acid oxidation and ketogenesis in the liver were strongly increased.
The CpG sites that were hypomethylated in the adult livers and hypermethylated in fetal liver were strongly enriched for metabolic pathways, such as the steroid metabolic process the regulation of lipid metabolic processes, regulation of generation of precursor metabolites and energy, and regulation of glycolysis (all with p-values < 1.15 × 10-44) (Table 1A).
Neoangiogenesis and the development of an abnormal angio-architecture in the liver are strongly linked with progressive fibrogenesis.
Tyrosinase-like activity in the frog liver was strongly stimulated by Zn2+ but suppressed by n-ZnO, Nfd and n-ZnO + Nfd.
Chronic inflammation in liver is strongly linked to the development of fibrosis, cirrhosis, and HCC [ 31].
Unexpectedly, INHA, barely detectable in disease-free liver, was strongly elevated in most HCC samples.
Nonalcoholic fatty liver disease, a condition in which excess fat accumulates in the liver, is strongly associated with the metabolic syndrome, including obesity and other related conditions.
In contrast, inhibin α, barely detectable in normal liver, was strongly increased in tumour-adjacent liver and dramatically enhanced in HCC.
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