In liver, we identified 28 probe sets with statistically significant (p≤0.01 and absolute log2 fold change ≥0.2) changes in DNA methylation (Figure S2A and Table S5).
When requiring a significant motif to be present at least twenty times in either brain or liver, we identified 11 and 10 motifs in the brain and liver, respectively (Table 2).
Though inflammation is a crucial force to promote increase in ROS accumulation in Mdr2 −/− liver, we identified additional effects of Mdr2 deficiency that also contribute to oxidative stress.
In the M4 GHB perfused liver, we identified 8±2%2% of M4 succinate that subsequently enters into the citric acid cycle and 59±6%6% of M4 GABA.
In patients with a low number of HBV DNA copies per cell in the liver, we identified additional risk factor (HCV infection, alcohol intake or non-alcoholic steato-hepatitis) suggesting a cooperative effect for HBV-induced carcinogenesis.
In the [2,3,4-C3]-GHB [2,3,4-C3]-GHB [2,3,4-C3]-GHB M3 GHB-CoA, M3 3,4-dihydroxybutyryl-CoA, M2 3-hydroxyperfusedliver, and M1 formate, weidentified clear precursor-to-product relationship.
Using bioinformatic analyses of gene sets regulated (1) by glucose (2) differentially expressed in both cell lines in comparison to HCC and to healthy liver, we identified and validated on xCELLigence cell signaling pathways linked to the regulation of gene expression by glucose and dysregulated in HepG2 cells.
In a study of liver gene expression in preparation, fatty acid desaturases SCD and FADS1 were significantly downregulated in liver, where we identified a multifunctional protein TOB1 which is significantly upregulated.
In the mouse liver network, we identified 98 modules (Table S2).
Using fucose-specific lectins to identify the proteins that become fucosylated in patients with liver disease, we identified more than 100 glycoproteins from patients with HCC and/or cirrhosis that contained increased fucosylation [19].
