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In fetal livers, the majority (86%) of the differentially methylated CpG sites that are located within CpG islands (CGI) were hypomethylated, whereas this was not the case for CpG sites outside CGIs, where roughly 50% of the CpG sites were either hypo- or hypermethylated in fetal livers.
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Like (vTK− SCID/uPA mouse liver, the majority of the liver parenchyma in vTK+SCID/uPA mice was occupied by intensely red colored RN surrounded by pale liver parenchyma (Fig. 5, upper panels).
As with adult liver, the majority (~94%) of sex-biased differences were autosomal in origin (Additional file 2: Figure S8).
In contrast, in female liver, the majority of sex-biased genes showed no significant change in expression over the same period.
Our results revealed a range of phenotypes: some morphants had unaltered livers, but the majority of morphants (8/14) exhibited smaller livers at 72 hpf compared with controls, and a subset of those morphants demonstrated a smaller progenitor population and showed enhanced susceptibility to APAP-induced liver injury.
Various forms of microcystin (MCY-RR, -LR and -desmethyl LR) were detected in sea otter livers, with the majority of otters (19/21) testing positive for MCY-RR, compared to 2/21 and 1/21 for MCY-LR and MCY-desmethyl-LR, respectively.
Although the liver contributes the majority of bound IGF-I in the circulation, liver-specific IGF-I knockouts revealed that hepatic IGF-I secretion is not essential for growth and suggested that growth-promoting IGF-I can be provided by other tissues (Yakar et al., 1999).
The presence of a CD8+ rich inflammatory infiltrate suggests an ongoing immune response in the liver, supporting the view that HCV may persist in the liver in the majority of HCV RNA negative cases.
Whereas the normal liver receives the majority of its blood supply from the portal venous system, liver tumours obtain the majority of theirs from the hepatic artery.
Among the patients with non-cirrhotic non-alcoholic liver disease, the majority had hepatitis, acute, subacute or chronic, (60/133, 45%) or other unspecified liver diseases (58/133, 44%).
To gain some perspective, however, the liver supplies the majority of yolk proteins in egg-laying species, and ultrastructural sex differences in the liver are required to accommodate this massive protein production in females [ 94].
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