1 r disease, including hepatitis, fatty liver, enlarged liver and cirrhosis, was validated with healthc

2 is likely that these cells contribute to the enlarged livers and hepatomas that we observe in sav1 an

3 ith CRLF2-d were more likely to present with enlarged livers and spleens (38% vs 18%, P < .001).

4 e, neutrophils were observed in sinusoids of enlarged livers and spleens, suggesting that IL-15 media

5  9 months of age, PDGF-C transgenic mice had enlarged livers associated with increased fibrosis, stea

6 uced DNA damage, could yield a population of enlarged liver cells with nuclear atypia and pleomorphis

7                                       In the enlarged livers, cyclin E-Cdk2 complexes were present in

8 mst2 in hepatocytes results in significantly enlarged livers due to excessive proliferation.

9 iated with HGF/SF-transgenic mice, including enlarged livers, ectopic skeletal-muscle formation, prog

10 on all liver disease (n = 647 cases), nor on enlarged liver, fatty liver, and cirrhosis only (n = 427

11  of high-density intrahepatic bile ducts and enlarged liver in Rosa(NICD/-)::AlbCre mice could be at

12 e 10 days or more after injury commonly have enlarged livers often twice or more normal size for thei

13 coded by Lipa) in mice (lal(-/-)) results in enlarged liver size due to neutral lipid storage in hepa

14 nths, Mgat3+/+ and Mgat3+/- mice had grossly enlarged livers that contained numerous tumors.

15                   APC(+/-) embryos developed enlarged livers through biased induction of hepatic gene

16  the haploinsufficiency seen in HCC produced enlarged livers with a gene expression profile of persis

17                       Transgenic embryos had enlarged livers, with prominent biliary epithelial hyper