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1 ic changes in the adjacent lung alongside an enlarged liver.
2 n klf9(-/-) mutants is due to development of enlarged livers.
3 r disease, including hepatitis, fatty liver, enlarged liver and cirrhosis, was validated with healthc
4 is likely that these cells contribute to the enlarged livers and hepatomas that we observe in sav1 an
6 e, neutrophils were observed in sinusoids of enlarged livers and spleens, suggesting that IL-15 media
7 9 months of age, PDGF-C transgenic mice had enlarged livers associated with increased fibrosis, stea
8 uced DNA damage, could yield a population of enlarged liver cells with nuclear atypia and pleomorphis
11 iated with HGF/SF-transgenic mice, including enlarged livers, ectopic skeletal-muscle formation, prog
12 on all liver disease (n = 647 cases), nor on enlarged liver, fatty liver, and cirrhosis only (n = 427
14 of high-density intrahepatic bile ducts and enlarged liver in Rosa(NICD/-)::AlbCre mice could be at
15 e 10 days or more after injury commonly have enlarged livers often twice or more normal size for thei
16 coded by Lipa) in mice (lal(-/-)) results in enlarged liver size due to neutral lipid storage in hepa
19 enotype was also of mild cystic kidneys, but enlarged livers were rare; for both genes, CKD or kidney
20 the haploinsufficiency seen in HCC produced enlarged livers with a gene expression profile of persis