The relatively normal fetal liver development of UPF2 null livers is further supported by the lack of anemia in these embryos (data not shown), which would be predicted if the liver experienced gross developmental abnormalities.
The formation of tumours in the lungs and livers was further confirmed by H&E staining as indicated in Figure 4e.
Such an effect in liver is further evidenced by reversal of hepatic steatosis and oxidative stress in ob/ob mice following exenatide treatment [43], and is supported in type 2 diabetic patients by amelioration of surrogate markers of nonalcoholic fatty liver disease [44].
Liver was further weighed and hepatosomatic index (HSI) calculated as HSI = LW/BW*100, where LW is the liver weight (g) and BW is the body weight.
Enrichment of the putative novel transcripts in testes and liver was further examined experimentally using mouse heart, testes, liver, kidney, brain and lung tissues by qRT-PCR and RT-PCR, to determine the expression levels and patterns.
The size of spleen and liver was further measured by ultrasonography, and an age and gender matched reference range was used for the diagnosis of splenomegaly and hepatomegaly [ 11].
After a gene chip-based screening, the data of gene expression in the liver, was further dissected by ANOVA analysis, gene expression profiles, gene network construction and real-time RT-PCR.
Recent advances on the diverse roles of natural killer and natural killer T cells in hepatocellular damage, liver fibrogenesis, and liver regeneration were further discussed.
Liver biopsies were further studied histologically, with morphometric analyses and immunostaining techniques.
Liver metastases were further examined by immunohistochemistry, Real Time PCR, and TUNEL assay.
