Liver triglycerides did not change with age in the Casp2 −/− liver; however, a small but significant decrease was observed in serum.
2, 3 However, Mensa et al. conclude that claudin-1 is solely located at the apical pole of hepatocytes, in contrast to reports by Reynolds et al. and Zadori et al. 2, 3 We agree that claudin-1 is predominantly expressed at the apical membrane of hepatocytes in normal liver; however, a minor pool of claudin-1 is observed at the basolateral membrane (Fig. 1).
Comparison of relevant studies show an impaired hypertrophy response compared with normal livers; however, statistical significance has not been demonstrated.
As shown in Fig. 4, few PCNA-positive hepatocytes were detected in control livers, however, many were observed in hAMCs group.
Regenerative ability is not equal in all livers, however.
The staining of Kupffer cells was variable among normal and cirrhotic livers, however, no distinct pattern emerged.
In the absence of liver dysfunction, the additional ammonia can be managed by the liver; however, in a damaged liver, the extra ammonia cannot be managed, resulting in hyperammonemia.
The liver however has a unique immunological environment in which the lymphoid population is weighted with innate immune cells [ 12, 13].
The liver, however, is an enormously complex organ whose function is difficult to characterize succinctly or comprehensively.
There is no data with regard to the progression of hepatic injury with continued therapy in patients with mildly elevated liver enzymes; however, a recent study showed that patients with mild aminotransferase elevation at baseline did not show a progressive rise in liver enzymes after a mean follow-up of 2 years of therapy [ 74].
