In addition to the mouse models mentioned above, transgenic mice over-expressing the cut-homeodomain transcription factor Hepatic nuclear factor 6 (Hnf6) specifically in the pancreatic endocrine cell lineage showed disrupted islet morphogenesis and a form of insulin-dependent diabetes [15].
In contrast to the OM mouse models mentioned earlier (such as Eya4/+ and Jf/+), OME in Df1/+ mice has been shown to be frequently unilateral (38).
This effect is most clearly seen in mice of the four core genotype model mentioned above: after removal of the gonads, XX females have twice the adipose tissue as XY females and are much more likely to develop fatty liver [ 86].
The model mentioned is really comprehensive.
Using the four core genotype mice in the mouse model for MS mentioned above, XY lymph node cells show a smaller immune response in the induction phase regardless of the gonad type of the donor [ 108].
Wild-type oligodendroglioma cells from mentioned mouse model were transplanted into the brain of C57/Bl6 mice, which generated lethal tumors.
To date, the relevant route of exposure models mentioned here (with 'normal' inbred mice and/or Brown Norway rats) has been tested with only a few chemicals, and the PLNA, although tested with over 100 chemicals, is not validated as yet.
As mentioned above, a mouse model with hepatocyte-specific inducible expression of ATZ was used to show that the autophagic response is activated when ATZ accumulates in the liver, providing evidence for the importance of autophagy as a proteostatic response to hepatic ATZ accumulation (Kamimoto et al., 2006).
The association with a cribriform pattern is also mentioned in the RET/PTC1 mouse model (Jhiang et al, 1996).
However, the other studies mentioned were based on mouse model experiments [ 5, 6], whilst the present study included ICU patients.
