We have observed that the Mecp2-null mice presented with episodes of diarrhea, and decided to study the intestinal phenotype in these mice.
Their main findings were that mice presented with a progressive drop in whole body O2 uptake and a concurrent fall in body temperature, which was only partially restored by external warming.
As we have previously demonstrated, the absence of ClC-2 produces a severe reduction of NaCl absorption [29], and Scl9a3 −/− (Nhe3-null) mice presented with slight diarrhea due to reduced sodium absorption in the colon [30].
Double transgenic mice presented with enlarged spleens and kidneys, enlarged, disorganized blood vessels located near the surface of the liver, sprouting, dilation, and disorganization of liver lymphatics, and turbulent flow in about 1/4 of the blood vessels sampled.
Finally, the AE3−/− null mice presented with late onset photoreceptor cell death (Fig. 7A).
Furthermore, unlike ApcMin/+ mice, ApcMin/+/Faslpr mice presented with invasive lesions in all animals at 30 weeks (Fig. 2).
The ACE.2 mice presented with a much milder form of the renal medullary and papillary underdevelopment.
Over 65% of IL-6KO mice presented with infiltrating lesions and fibrosis with grade 4 severity, while 93% of wt mice had grade 2 or less heart pathology.
Interestingly, bid-deficient mice presented with a relatively mild phenotype, but showed a prominent resistance to Fas-dependent apoptosis of hepatocytes [33].
However, ApcMin/+/Faslpr mice presented with a dramatic increase in tumor burden relative to ApcMin/+ mice and invasive lesions at advanced ages.
Surprisingly, dystrophin-deficient mdx and ms-DKO mice presented with comparable levels of myofiber necrosis, membrane instability, and deficits in muscle function.
