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Homozygous (Casr null) mice have severe hypercalcemia and hyperparathyroidism, and die within several weeks of birth.
While heterozygotes are healthy, homozygous W mice have severe macrocytic anemia and die within days.
During development, E2f4 null mice have severe disruption of liver-based erythropoiesis [17].
In detail, Dll4 deficient mice have severe vascular defects, similar to Notch 1 and 4 knock-outs [8], [9].
At this time point, Il10−/− and DKO mice have severe chronic colitis, while Tnf−/− and mast cell-deficient sash mice do not (Figure 3).
Consistent with this, all mouse mutants lacking otoconia (such as tilted, head slant, and head tilt mice) have severe balance deficits [20], [21], [22], [23].
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In contrast, one Prnp −/− and two Tg20 mice had severe seizures and died.
The results of the blood chemistry analysis demonstrated that Wwox KO mice had severe metabolic defects.
Some Osx-Cre expressing mice (Hdac3 wildtype) also had mild skull defects (Figure S5); however, all Hdac3 CKO mice had severe craniofacial abnormalities.
However, in present study, since kainate-treated mice had severe and conclusive seizure, therefore we could not fix mice for anesthesia.
We found that both NT3.lysM and NT3.catK mice had severe osteoporosis at 8 weeks of age, with an approximate 50% loss in trabecular bone volume.
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