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However, once neuron development is initiated, these mice develop severe hippocampal abnormalities, absence of cerebellar foliation, disorganization of cortical neurons and lethality by postnatal day 7, attributed to a failure of neuronal precursors to differentiate into mature neurons and excessive cell death (Montgomery et al. 2009).
Bovine growth hormone (bGH) transgenic mice develop severe kidney damage.
The spontaneous leptin mutation model ob/ob mice develop severe diabetes with marked hyperglycemia and a propensity to overeat, resulting in obesity and the development of hepatic steatosis (Mayer et al., 1951).
Since IL-10-deficient mice develop severe inflammatory bone-loss in arthritis models, which is mediated by inflammasome activation and IL-1 release, our observations contribute to a better understanding of the molecular pathophysiology of CNO.
These mice develop severe cardiomyopathy with early death at 28 weeks in a gene dosage-dependent manner.
We have previously reported that γB-crystallin S11R mutation leads to a dominant congenital cataract, and homozygous CrygbS11R/S11R mutant mice develop severe nuclear cataracts regardless of the genetic background in the A/J, C57BL/6 and 129 strains [13].
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Mst1 transgenic (Tg) mice developed severe dilated cardiomyopathy at a young age and died prematurely due to heart failure.
Adult mutant mice developed severe thymic hypoplasia, which included alterations in the cortical TEC architecture that coincided with the loss of thymocytes.
From day two on infected mice developed severe clinical symptoms and died within 6 and 10 days.
By 24 months of age, Tax transgenic mice developed severe arthropathy with a cumulative incidence of 22.8%.
WT mice developed severe whole body (hepatic and skeletal muscle) insulin resistance after HFD, as measured by hyperinsulinemic euglycemic clamp.
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