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Also, the mutant mice exhibited severe skeletal deformities from defective intramembranous and endochondral ossification, owing to delayed chondrocyte maturation and impaired osteoblast differentiation.
Our findings showed that TiO2 NP-exposed mice exhibited severe inflammation and vascular endothelial dysfunction, implying that the lesions may be involved in NOx reduction and ET-1 overexpression due to TiO2 NP exposure.
The affected mice exhibited severe respiratory syndromes and diffuse lung injury.
Transgenic mice exhibited severe impairment in glucose-induced Insulin secretion in vivo.
As expected wild type C57BL/6 mice exhibited severe weight loss and intestinal inflammation following acute DSS administration (Figure 1A).
Here we show that PACAP-deficient mice exhibited severe dysfunctions of entrainment in a time-dependent manner.
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However, contrary to expectations, we found that these mice exhibit severe diabetic phenotype.
Consistent with this, PMCA2-null mice exhibit severe balance deficits resulting from the complete absence of otoconia [34].
We have previously reported that intestinal epithelium-specific TAK1 deleted mice exhibit severe inflammation and mortality at postnatal day 1 due to TNF-induced epithelial cell death.
NDUFS4 knockout mice exhibit severe RCCI with features similar to those of Hq mice (growth retardation, blindness, ataxia, and baldness) but greater disease severity leading to death at 7 weeks of age after only 2 weeks with symptoms.
We show that homozygous Dicer mutant mice exhibit severe axon guidance defects in the visual system, including an increased ipsilateral projection, axons extending ectopically outside the region of the optic chiasm, the formation of a secondary optic tract, and aberrant growth of RGC axons into the contralateral optic nerve and eye.
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