Mice were left for 8 weeks for the OVx mice to develop osteopenia.
Kassan et al123 observed that Ang II led mice to develop an increase in blood pressure, cardiac hypertrophy and fibrosis.
Mochizuki-Kashio, M. et al. Ezh2 loss in hematopoietic stem cells predisposes mice to develop heterogeneous malignancies in an Ezh1-dependent manner.
Recently, we have obtained ERα floxed mice and have bred them with nestin-CRE mice to develop mice lacking estrogen receptors in neurons.
Inactivation of one Cdx2 allele predisposes mice to develop colon polyps, and loss of CDX2 expression is a feature of some poorly differentiated colon carcinomas in humans.
Researchers at Carnegie Mellon University and the University of Pittsburgh have successfully directed adult stem cells from mice to develop into bone and muscle cells with the aid of a custom-designed ink-jet printer.
In addition, we combined neurobehavioral metrics of nociception and sensorimotor performance of individual mice to develop a novel composite toxicity score that reveals and quantifies peripheral neurotoxicity, a debilitating long-term systemic toxicity of paclitaxel therapy.
Genetic ablation of iron regulatory protein 2 (IRP-2), a protein responsible for post-transcriptional regulation of expression of several iron metabolism proteins, predisposes IRP-2 −/− mice to develop adult onset neurodegenerative disease.
Tumor volume was calculated by using the formula: tumor volume (mm3)=1/2 length (mm Ãwidth (mm 2.40 In another set of experiments, 1×106 HCC1806 cells were injected into the mammary fat pad of 6 8-week-old NOD/scid mice to develop tumors first.
Accordingly, dietary or genetically induced obesity, which does not lead to any pathological indication other than simple fat accumulation in the liver of wild-type (WT) mice, can provoke Sestrin2-deficient mice to develop severe ER stress-associated liver pathologies such as extensive liver damage, steatohepatitis and fibrosis.
The failure of NKT cell-deficient mice to develop AHR is not due to an inability of these mice to produce type 2 T-helper (Th2) responses because NKT cell-deficient mice that are immunized subcutaneously at non-mucosal sites produce normal Th2-biased responses.
