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In addition, recent advances on genetically engineered techniques such as cell-specific and inducible knockout as well as knockin mouse systems have brought novel concepts on IBD pathogenesis to the fore.
A few studies in mouse systems have reported that, in vivo, allogeneic mismatched MSCs were rejected by the host and could not form ectopic bone, while syngeneic recipient allowed ectopic bone formation, despite the fact that, in vitro, the MSCs showed immunosuppressive activity [ 40, 41].
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Recent studies in the house mouse system have shown that epistatic genes could indeed be involved in reproductive isolation mechanisms at the post-and pre-zygotic level [ 42].
Studies in a mouse system have documented, that co-culture of BM-MSC with B cells reduced the proliferative capacity and the immunoglobulin (Ig) production of the previously LPS-stimulated immune cells [ 88].
Although several epidemiological studies in humans and a limited number of genetic studies in mouse model systems have indicated that clock disruption may predispose mammals to cancer, well-controlled genetic studies in mice have not supported the commonly held view that circadian clock disruption is a cancer risk factor.
Novel techniques and genetically engineered mouse model systems have increased our understanding of thyroid hormone receptor (TR) action, and shed new light on the underlying molecular mechanisms for RTH.
Previous studies in cell and mouse model systems have demonstrated that these proteins play roles in the metabolism of the amyloid precursor protein (APP), including processes involved in the generation, catabolism and deposition of β-amyloid (Aβ) peptides.
Studies in mouse model systems have revealed that hundreds of genes are involved in the host defense against microbial infections and that the interaction of these genes and pathways is very complex [27], [31] [37].
In addition, mapping studies in mouse model systems have identified genetic variants for brain structure variation with great power.
Finally, cell culture and mouse model systems have begun to identify mammary stem cells that may provide progenitors for oncogenic transformation [ 13] and have led to an appreciation of the microenvironment for oncogenesis [ 14, 15].
That is partly because the tumors used in mouse studies are somewhat artificial, often injected into mice whose immune systems have first been disabled.
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