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Therapeutic studies using transgenic rodent models often fail to predict efficacy and outcome in human patients.
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These studies are usually conducted either in vitro using cell culture or in vivo using transgenic rodents, either with knockouts to assess the effect of removing the gene or with knockins to assess the affect of adding the gene.
Studies using transgenic rodents have shown a BM origin of a limited fraction of renal myofibroblasts after ischemia/reperfusion injury (Broekema et al. 2007) and in the model of adriamycin-induced chronic renal failure (Li et al. 2007).
Among them, transgenic in vivo genotoxicity assays, which use transgenic rodents carrying reporter genes to detect genetic alterations, enable us to evaluate organ-specific in vivo genotoxicity.
Moreover, because we attempted to quantify MOG specific T cells within the context of the natural repertoire of a rodent, instead of using transgenic animals with single TCR specific for MOG (which may have simplified the identification of MOG specific T-cells), quantification was done in different animals and individual dynamics were extrapolated from the population analysis.
"If we understand how this works, we can grow plants using transgenic approaches".
Using transgenic mice, Berer et al.
Studies using the transgenic rodent (TGR) mutation reporter assay are very efficient and commonly used.
But because rodents don't naturally produce the plaques, those studies used transgenic mice and rats.
"I will go broke if I don't get to use transgenic beans.
We used rodent transgenic cell lines containing 50 70 copies of a LacI transgene to provide the enhanced sensitivity required to quantify mutational frequency and type in the 1100-bp LacI target as well as assessment of DNA damage to the entire 45-kbp construct.
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