For in vivo MRI studies, the engineered nanocages were evaluated using the KrasG12D; Trp53R172H; Pdx-1Cre (KPC) transgenic mouse models, which develop clinically relevant pancreatic tumor under normal processes of angiogenesis, immune function and inflammation.
This has been partly circumvented through the use of non-human primate models, which develop a form of TB that exhibits many of the hallmarks of the human infection [12].
Xenograft models provide a complement to genetically engineered mouse models which develop over a longer time and reside in an immunocompetent host but do not always capture all aspects of human cancer.
A geometric model, which develops the basis of a ray-tracing technique for performing the optical analysis, is also described.
We have recently characterized a rat ciliopathy model which develops primary photoreceptor degeneration and secondary vasoregression.
Indeed, in earlier studies, using a MPTP-treated mouse model which develops tauopathy, we have shown that activated p-GSK-3β co-immunoprecipitates with α-Syn and with pSer396/404 Tau [24].
Sle3 bicongenic mouse model, which develops a more robust lupus-like phenotype was next utilized.
We utilised two mouse models, each manifesting distinct AD-related pathologies: the K3 tau transgenic model, which develops NFTs [ 21, 22]; and the APP/PS1 transgenic model, which develops amyloid plaques [ 23].
This point is illustrated by the protein tyrosine kinase Lyn-deficient mouse model, which develops a lupus-like autoimmune syndrome.
However, these studies are specific to the mouse experimental model, which develops a single set of teeth with no replacements.
