In addition, Muc19, a single-copy gene in human and mouse, was demonstrated to be a putative ortholog of spiggin.
On the other hand, TSP-1-deficient mice were demonstrated to have an only slightly different phenotype than their control group, possibly due to compensation by genetic adaption [24, 25].
Previously, higher vasomotor capacities in medium- to small-sized arteries and improved perfusion in hDDAH-1 transgenic mice were demonstrated [2], [9].
All arthritic mice displayed high serum levels of IgG and anti-CII antibodies, but no significant differences between the ovariectomized and sham-operated mice were demonstrated.
Furthermore, iNOS-deficient mice were demonstrated to be highly susceptible to TB infection (Refs 42, 47, 48), and NO was shown to be crucial in maintaining a latent TB infection in mice (Ref. 49).
Furthermore, inwardly rectifying K+ channel 6.2 (Kir6.2) deficient mice were demonstrated to be more susceptible to stretch-induced ANP release compared to wild type, suggesting a negative feedback axis between KATP and cardiac natriuretic peptide release [ 38].
Human breast epithelial cells with Hoechst dye-effluxing 'side population' (SP) properties characteristic of mammary stem cells in mice were demonstrated to be undifferentiated cells by lack of expression of myoepithelial and luminal epithelial membrane markers.
Moreover, in vivo efficacy in an oral glucose tolerance test in lean mice is demonstrated.
Cellular and humoral immunogenicity in mice was demonstrated using a DNA prime/rFPV boost and vaccinia virus challenge model.
By conjugating poly ethylene glycol) (PEG) and cyclic-RGD onto SPNs-SiO2, targeted PA imaging of tumor in living mice is demonstrated after systemic administration, showing a high signal to background ratio.
