A recombinant P. aeruginosa PAO1ΔpscD::exlBA strain, deficient for T3SS but engineered to express ExlA, gained lytic capacity on endothelial cells and full virulence in mice, demonstrating that ExlA is necessary and sufficient for pathogenicity.
Initial analysis of biochemical markers, which previously displayed kindling-dependent alterations in rat hippocampal synaptosomes, showed similar trends in both wild-type and VAMP2+/− mice, demonstrating that kindled rat and mouse models are comparable.
Synthetic, protein-only prions can cause a mad cow like disease in mice, as can brain tissue from these mice, demonstrating that misfolded proteins are the infectious agents in prion disease.
As previously reported [8], no reproductive phenotype was identified in adult SM Cre positive, ARflox negative male mice demonstrating that expression of Cre alone had no effect (data not shown).
We tested this hypothesis with experiments in mice, demonstrating that stress causes both molecular changes, which are partly reversible and can be elicited by the administration of corticosterone.
Rapamycin abrogated differences in regenerating liver weights between control and LKO mice, demonstrating that let-7b/c2 loss promotes additional mTOR activation to enhance regeneration.
However, depleting CD4+ T cells did not modify the viremia in both WT and Tlr3 −/− mice, demonstrating that virus replication is independent of CD4+ T cells.
p65EHT mice developed papillomas similarly to p65FL mice demonstrating that heterozygous loss of p65 in the epidermis was not sufficient to prevent tumour development (Fig 1D and E).
Figure 5 shows representative FISH analyses performed on wild-type, hemizygous, and homozygous β+IVSI-6 transgenic mice, demonstrating that integration occurred at band F2 of the mouse chromosome 7.
Auditory thresholds increased from 84 dB on P17 18 to more than 100 dB in adult Cx30−/− mice, demonstrating that hearing impairment was more severe in Cx30−/− mice than in Cx26OtogCre mice.
However, the disease course and histological features of the arthritic joints following K/BxN serum injection were comparable between WT and PAD4-deficient mice, demonstrating that PAD4 is not required for the effector phase of arthritis.
