Using apical intramyocardial microinjection of recombinant IL-6 protein in neonatal 1-day-old mice, we further explored whether IL-6 could induce cardiomyocyte proliferation without apparent cardiac lesions.
Having confirmed via histology, haematology and clinical biochemistry analyses that OPP is not toxic to mice, we further explored the gene expression changes caused by OPP through statistical and functional analyses using Illumina microarrays.
In view of the increase in apparent cell number (Fig. 4A), but diminished number of axons (Fig. 2C), in foci in the spinal cord of βLKB1KO mice, we next explored the possibility that inflammatory macrophage infiltration might be involved in the present model.
This is accentuated by our data in mice, where we explored for the first time a therapeutic MKL1 and MKL2 knockdown approach in tumours.
Although activation of HSCs with IFN α could so far only be shown in mice, we here explore whether and under which conditions a potentially similar effect in the human situation could improve TKI therapy of CML patients.
To extend these studies and identify candidate cell types that might contribute to oncogenesis in mouse models, we explored the link between the mouse mammary epithelial hierarchy and models of mammary tumorigenesis.
As Cldn13 appears to be mouse specific, we explored its phylogenetic relationship with other Claudin family members.
Using mouse models, we explored the neuroprotective effect of near infrared light (NIr) treatment, delivered at an age when substantial pathology is already present in the cerebral cortex.
Using these mice, we hope to explore the full range of inflammatory stimuli for which this QTL explains interstrain differences.
