Studies in the spiny mouse strain demonstrated that maternal dietary supplementation with 5 % Cr (approximately 1.36 g/kg/day) from mid-pregnancy onwards promoted neonate survival and postnatal growth after intrapartum hypoxic insult [70].
Additionally, sympathetic sprouting into the DRG develops normally in the Nav1.3, 1.8, and 1.9 global knockout mouse strains, demonstrating that only Nav1.7 is required for sympathetic sprouting following SNT surgery.
A survey of genomic DNA from 51 mouse strains demonstrated CAG repeat length range from 7 - 17.
Since this gene is known to be a major variant in inbred mouse populations [31], [32], [33], [34], [35], with some strains carrying a premature stop codon and thus effectively being Hc-null, and further recognizing B6 mice as Hc-positive and FVB as Hc-null, we decided to see if other mouse strains demonstrated the PECAM-independent inflammatory phenotype in correlation with their Hc status.
Due to their isogenicity, inbred mouse strains demonstrate low biological variability within each strain[ 1, 2].
Each of these mouse strains demonstrates innate airway hyperresponsiveness that is not the result of differences in absolute lung volume or tidal volume.
Their study using various mouse strains demonstrated that the course of TB was different and dependent on the mouse strain used, which is also reflected in their IGRA results [ 17].
In addition, microarray studies in the hippocampus of eight mouse strains demonstrated highest expression of Comt in C57, amongst all the strains (including DBA), and a significant inverse correlation of Comt expression with aggressive behaviors [ 17].
Crucially, these two mouse strains demonstrated that it was possible to use phenotype-genotype comparisons to map causative dosage-sensitive genes, thus establishing the concept of a mouse mapping panel.
Comparing genomic changes in mice strains demonstrating physiologic differences with pathologic insults is a novel approach to elucidate potential mechanisms.
They showed comparable IEC apoptosis and shedding to their heterozygous counterparts and WT mice of the same strain, demonstrating that peripheral TLR signaling is required for LPS-induced small intestinal injury.
