Moreover, these mice were highly susceptible to experimental triggers of colitis.
FFI mice were highly resistant to infection by pre-existing prions, confirming infectivity did not arise from contaminating agents.
Further analysis revealed that the DN3 cell numbers from Rag2 KI mice were highly accumulated, whereas the DN4 cell numbers were reduced, indicating the arrest of thymocyte development at the DN3 stage (Fig. 2B and Supplementary Fig. S2).
Consistent with the development of diffuse lesions, genes that were differentially expressed in CD45− tissue cells from the lung of wild-type and Ccr2−/− mice were highly enriched in human diffuse, progressive PF.
In this work, we showed that mice deficient in the alpha/beta interferon receptor (IFNAR mice) were highly susceptible to USUV infection and provided a lethal challenge model for vaccine testing.
Since jnk1−/− mice were highly resistant to ventilator-induced lung injury, we performed comprehensive gene expression profiling of ventilated wild-type or jnk1−/− mice to identify novel candidate genes which may play critical roles in the pathogenesis of ventilator-induced lung injury.
Although we observed comparable escape latencies for male TTC9A+/+, male TTC9A−/−, and female TTC9A−/− in the home-cage emergence test, we cannot interpret that both the TTC9A+/+ and TTC9A−/− male mice were highly anxious as other behavioral tests showed no significant difference in their exploratory and anxiety-related behaviors.
Our findings indicate that the Incremental Repeated Acquisition (IRA) and trace fear conditioning tasks, neither of which have previously been published with these mice, were highly sensitive to P301L tau expression, whereas the Morris water maze, the most commonly used task with this model, was the least sensitive.
The lung tumors in Kras LA1) mice were highly fibrotic and contained cancer-associated fibroblasts (CAF) that produced collagen and generated stiffness in collagen gels.
In these animals, there was no gender gap in heart disease, and female mice were highly susceptible to oxidative damage from free radicals, which boost plaque formation in arteries.
The importance of GR expression for survival of septic shock has been further demonstrated by Kleiman et al. who showed that GR dimerization-deficient mice were highly susceptible to endotoxic shock, suggestively by their inability to downregulate the pro-inflammatory cytokine IL-1β [18].
