Compared to hearts from uninfected mice (Figure 3A and B) infected mice displayed increased inflammation and pseudocysts along with increased cellularity, mostly resulting from influx of inflammatory cells (Figure 3C and D).
At day 7 p.i. TIMP-1−/− mice displayed increased MMP-9 activity, supporting a role of TIMP-1 as a major inhibitor of MMP9 activity in WT mice (Roderfeld et al., 2007).
In another model, CB2 receptor KO mice displayed increased allergic responses in the skin, which was secondary to increased production of proinflammatory cytokines [54].
In addition, EphA2-deficient gene-trap mice displayed increased susceptibility to chemical carcinogen-induced skin cancer, accompanied by increased tumor cell proliferation and phosphorylation of Erk [ 36].
ACV mice displayed increased heart rates and fractional shortening as assessed by echocardiography.
k, Dmrt3−/− mice displayed increased burst and interburst durations compared to control animals, analysis made on L2s (n = 6 per genotype, P = 0.02, burst; P = 0.001, interburst).
MTKO mice displayed increased B cell differentiation following OVA challenge and an enhanced lymphoproliferative response to mitogenic stimulation.
Compared to cells obtained from control animals, splenic DCs from SDR mice displayed increased levels of MHC I, CD80, and CD44, indicative of an activated phenotype.
When the researchers disrupted either the organ or the production of the pheromone, the older mice displayed increased mating behavior toward the juveniles.
Late-onset (day 7) tumors from CLP-operated mice displayed increased proportions of F4/80High.
Irgm1-deficient mice displayed increased susceptibility to this bacterium that was reflected in increased bacterial loads in spleen and liver and decreased maturation of S. typhimurium granulomas.
