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In female BALB/c mice the mortality rate was 20%, which correlated with extensive hepatic necrosis.
In untreated (vehicle) wild-type (WT) CF-1 mice, the mortality rate was 90% from CLP-induced sepsis over a 7-days period (Fig 3A).
In control mice, the mortality rates were 90%and69%9% after 25 h of infection with the hGISA and GISA strains, respectively.
In the bleomycin-injury lung model used in this study (intratracheal administration of bleomycin 2 mg/kg to 10- to 12-week-old mice), the mortality was as high as 70% by day 12.
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This result suggests that 10 mg/Kg CDDO-Im is not intrinsically toxic to mice, and that the mortality of CLL/SBL mice might be related to the effect of the drug on the leukemic cells.
Together, these findings are consistent with the notion that MMP-1a released from the endothelium of endotoxemic mice contributes to the mortality observed in the mouse sepsis models.
After i.v. infection with 102 cfu of S. typhimurium, only 5% of the LDLR−/− mice died, whereas the mortality of control LDLR+/+ was 100% within 12 days of infection (P<.001; Fig. 1).
Treatment with WNIG offered complete protection to mice injected with dexamethasone, while the mortality among control infected mice injected with dexamethasone exceeded 80%.
Surprisingly, pretreatment of mice with the vehicle (DMSO), increased the mortality in NMDA-injected mice by 25%.
Ferret models suggest that virulence is not increased by adamantane resistance in influenza A (H3N2) infections (8 ), although experimental studies with recombinant influenza (H1N1) in mice have suggested that the mortality rate is increased by a double mutation conferring adamantane resistance (9 ).
Blocking endogenous murine protein C with an anti-mouse monoclonal antibody increased the mortality rate significantly from 62% to 91%.
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