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Pharmacological inhibition of miR-21 using antagomiR-21 significantly increased mortality in two models of lethal infections (P < 0.01, endotoxinemia and peritonitis).
Existing mouse models of lethal Ebola virus infection do not reproduce hallmark symptoms of Ebola hemorrhagic fever, neither delayed blood coagulation and disseminated intravascular coagulation, nor death from shock, thus restricting pathogenesis studies to non-human primates.
Existing mouse models of lethal Ebola virus infection do not reproduce hallmark symptoms of Ebola hemorrhagic fever, neither delayed blood coagulation and disseminated intravascular coagulation nor death from shock, thus restricting pathogenesis studies to nonhuman primates.
To understand the role of fetuin-A in LSI, we measured its circulating levels in murine models of lethal endotoxemia and sepsis.
These observations are consistent, in part, with the transcriptional alterations reported in models of lethal ischemic injuries which are preceded by ischemic or pharmacological preconditioning.
In light of the capacity of EGCG in inhibiting LPS-induced HMGB1 release and cytokine activities, we explored its efficacy in animal models of lethal endotoxemia and sepsis (induced by cecal ligation and puncture).
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This experiment was designed to test the impact of this strategy on neuronal and astroglial damage in a swine model of lethal hemorrhage.
Ab513 mitigates thrombocytopenia in a humanized mouse model, resolves vascular leakage, reduces viremia to nearly undetectable levels, and protects mice in a maternal transfer model of lethal antibody-mediated enhancement.
Three mAbs targeting distinct epitopes on the four DENV serotypes and engineered to prevent FcγR binding did not enhance infection and neutralized DENV in vitro and in vivo as postexposure therapy in a mouse model of lethal DENV infection.
The synthetic random copolymer of the amino acids, L-Glu, L-Lys, L-Ala and L-Tyr, termed GLAT, with promiscuous binding to multiple MHC class II alleles, reduces the incidence, onset and severity of disease in the BIO.D2 --> BALB/c mofelethalethal GVHD.
We have therefore tested the effect of exogenous administration of IL-23 in the model of lethal infection with 10×LD50.
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