Sentence examples for mice from endotoxic from inspiring English sources

We previously observed that a cyclic peptide derived from the Limulus anti-LPS factor (LALF), which partially protect mice from endotoxic shock lethality, has the ability to modulate cytokine secretion in vitro.

Similar findings have been obtained from in vivo animal studies using a different p38 MAPK inhibitor, SB203580 (Calbiochem) which protected mice from endotoxic shock following administration of a lethal dose of LPS [8].

Ang-1 has also been shown to protect mice from endotoxic shock [ 27].

The extent of inhibition afforded by hBD3 was comparable to that conferred by 1 μg IL-10, which protects mice from endotoxic shock 23, so hBD3 may provide similar protection.

Studies using GSNOR-null (GSNOR−/−) mice showed that GSNOR is critical for protecting mice from endotoxic and septic shock by preventing hazardous increase of protein S-nitrosylation and extensive cell death in liver and lymphoid tissues (3).

It has also been reported that the administration of recombinant MIF increased the systemic toxicity of endotoxin, whereas anti-MIF antibody fully protected mice from endotoxic shock and death [ 17].

We found an increased resistance of cIAP-1 mice for endotoxic shock induced by LPS treatment.

PI3Kδ can mediate a switch between TIRAP dependent pro-inflammatory cytokine secretion and TRAM-dependent IL-10 secretion, thereby limiting inflammation and protecting mice from LPS induced endotoxic shock [ 21].

Noncleavable transmembrane TNF transgenic mice were fully protected from endotoxic shock, pointing towards the importance of TNF cleavage in the endotoxemia model (Mueller et al, 1999).

In contrast, dexmedetomidine improves mortality from endotoxic shock in rats [ 22] and cecal ligation and intestinal puncture in mice [ 23] associated with an anti-inflammatory effect.

In vivo PAF treatment immediately after LPS challenge markedly improved the survival rate against mortality from endotoxic shock.