Sentence examples for mediator of lethality from inspiring English sources

In particular, the thrombin-rhTM complex demonstrates an anti-inflammatory ability through neutralizing HMGB-1 [48] 48], which is known to be a mediator of lethality and is released from necrotic cells or macrophages/activated dendritic cells with potent pro-inflammatory function, which in turn causes shock or MODS when being disseminated in the systemic circulation [49 51].

HMGB-1, also a DNA-binding protein, is released from cells due to necrosis or via a non-classical secretion pathway and is a late-stage mediator of lethality in a murine model of sepsis.

Subsequently, these findings were extended by Yang and colleagues [ 13], who showed that HMGB1 is also a mediator of lethality in mice rendered septic by the induction of polymicrobial bacterial peritonitis.

HMGB1 is a late mediator of lethality, and contributes to the increased levels of circulating and tissue cytokines that are present hours to days after the initial exposure to LPS [ 56].

Here, we demonstrated that activation of PPAR- δ and - γ by specific ligands, GW501516 and rosiglitazone, respectively, inhibits the LPS-primed release of HMGB1, a late mediator of lethality in endotoxic shock.

For many years the extranuclear functions of HMGB1 were little studied (with the notable exception of studies on amphoterin, the other name of HMGB1, by Rauvala and coworkers [4]), until Wang et al. [5] strikingly showed that, in addition to its nuclear functions, HMGB1 was involved in sepsis as a late mediator of endotoxin lethality in mice.

Recently, high mobility group box 1 (HMGB1) was identified as a late mediator of endotoxin lethality.

Recent studies have shown that the monocyte-derived HMGB1 is a late-acting cytokine mediator of endotoxin lethality.

It later became evident that HMGB1 is actively secreted from cells, has cytokine activities and is a late mediator of endotoxin lethality in mice [ 4].

It is interesting to note that high-mobility-group box protein-1 (HMGB1), which is specifically released from necrotic but not apoptotic cells, is systemically elevated in human sepsis and functions as a mediator of endotoxin lethality in mice [ 12].

In the periphery, released HMGB1 has pleitropic pro-inflammatory effects, including action as a late mediator of endotoxin lethality in mice (Wang et al., 1999; Lotze and Tracey, 2005).