Copper stimulates the synthesis and release of interleukin-8 in human endothelial cells: a possible early role in systemic inflammatory responses.

Endogenous copper can play an important role in postischemic reperfusion injury, a condition associated with endothelial cell activation and increased interleukin 8 (IL-8) production. Excessive endothelial IL-8 secreted during trauma, major surgery, and sepsis may contribute to the development of systemic inflammatory response syndrome (SIRS), adult respiratory distress syndrome (ARDS), and multiple organ failure (MOF). No previous reports have indicated that copper has a direct role in stimulating human endothelial IL-8 secretion.

Low albumin level in the emergency department: a potential independent predictor of delayed mortality in blunt trauma.

Albumin is an abundant plasma protein with multiple physiologic functions, and low serum albumin levels have been associated with increased mortality in hospitalized patients. In a retrospective matched-pair study, we investigated whether emergency department (ED) albumin levels predict delayed mortality for patients initially stabilized after blunt trauma. Fifty-one hospital non-survivors who died more than 24 h after admission to a trauma center ED were matched by Injury Severity Score, type and location of injury, age, and gender with 51 survivors.

Copper inhibits activated protein C: protective effect of human albumin and an analogue of its high-affinity copper-binding site, d-DAHK.

Activated protein C (APC) is useful in the treatment of sepsis. Ischemia and acidosis, which often accompany sepsis, cause the release of copper from loosely bound sites. We investigated (i) whether physiological concentrations of copper inhibit APC anticoagulant activity and (ii) if any copper-induced APC inhibition is reversible by human serum albumin (HSA) or a high-affinity copper-binding analogue of the human albumin N-terminus, d-Asp-d-Ala-d-His-d-Lys (d-DAHK).