Extracorporeal life support for severe ARDS in adults is a successful therapeutic option in those patients who do not respond to conventional mechanical ventilator strategies.

Although no difference in ISS was identified between the lean and obese cohorts, there was an increase in mortality with the obese cohort. The severity of lower extremity injuries increased with increasing BMI. The overweight cohort was associated with lower ISS and abdominal mAIS score compared with the lean cohort. This protection may be attributable to an increase in insulating tissue, or a "cushion effect," without a significant increase in mass and momentum.

Among adults admitted for trauma in Washington State, 3-year cumulative mortality was 16% despite a decline in in-hospital deaths. Discharge to a skilled nursing facility at any age following trauma admission was associated with a higher risk of subsequent mortality.

Defective cardiac function during sepsis has been referred to as “cardiomyopathy of sepsis.” It is known that sepsis leads to intensive activation of the complement system. In the current study, cardiac function and cardiomyocyte contractility have been evaluated in rats after cecal ligation and puncture (CLP). Significant reductions in left ventricular pressures occurred in vivo and in cardiomyocyte contractility in vitro. These defects were prevented in CLP rats given blocking antibody to C5a. Both mRNA and protein for the C5a receptor (C5aR) were constitutively expressed on cardiomyocytes; both increased as a function of time after CLP. In vitro addition of recombinant rat C5a induced dramatic contractile dysfunction in both sham and CLP cardiomyocytes, but to a consistently greater degree in cells from CLP animals. These data suggest that CLP induces C5aR on cardiomyocytes and that in vivo generation of C5a causes C5a–C5aR interaction, causing dysfunction of cardiomyocytes, resulting in compromise of cardiac performance.

More than half of older trauma patients in this study had sarcopenia, osteopenia, or both. Each factor was independently associated with increased 1-year mortality. Given the prevalent use of abdominopelvic CT in trauma centers, opportunistic screening for radiologic indicators of frailty provides an additional tool for early identification of older trauma patients at high risk for poor outcomes, with the potential for targeted interventions.

No abstract

Lipopolysaccharide (LPS) is a key inflammatory mediator. It has been proposed to function as an important molecule that alerts the host of potential bacterial infection. Although highly conserved, LPS contains important structural differences among different bacterial species that can significantly alter host responses. For example, LPS obtained from Porphyromonas gingivalis, an etiologic agent for periodontitis, evokes a highly unusual host cell response. Human monocytes respond to this LPS by the secretion of a variety of different inflammatory mediators, while endothelial cells do not. In addition, P. gingivalis LPS inhibits endothelial cell expression of E-selectin and interleukin 8 (IL-8) induced by other bacteria. In this report the ability of P. gingivalis LPS to activate p38 mitogen-activated protein (MAP) kinase was investigated. It was found that p38 MAP kinase activation occurred in response to P. gingivalis LPS in human monocytes. In contrast, no p38 MAP kinase activation was observed in response to P. gingivalis LPS in human endothelial cells or CHO cells transfected with human Toll-like receptor 4 (TLR-4). In addition, P. gingivalis LPS was an effective inhibitor of Escherichia coli-induced p38 MAP kinase phosphorylation in both endothelial cells and CHO cells transfected with human TLR-4. These data demonstrate that P. gingivalis LPS activates the LPS-associated p38 MAP kinase in monocytes and that it can be an antagonist for E. coli LPS activation of p38 MAP kinase in endothelial and CHO cells. These data also suggest that although LPS is generally considered a bacterial component that alerts the host to infection, LPS from P. gingivalis may selectively modify the host response as a means to facilitate colonization.The innate host defense system protects mammalian hosts against microbial infection through an orchestrated response to the presence of nonself components (31, 32). Lipopolysaccharide (LPS), a component of the gram-negative bacterial cell wall, is a key structure recognized by a variety of different innate host defense proteins, allowing the host to "sense" a potential bacterial infection (8,62). LPS is evolutionarily an ideal target, since it is a conserved structure found on a wide variety of pathogenic bacteria and is sufficiently different from host components to allow a safe selective response (38). However, there are important structural differences in LPS composition between different bacterial species, such as fatty acid acyl chain composition and charge, which can significantly affect the host response (33,36,42,49,64). Different binding affinities for LPS binding protein and CD14 may only partly explain the lowered inflammatory response to some LPS species that has been observed (14), consistent with the notion that the major role of LPS binding protein and CD14 is to concentrate LPS at host cell surfaces (65). Recently it has been demonstrated that cell surface Toll-like receptor (TLR) proteins participate in the ability of the host to discriminate different LPS structural f...

beta-blocker therapy is safe and may be beneficial in selected trauma patients with or without head injury. Further studies looking at beta-blocker therapy in trauma patients and their effect on cerebral metabolism are warranted.