Manual vs. Mechanical Chest Compressions in Out-of-Hospital Cardiac Arrest

Objective: The objective was to conduct an analysis of literature that examined whether the use of mechanical vs. manual chest compressions results in outcomes (e.g. quality of CPR, return of spontaneous circulation (ROSC), neurologic outcome, survival) that are significantly increased or decreased in adults that experienced out of hospital cardiac arrest (OHCA). Methods: Systematic searches were conducted through the James Madison University Library. The inclusion criteria included human adults that experienced out of hospital cardiac arrest that were treated by Emergency Medical Services (EMS) with and/or without a mechanical chest compression device. Results: A statistically significant difference was not found between the manual chest compression study arm and the automated chest compression study arm. Conclusion: Because P-values were not statistically significant, when comparing manual to automated chest compressions, the researchers were unable to confidently state recommendations. However, there was moderate clinical significance for improved outcome with manual chest compressions

A Francisella Mutant in Lipid A Carbohydrate Modification Elicits Protective Immunity

Francisella tularensis (Ft) is a highly infectious Gram-negative bacterium and the causative agent of the human disease tularemia. Ft is designated a class A select agent by the Centers for Disease Control and Prevention. Human clinical isolates of Ft produce lipid A of similar structure to Ft subspecies novicida (Fn), a pathogen of mice. We identified three enzymes required for Fn lipid A carbohydrate modifications, specifically the presence of mannose (flmF1), galactosamine (flmF2), or both carbohydrates (flmK). Mutants lacking either galactosamine (flmF2) or galactosamine/mannose (flmK) addition to their lipid A were attenuated in mice by both pulmonary and subcutaneous routes of infection. In addition, aerosolization of the mutants (flmF2 and flmK) provided protection against challenge with wild-type (WT) Fn, whereas subcutaneous administration of only the flmK mutant provided protection from challenge with WT Fn. Furthermore, infection of an alveolar macrophage cell line by the flmK mutant induced higher levels of tumor necrosis factor-α (TNF-α) and macrophage inhibitory protein-2 (MIP-2) when compared to infection with WT Fn. Bone marrow–derived macrophages (BMMø) from Toll-like receptor 4 (TLR4) and TLR2/4 knockout mice infected with the flmK mutant also produced significantly higher amounts of interleukin-6 (IL-6) and MIP-2 than BMMø infected with WT Fn. However, production of IL-6 and MIP-2 was undetectable in BMMø from MyD88−/− mice infected with either strain. MyD88−/− mice were also susceptible to flmK mutant infection. We hypothesize that the ability of the flmK mutant to activate pro-inflammatory cytokine/chemokine production and innate immune responses mediated by the MyD88 signaling pathway may be responsible for its attenuation, leading to the induction of protective immunity by this mutant

Relative availability of selected trace elements from coal fly ash and Lake Michigan sediment

The concentration of greater than 1 ..mu..m coal fly ash particles in Lake Michigan surface waters was found to be 10/sup 5/ to 10/sup 6/ per liter. With an expected residence time of one year, this concentration implies a flux to the sediment of 10/sup 6/ to 10/sup 7/ particles/cm/sup 2//yr, or about 10/sup -6/ to 10/sup -5/ g/cm/sup 2//yr. The release of trace elements from fly ash and sediment has been studied using Chelex-100 resin to simulate leaching at high dilutions in natural media. Mn, Pb and Zn, but not Fe, are released more readily from Lake Michigan sediment than from fly ash