Microvesicles are cell-derived signaling particles emerging as important mediators and biomarkers of systemic inflammation, but their production in severe burn injury patients has not been described. In this pilot investigation, we measured circulating microvesicle levels following severe burns, with severe sepsis patients as a comparator group. We hypothesized that levels of circulating vascular cell-derived microvesicles are elevated acutely following burns injury, mirroring clinical severity due to the early onset and prevalence of systemic inflammatory response syndrome (SIRS) in these patients.
View Article and Find Full Text PDFObjective: To evaluate the efficacy of eLearning in the widespread standardised teaching, distribution and implementation of the Chelsea Critical Care Physical Assessment (CPAx) tool-a validated tool to assess physical function in critically ill patients.
Design: Prospective educational study. An eLearning module was developed through a conceptual framework, using the four-stage technique for skills teaching to teach clinicians how to use the CPAx.
Introduction: Severe burn leads to a state of hypercatabolism, resulting in rapid muscle loss and long-term disability. As survival rates from severe burn are improving, early rehabilitation is essential to facilitate functional recovery. However, there is no way of measuring the degree of disability in the acute stages, and hence, no marker of functional recovery.
View Article and Find Full Text PDFIntroduction: Intensive care unit-acquired weakness (ICU-AW) is common in survivors of critical illness, resulting in global weakness and functional deficit. Although ICU-AW is well described subjectively in the literature, the value of objective measures has yet to be established. This project aimed to evaluate the construct validity of the Chelsea Critical Care Physical Assessment tool (CPAx) by analyzing the association between CPAx scores and hospital-discharge location, as a measure of functional outcome.
View Article and Find Full Text PDFTumor necrosis factor α-converting enzyme (TACE) is responsible for the shedding of cell surface TNF. Studies suggest that reactive oxygen species (ROS) mediate up-regulation of TACE activity by direct oxidization or modification of the protein. However, these investigations have been largely based upon nonphysiological stimulation of promonocytic cell lines which may respond and process TACE differently from primary cells.
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