The Journal of surgical research
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Acellular dermal matrix (ADM) has been used successfully in the treatment of full-thickness skin injuries as an allogenic dermal substitute. To assess the efficacy of xenogenic ADM in such wounds, we examined the long-term wound healing and immunological responses to porcine ADM in a rat model. ⋯ In wounds implanted with xenogenic ADM, a short-lived acute inflammatory response, long-lasting humoral and cell-mediated immune responses, and generally poor wound healing were observed.
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Randomized Controlled Trial Clinical Trial
Increased urinary excretion of bilirubin oxidative metabolites in septic patients: a new marker for oxidative stress in vivo.
Bilirubin oxidative metabolites (BOMs) are generated from bilirubin as a result of its scavenging action against free radicals. During sepsis, excess amounts of free radicals are produced, and they play an important role in the pathophysiological process. We studied whether urinary excretion of BOMs would increase under septic conditions in humans and compared BOM levels with other well-established clinical parameters of inflammation. ⋯ These results demonstrated a urinary increase in BOMs in septic patients. This increase indicates that urinary BOM level is a possible marker for continuous monitoring of sepsis severity in clinical practice.
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Severe acute pancreatitis (AP)(2) is associated with exaggerated leukocyte adherence and activation. Endothelial cellular adhesion molecules (CAMs) can be induced by cytokines, but also directly by oxygen free radicals (OFRs), mediated by nuclear factor kappa-B (NF-kappa B). We investigated the behavior of inducible CAMs in relation to pancreatic oxidative stress. Our novel modification of cerium capture histochemistry (reaction of OFRs with cerium produces laser reflective Ce perhydroxide precipitates) combined with reflectance confocal laser scanning microscopy (CLSM) allows the histological codemonstration of in vivo OFR production and immunolabeled CAMs, or NF-kappa B. ⋯ The early acinar oxidative stress is colocalized with NF-kappa B activation, preferential P-selectin, and ICAM upregulation in this AP model. Subsequently, adherent, activated PMNs become the major source of OFRs, thereby contributing to tissue damage.