J Trauma
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The incidence of periprosthetic fractures after total knee arthroplasty is continuously rising because of an increasing number of knee joint replacements and an enhanced survivorship of the elderly population after knee arthroplasty. The purpose of this study was to analyze the practicability and effectiveness of the various treatment methods for management of periprosthetic fractures after total knee arthroplasty, and to determine the clinical and radiographic long-term results of patients following surgical and nonoperative treatment of these injuries. ⋯ Compared with current data in literature, we had a satisfactory outcome in following individualized treatment of periprosthetic fractures after knee joint replacement. Referring to the wide field of treatment options and high rates of complications, periprosthetic femoral fractures around the knee commonly constitute a challenging problem for the treating surgeons and require an adequate analysis of fracture etiology and a corresponding transfer into an individual treatment concept.
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Severe injury can cause intestinal permeability through decreased expression of tight junction proteins, resulting in systemic inflammation. Activation of the parasympathetic nervous system after shock through vagal nerve stimulation is known to have potent anti-inflammatory effects; however, its effects on modulating intestinal barrier function are not fully understood. We postulated that vagal nerve stimulation improves intestinal barrier integrity after severe burn through an efferent signaling pathway, and is associated with improved expression and localization of the intestinal tight junction protein occludin. ⋯ Vagal nerve stimulation performed before injury improves intestinal barrier integrity after severe burn through an efferent signaling pathway and is associated with improved tight junction protein expression.
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Tissue injury from mechanical trauma modulates innate immunity. The resultant systemic inflammatory response syndrome (SIRS) closely mimics clinical sepsis, and bacterial n-formyl peptides are septic mediators. Similar formyl peptides exist in mitochondria but little is known about their actions on human neutrophils (PMN). ⋯ Formylated mitochondrial proteins are potent immune activators. Acting through the FPR-1 receptor on professional phagocytes, MDP elicits [Ca]i release responses and Ca entry via G-protein-coupled pathways. MDP activates chemotaxis and respiratory burst. Our findings suggest a novel paradigm wherein one root cause of SIRS after trauma may be the release of mitochondrial fragments from mechanically damaged tissues. In this paradigm, mitochondrial debris "alarmins" alter host PMN phenotype, activating or suppressing immunity, predisposing to SIRS, sepsis or organ failure.