Traumatic spinal cord injury (SCI) is followed by an instant increase in expression of the microglial-derived proinflammatory cytokine tumor necrosis factor (TNF) within the lesioned cord. TNF exists both as membrane-anchored TNF (mTNF) and as cleaved soluble TNF (solTNF). We previously demonstrated that epidural administration of a dominant-negative inhibitor of solTNF, XPro1595, to the contused spinal cord resulted in changes in Iba1 protein expression in microglia/macrophages, decreased lesion volume, and improved locomotor function.
View Article and Find Full Text PDFNuclear factor-kappa B (NF-κB) is a key modulator of inflammation and secondary injury responses in neurodegenerative disease, including spinal cord injury (SCI). Inhibition of astroglial NF-κB reduces inflammation, enhances oligodendrogenesis and improves functional recovery after SCI, however the contribution of neuronal NF-κB to secondary inflammatory responses following SCI has yet to be investigated. We demonstrate that conditional ablation of IKK2 in Synapsin 1-expressing neurons in mice (Syn1creIKK2) reduces activation of the classical NF-κB signaling pathway, resulting in impaired motor function and altered memory retention under naïve conditions.
View Article and Find Full Text PDFThe treatment of oesophageal perforations (EP) has primarily been a surgical issue and despite significant advances in surgery and intensive care medicine EP is continuously associated with high morbidity and mortality. Implementation of an effective treatment algorithm which steps away from the traditional surgical approach is essential for achieving a better clinical outcome. A modern treatment algorithm includes contrast computed tomography and endoscopy diagnostics and use of non- or semi-invasive procedures like selfexpanding metal stents, selective digestive decontamination and the establishment of a controlled fistula.
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