Front Endocrinol (Lausanne)
January 2025
Background: In patients undergoing orthopaedic trauma surgery, acute kidney injury (AKI) can develop post-operatively and is a major cause of increased mortality and hospital stay time. Development of AKI is associated with three main processes: inflammation, ischaemia-reperfusion injury (IRI) and hypoperfusion. In this study, we investigated whether ratios of urine and blood anti-inflammatory biomarkers and biomarkers of hypoperfusion, IRI and inflammation are elevated in patients who develop post-trauma orthopaedic surgery acute kidney injury (PTOS-AKI).
View Article and Find Full Text PDFType I interferon (IFN-I) and IFN-γ foster antitumor immunity by facilitating T cell responses. Paradoxically, IFNs may promote T cell exhaustion by activating immune checkpoints. The downstream regulators of these disparate responses are incompletely understood.
View Article and Find Full Text PDFIonizing radiation (IR) can reprogram proteasome structure and function in cells and tissues. In this article, we show that IR can promote immunoproteasome synthesis with important implications for Ag processing and presentation and tumor immunity. Irradiation of a murine fibrosarcoma (FSA) induced dose-dependent de novo biosynthesis of the immunoproteasome subunits LMP7, LMP2, and Mecl-1, in concert with other changes in the Ag-presentation machinery (APM) essential for CD8+ T cell-mediated immunity, including enhanced expression of MHC class I (MHC-I), β2-microglobulin, transporters associated with Ag processing molecules, and their key transcriptional activator NOD-like receptor family CARD domain containing 5.
View Article and Find Full Text PDFTraumatic brain injury (TBI) is an increasingly recognized diagnosis with significant, and often costly, associated consequences. Yet, despite their increased recognition, TBIs remain underdiagnosed. This issue is especially prominent in the context of mild TBI (mTBI), where there often exists little to no objective evidence of brain injury.
View Article and Find Full Text PDFBackground: Resistance to existing therapies is a significant challenge in improving outcomes for glioblastoma (GBM) patients. Metabolic plasticity has emerged as an important contributor to therapy resistance, including radiation therapy (RT). Here, we investigated how GBM cells reprogram their glucose metabolism in response to RT to promote radiation resistance.
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