Inflammatory markers such as C-reactive protein are frequently elevated in patients treated by dialysis. Serum concentration of these markers are much higher than in the general population, in which it has been clearly shown that chronic inflammation is associated to the occurrence of cardiovascular events. The mechanisms leading to chronic inflammation in dialysis patients may be related to chronic inflammation per se, or to dialysis. Furthermore, in these patients, raised inflammatory markers are associated to malnutrition and increased cardiovascular morbidity and mortality. The association of inflammation, malnutrition and atherosclerosis defines the so-called MIA syndrome.
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J Infect Dev Ctries
December 2024
Nephrology Department, UHC Mother Tereza, Tirane, Albania.
Introduction: Acute kidney injury involves inflammation and intrinsic renal damage, and is a common complication of severe coronavirus disease 2019 (COVID-19). Baseline chronic kidney disease (CKD) confers an increased mortality risk. We determined the renal long-term outcomes of COVID-19 in patients with baseline CKD, and the risk factors prompting renal replacement therapy (RRT) initiation and mortality.
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Institute for Clinical Chemistry and Laboratory Medicine, Faculty of Medicine and University Hospital Carl Gustav Carus, Technische Universität Dresden, Fetscherstrasse 74, 01307, Dresden, Germany.
Metabolic flexibility is key for the function of myeloid cells. Arginine metabolism is integral to the regulation of myeloid cell responses. Nitric oxide (NO) production from arginine is vital for the antimicrobial and pro-inflammatory responses.
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January 2025
Department of Biomedical Engineering, University of Rochester, Rochester, NY, USA.
The aberrant vascular response associated with tendon injury results in circulating immune cell infiltration and a chronic inflammatory feedback loop leading to poor healing outcomes. Studying this dysregulated tendon repair response in human pathophysiology has been historically challenging due to the reliance on animal models. To address this, our group developed the human tendon-on-a-chip (hToC) to model cellular interactions in the injured tendon microenvironment; however, this model lacked the key element of physiological flow in the vascular compartment.
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Department of Neurosurgery, General Hospital of Northern Theater Command, Postgraduate Training Base of General Hospital of Northern Theater Command of Jinzhou Medical University, Shenyang, Liaoning, China.
Traumatic brain injury (TBI) is identified as a risk factor for Parkinson's disease (PD), which is a neurodegenerative disease characterized by the loss of dopaminergic neurons in the substantia nigra (SN). However, the precise mechanism by which chronic TBI initiates PD pathogenesis is not yet fully understood. In our present study, we assessed the chronic progression and pathogenesis of PD-like behavior at different intervals in TBI mice.
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Graduate Institute of Biomedical Materials and Tissue Engineering, College of Biomedical Engineering, Taipei Medical University, Shuang-Ho Campus, New Taipei City 235603, Taiwan; International PhD Program in Biomedical Engineering, College of Biomedical Engineering, Taipei Medical University, Shuang-Ho Campus, New Taipei City 235603, Taiwan; International PhD Program in Cell Therapy and Regenerative Medicine, College of Medicine, Taipei Medical University, Taipei 11031, Taiwan. Electronic address:
Autologous or allogeneic platelet-derived extracellular vesicles (pEVs) show potential in enhancing tissue recovery and healing chronic wounds. pEVs promote neovascularization and cell migration while reducing inflammation, oxidative stress, and scarring. However, their efficacy in clinical settings is challenged by their susceptibility to washout by wound exudate.
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