Hepatocellular carcinoma (HCC) invariably develops within a setting of chronic inflammation caused by either hepatotropic viruses, toxins, metabolic liver disease or autoimmunity. Mechanisms that link these two processes are not completely understood, but transcription factors of the NF-κB family and signal transducer and activator of transcription 3 (STAT3), cytokines such as IL-6 and IL-1α and ligands of the epidermal growth factor receptor (EGFR) family are clearly pivotal players. HCC may have its origins in either hepatocytes or hepatic progenitor cells (HPCs), and HCCs, like other solid tumours appear to be sustained by a minority population of cancer stem cells.
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http://dx.doi.org/10.1007/978-3-642-03503-6_8 | DOI Listing |
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.
View Article and Find Full Text PDFSemin Immunopathol
January 2025
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.
View Article and Find Full Text PDFSci Rep
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.
View Article and Find Full Text PDFTransl Psychiatry
January 2025
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.
View Article and Find Full Text PDFTrends Biotechnol
January 2025
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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