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Cytochrome c as a Potentially Clinical Useful Marker of Mitochondrial and Cellular DamageFactors affecting effectiveness of vaccination against hepatitis B virus in hemodialysis patientsMalate dehydrogenase-2 inhibitor LW6 promotes metabolic adaptations and reduces proliferation and apoptosis in activated human T-cells.Angiogenin is upregulated during the alloreactive immune response and has no effect on the T-cell expansion phase, whereas it affects the contraction phase by inhibiting CD4+ T-cell apoptosis.Toll-like receptors and their role in renal pathologies.Hepatitis C virus core+1/ARF protein decreases hepcidin transcription through an AP1 binding site.Asymptomatic hyperuricemia and chronic kidney disease: Narrative review of a treatment controversial.Preconditioning of primary human renal proximal tubular epithelial cells without tryptophan increases survival under hypoxia by inducing autophagy.Hepatitis C virus modulates lipid regulatory factor Angiopoietin-like 3 gene expression by repressing HNF-1α activity.Serum copper and ferroportin in monocytes of hemodialysis patients are both decreased but unassociated.Urate crystals directly activate the T-cell receptor complex and induce T-cell proliferation.Late onset of clinically apparent central vein stenosis due to previous central venous catheter in a patient with inherited thrombophilia.Plasma vascular endothelial growth factor and angiogenin are positively related to erythropoietin dose in hemodialysis patients.CD8+ T-cell auto-reactivity is dependent on the expression of the immunoproteasome subunit LMP7 in exposed to lipopolysaccharide antigen presenting cells and epithelial target cells.Allopurinol protects human glomerular endothelial cells from high glucose-induced reactive oxygen species generation, p53 overexpression and endothelial dysfunction.Tryptophan depletion under conditions that imitate insulin resistance enhances fatty acid oxidation and induces endothelial dysfunction through reactive oxygen species-dependent and independent pathways.Activation of general control nonderepressible 2 kinase protects human glomerular endothelial cells from harmful high-glucose-induced molecular pathways.Late-onset Pompe's disease in a hemodialysis patient: A first case report.Increased visfatin in hemodialysis patients is associated with decreased demands for recombinant human erythropoietin.In human cell cultures, everolimus is inferior to tacrolimus in inhibiting cellular alloimmunity, but equally effective as regards humoral alloimmunity.Correction to: Tryptophan depletion under conditions that imitate insulin resistance enhances fatty acid oxidation and induces endothelial dysfunction through reactive oxygen species-dependent and independent pathways.Uric acid increases cellular and humoral alloimmunity in primary human peripheral blood mononuclear cells.Comparison of the effect of the aerobic glycolysis inhibitor dichloroacetate and of the Krebs cycle inhibitor LW6 on cellular and humoral alloimmunity.Indoleamine 2,3-dioxygenase, by degrading L-tryptophan, enhances carnitine palmitoyltransferase I activity and fatty acid oxidation, and exerts fatty acid-dependent effects in human alloreactive CD4+ T-cells.Proteasome or immunoproteasome inhibitors cause apoptosis in human renal tubular epithelial cells under normoxic and hypoxic conditions.Differential effects of the two amino acid sensing systems, the GCN2 kinase and the mTOR complex 1, on primary human alloreactive CD4⁺ T-cells.Indoleamine 2,3‑dioxygenase downregulates T‑cell receptor complex ζ‑chain and c‑Myc, and reduces proliferation, lactate dehydrogenase levels and mitochondrial glutaminase in human T‑cells.Indoleamine 2,3-dioxygenase depletes tryptophan, activates general control non-derepressible 2 kinase and down-regulates key enzymes involved in fatty acid synthesis in primary human CD4+ T cells.In human alloreactive CD4⁺ T-cells, dichloroacetate inhibits aerobic glycolysis, induces apoptosis and favors differentiation towards the regulatory T-cell subset instead of effector T-cell subsets.Indoleamine 2,3-dioxygenase increases p53 levels in alloreactive human T cells, and both indoleamine 2,3-dioxygenase and p53 suppress glucose uptake, glycolysis and proliferation.Inhibition of indoleamine 2,3-dioxygenase in mixed lymphocyte reaction affects glucose influx and enzymes involved in aerobic glycolysis and glutaminolysis in alloreactive T-cells.IDO decreases glycolysis and glutaminolysis by activating GCN2K, while it increases fatty acid oxidation by activating AhR, thus preserving CD4+ T‑cell survival and proliferation.The contribution of genetic variants of SLC2A1 gene in T2DM and T2DM-nephropathy: association study and meta-analysisPerilipin-1 in hemodialyzed patients: association with history of coronary heart disease and lipid profilePlasma indoleamine 2,3-dioxygenase and arginase type I may contribute to decreased blood T-cell count in hemodialysis patientsSerum osteoprotegerin is markedly increased and may contribute to decreased blood T cell count in hemodialysis patientsKynurenine, by activating aryl hydrocarbon receptor, decreases erythropoietin and increases hepcidin production in HepG2 cells: A new mechanism for anemia of inflammationIncreased plasma angiogenin level is associated and may contribute to decreased T-cell zeta-chain expression in hemodialysis patientsDamage-associated molecular patterns derived from mitochondria may contribute to the hemodialysis-associated inflammationInhibition of indoleamine 2,3-dioxygenase not only blocks autoreactive B cell activation, but it also reduces production of antibodies in general: comment on the article by Pigott and Mandik-Nayak
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P50
description
researcher ORCID ID = 0000-0001-5194-6849
@en
wetenschapper
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name
Georgios Pissas
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Georgios Pissas
@en
Georgios Pissas
@es
Georgios Pissas
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type
label
Georgios Pissas
@ast
Georgios Pissas
@en
Georgios Pissas
@es
Georgios Pissas
@nl
prefLabel
Georgios Pissas
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Georgios Pissas
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Georgios Pissas
@es
Georgios Pissas
@nl
P1153
55208927800
P31
P496
0000-0001-5194-6849