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Background And Purpose: Guillain-Barré syndrome (GBS) is an autoimmune-mediated disorder characterized by demyelinating or axonal injury of the peripheral nerve. Our aim is to determine whether serum amyloid A (SAA) is a biomarker of demyelinating injury and disease severity in patients with GBS.
Methods: This study retrospectively enrolled 40 patients with either the demyelinating or axonal GBS and sex- and age-matched controls with other neurological diseases as well as healthy subjects. The demographic and clinical features at entry were collected. The serum levels of the SAA isoforms SAA1, SAA2, and SAA4 were determined in the patients with GBS and the controls using the enzyme-linked immunosorbent assay and analyzed for the associations between levels of different SAA isoforms and the clinical features of the patients.
Results: The levels of SAA2 and SAA4 were significantly higher in patients with GBS than in both the other neurological disease controls and the healthy subjects (<0.05 for all). The level of SAA1 did not differ between patients with GBS and the controls. The level of SAA2 was considerably higher in GBS patients with antecedent infection than in those without infection (=0.020). The levels of different SAA isoforms were not associated with the disease severity or other clinical features of patients with GBS (>0.05 for all).
Conclusions: Increased levels of SAA2 and SAA4 may only represent the acute inflammatory status and so cannot be utilized as biomarkers of the disease severity or demyelinating injury in patients with GBS.
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http://dx.doi.org/10.3988/jcn.2024.0469 | DOI Listing |
J Mater Chem B
June 2025
Department of Industrial Systems Engineering and Design, Universitat Jaume I, Castellon de la Plana, Spain.
Quercetin (QUE), a natural flavonoid found in various fruits and vegetables, has diverse biological functions, including anti-inflammatory effects, regulation of cell adhesion and oxidative stress mitigation. In this study, sol-gel materials with increasing concentrations of quercetin (0.5, 1 and 2 wt%) were synthesised and applied onto titanium (Ti) surfaces as coatings.
View Article and Find Full Text PDFJ Clin Neurol
May 2025
Medical Research Center, Affiliated Hospital of Jining Medical University, Jining, Shandong Province, China.
Background And Purpose: Guillain-Barré syndrome (GBS) is an autoimmune-mediated disorder characterized by demyelinating or axonal injury of the peripheral nerve. Our aim is to determine whether serum amyloid A (SAA) is a biomarker of demyelinating injury and disease severity in patients with GBS.
Methods: This study retrospectively enrolled 40 patients with either the demyelinating or axonal GBS and sex- and age-matched controls with other neurological diseases as well as healthy subjects.
Front Immunol
May 2025
Department of Laboratory Medicine, Lund University, Lund, Sweden.
Serum Amyloid A (SAA) proteins are acute-phase reactants with critical roles in sterile and bacterial inflammation. Through and experiments, we demonstrate that SAA proteins amplify cytokine and chemokine responses during sterile inflammation and enhance bacterial clearance in infectious conditions. Mechanistically, SAA proteins augment NF-κB signaling, driving pro and anti-inflammatory mediator production.
View Article and Find Full Text PDFInt J Mol Sci
November 2024
Faculty of Medicine, University of P. J. Šafárik, 041 90 Košice, Slovakia.
Long-term treatment with bisphosphonates is accompanied by an increased risk of medication-related osteonecrosis of the jaw (MRONJ). Currently, no clinically useful biomarkers for the predictive diagnosis of MRONJ are available. To investigate the potential key proteins involved in the pathogenesis of MRONJ, a proteomic LC-MS/MS analysis of saliva was performed.
View Article and Find Full Text PDFVirus Res
November 2024
Department of Virology, School of Public Health, Tehran University of Medical Sciences, Tehran, Iran. Electronic address:
Chronic hepatitis C virus infection is a major cause of mortality due to liver cirrhosis globally. Despite the advances in recent therapeutic strategies, there is yet a high burden of HCV-related cirrhosis worldwide concerning low coverage of newly developed antiviral therapies, insufficient validity of the current diagnostic methods for cirrhosis, and incomplete understanding of the pathogenesis in this stage of liver disease. Hence we aimed to clarify the molecular events in HCV-related cirrhosis and identify a liver-specific gene signature to potentially improve diagnosis and prognosis of the disease.
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