An attack of gout is extremely painful. Recurrent attacks of arthritis in one or more joints or tendon sheaths accompanied by intense pain are typical of this commonly occurring condition. As these symptoms indicate acute inflammation due to uric acid crystal deposition, good diagnostics are essential to enable initiation of drug treatment which removes the crystals deposited in tissue.
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Biomimetic bioreactor for potentiated uricase replacement therapy in hyperuricemia and gout.
Front Bioeng Biotechnol
January 2025
Department of Rheumatology and Immunology, The Third Affiliated Hospital of Southern Medical University, Institute of Clinical Immunology, Academy of Orthopedics, Guangzhou, Guangdong, China.
Introduction: Uricase replacement therapy is a promising approach for managing hyperuricemia and gout but is hindered by challenges such as short blood circulation time, reduced catalytic activity, and excessive hydrogen peroxide (HO) production. These limitations necessitate innovative strategies to enhance therapeutic efficacy and safety.
Methods: We designed and synthesized RBC@SeMSN@Uri, a red blood cell-coated biomimetic self-cascade bioreactor, which encapsulates uricase (Uri) and a selenium-based nano-scavenger (SeMSN) within RBC membranes.
The Gut Microbiome in Hyperuricemia and Gout.
Arthritis Rheumatol
January 2025
Assistant Professor of Pathology and of Microbiology and Microbiology and Immunology, Stanford University, Stanford, CA, 94305.
Humans develop hyperuricemia via decreased urate elimination and excess urate production, consequently promoting monosodium urate crystal deposition and incident gout. Normally, approximately two thirds of urate elimination is renal. However, chronic kidney disease (CKD) and other causes of decreased renal urate elimination drive hyperuricemia in most with gout.
View Article and Find Full Text PDFTreatment of gouty lumbar spinal stenosis: a case report and bioinformatics analysis.
BMC Musculoskelet Disord
January 2025
General Hospital of Ningxia Medical University, Ningxia, 750004, China.
The case of Lumbar spinal stenosis (LSS) combined with tophi due to gout is rarely reported. In the course of our clinic work, we encountered a young male patient who was diagnosed with a history of gout for 5 years and was targeted as LSS combined with gouty tophi, and we would like to share this case. In addition, in order to further investigate the deep mechanism of LSS associated with gout, we obtained the intersecting genes of the two diseases based on a machine learning approach by obtaining the dataset GSE113212 related to LSS from the Gene Expression Omnibus (GEO) database, and the genes related to gout from the human gene database.
View Article and Find Full Text PDFCo-expression of the RPS6KB1 and PDPK1 genes for production of activated p70S6K1 using bac-to-bac baculovirus expression system.
Mol Biol Rep
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Department of Structural and Molecular Biology, University College London, London, WC1E 6BT, UK.
Background: Ribosomal protein S6 kinase 1 (p70S6K1) is a member of the AGC family of serine/threonine kinases which plays a role in various cellular processes, including protein synthesis, cell growth, and survival. Dysregulation of p70S6K1, characterized by its overexpression and/or hyperactivation, has been implicated in numerous human pathologies, particularly in several types of cancer. Therefore, generating active, recombinant p70S6K1 is critical for investigating its role in cancer biology and for developing novel diagnostic or therapeutic approaches.
View Article and Find Full Text PDFUsing Multi-Omics Methods to Understand Gouty Arthritis.
Curr Rheumatol Rev
January 2025
Department of Rheumatology, Beijing Jishuitan Hospital, Guizhou Hospital, China.
Gouty arthritis is a common arthritic disease caused by the deposition of monosodium urate crystals in the joints and the tissues around it. The main pathogenesis of gout is the inflammation caused by the deposition of monosodium urate crystals. Omics studies help us evaluate global changes in gout during recent years, but most studies used only a single omics approach to illustrate the mechanisms of gout.
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