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Articular Cartilage Pathology and Therapies
Published in Kyriacos A. Athanasiou, Eric M. Darling, Grayson D. DuRaine, Jerry C. Hu, A. Hari Reddi, Articular Cartilage, 2017
Kyriacos A. Athanasiou, Eric M. Darling, Grayson D. DuRaine, Jerry C. Hu, A. Hari Reddi
Gout is a buildup of uric acid crystals in the blood and synovial fluid, leading to inflammatory arthritis. This increase in uric acid levels in the blood can be due to a lack of uric acid excretion by the kidneys or increased dietary intake of foods high in purine, a uric acid precursor. Excessive alcohol consumption is also commonly associated with increased uric acid concentrations (Saker et al. 1967; Liberopoulos et al. 2004; Fam 2005; Zhang et al. 2006; Choi and Curhan 2007), although the role of alcohol in gout progression is increasingly being questioned (Hennigan and Terkeltaub 2007). Gout has been described since ancient times by both the Babylonians and Egyptians, with Hippocrates providing one of the classical descriptions in the fifth century BC, relating it to dietary intake of alcohol and certain foods. The most common joint affected is the first metatarsophalangeal joint (big toe). Other disorders associated with increased uric acid concentration include tophus formation (large MSU crystals) and renal calculi (Figure 3.7).
Treatment Devices
Published in Laurence J. Street, Introduction to Biomedical Engineering Technology, 2016
Kidney stones can form from a variety of chemicals. About 80% of stones are formed from calcium oxalate.Some stones are formed by the action of bacteria in relation to ammonia, which forms crystalline stones called struvites. These stones can become very large, filling the renal pelvis and taking on a “stag horn” shape. These stones can be very difficult to remove and very harmful to the kidneys. They are most often seen in women who have frequent urinary tract infections.Uric acid stones form due to an excess of, you guessed it, uric acid. Uric acid can also precipitate in joints, causing the painful condition known as gout.A rare genetic condition can cause high levels of the amino acid cystine in the urine, which can result in stone formation.
Fluorescent Quantum Dots for Biomedical Applications
Published in Vladimir Torchilin, Mansoor M Amiji, Handbook of Materials for Nanomedicine, 2011
Kelly Kenniff, Keith Payton, Swadeshmukul Santra
Uric acid represents the major catabolite of purine breakdown in humans. Therefore, it remains an important marker molecule for disorders associated with alterations of the plasma urea concentration such as hyperuricemia (gout), renal impairment, leukemia, ketoacidosis, Lesch-Nyhan syndrome and lactate excess.113 Uric acid may also act as an antioxidant in human body. Consequently its measurement for diagnosis and treatment of some disorders is routinely required. Zhang et al.114 developed a reagentless amperometric uric acid biosensor based on carboxyl modified, conductive zinc sulfide (ZnS) Qdots. The biosensor could detect uric acid without the presence of an electron mediator. The fabricated uricase/ZnS Qdot/l-cys biosensor exhibited higher amperometric response compared to the one without Qdots (uricase/l-cys biosensor). They were able to demonstrate a linear dependence on the uric acid concentration ranging from 5.0 × 10−6 to 2.0 × 10−3 mol L−1 with a detection limit of 2.0 × 10−6 mol L−1 at 3σ.
Characterization of a novel marine microbial uricase from Priestia flexa and evaluation of the effects of CMCS conjugation on its enzymatic properties
Published in Preparative Biochemistry & Biotechnology, 2023
YuLiang Jiao, YuYing Zhu, ShuMin Zeng, ShuFang Wang, Jing Chen, XiangHong Zhou, GuiZhen Ma
Uricase (EC 1.7.3.3), also referred to as urate oxidase, occurring widely in animals and microorganisms, catalyzes the oxidation of uric acid to allantonin, hydrogen peroxide, and carbon dioxide. The enzyme plays a key role in purine metabolism by keeping plasma uric acid at normal levels. In human and other apes, there is only a nonfunctional uricase pseudogen in lieu, which makes the serum uric acid higher in human or these animals than other mammals.[1] The high uric acid levels might contribute to the increase of life expectancy and intelligence of humans in evolution.[1] However, uric acid is a sword with two edges—accumulation of uric acid in excess in serum of humans can cause various diseases including the well-known intolerable arthritis gout, hyperuricemia complicating tumor lysis syndrome and even life-threatening conditions such as acute renal failure.[2]
Characterization of the antioxidant activity, total phenolic content, enzyme inhibition, and anticancer properties of Achillea millefolium L. (yarrow)
Published in Instrumentation Science & Technology, 2022
Nagihan Karaaslan Ayhan, Merve Goksin Karaaslan Tunc, Samir Abbas Ali Noma, Ali Kurucay, Burhan Ates
Excess uric acid production may cause hyperuricemia which causes gout.[19] High levels of XO can cause oxidative stress, mutagenesis, and perhaps cancer. Hence, the inhibition of XO reduces oxidative stress immediately after inflammation. Also, the inhibition of XO may be used for cancer therapy.[20] Allopurinol, a prototypical potent XO inhibitor with a purine moiety, has been the cornerstone of gout and hyperuricemia-related disorders for decades and has mild side effects such as gastrointestinal distress, hypersensitivity reactions, and renal toxicity.[21] In order to control hyperuricemia in gout patients, it is necessary to find a new non-purine XO inhibitor that is more potent than allopurinol and is selective.[22] Novel non-purine alternatives to allopurinol have been investigated with potent XO inhibitory activity and fewer side effects.[23]
Association between ambient air pollution and hyperuricemia in traffic police officers in China: a cohort study
Published in International Journal of Environmental Health Research, 2021
Yong-Xiang Tang, Michael S. Bloom, Zhengmin (Min) Qian, Echu Liu, Daire R. Jansson, Michael G. Vaughn, Hua-Liang Lin, Lv-Wu Xiao, Chuan-Wei Duan, Lie Yang, Xiao-Yun Xu, Yan-Ru Li, Ling Zhu, Guang-Hui Dong, Yi-Min Liu
We collected an overnight fasting blood sample from each study participant during the physical examination. Blood specimens were centrifuged at 3000 rpm for 10 min, and the serum was separated for laboratory assays. Serum uric acid was measured by photometry with a Siemens Advia 2400 instrument (Siemens Healthcare GMBH, Germany) using an enzymatic colorimetric test. Hyperuricemia was defined as serum uric acid >420 μmol/L in males and >350 μmol/L in females, which is a widely accepted diagnostic criteria (Ge and Xu 2013; Bardin and Richette 2014; Liu et al. 2015).