Short communicationCerebral uric acid increases following experimental traumatic brain injury in rat
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Cited by (33)
Association between Serum Uric Acid Level and Activity of Daily Living in Japanese Patients with Ischemic Stroke
2017, Journal of Stroke and Cerebrovascular DiseasesCitation Excerpt :Administration of uric acid, before ischemia or during the subsequent reperfusion period, caused a significant reduction in infarct volume and led to improved behavioral outcomes at 24 hours.30 In animal models, local uric acid concentrations significantly increase in acute brain infarction and can persist for several days after brain injury.31,32 Although these findings were obtained from the results of experiments on animals, uric acid is known to be one of the most important antioxidants abundant in humans.
The inflammasome and danger associated molecular patterns (DAMPs) are implicated in cytokine and chemokine responses following stressor exposure
2013, Brain, Behavior, and ImmunityCitation Excerpt :Activation of the inflammasome occurs in response to a variety of signals. Danger associated molecular patterns (DAMPs) (Gasse et al., 2009; Hoffman and Wanderer, 2010; Kono and Rock, 2008; Shi et al., 2003), including Hsp72 (Pittet et al., 2002) and uric acid (Jeevanandam et al., 1991; Namas et al., 2009; Tayag et al., 1996), and microbe associated molecular patterns (MAMPs) such as LPS (Ganz et al., 2011) all potently activate the inflammasome and are released in response to stressor exposure (Allen et al., 2012; Campisi et al., 2012; Fleshner et al., 2007, 2010; Johnson and Fleshner, 2006; Williams and Ireland, 2008). Importantly, in vivo neutralization of LPS that is shed from commensal bacteria during stress selectively inhibits the production of inflammasome-dependent cytokines without impacting inflammasome-independent inflammatory proteins (Maslanik et al., in press), suggesting that stress-induced release of MAMPs may signal the inflammasome, in vivo.
Acute brain injury triggers MyD88-dependent, TLR2/4-independent inflammatory responses
2007, American Journal of PathologyImpairment of the ability of the injured aged brain in elevating urate and ascorbate
2006, Experimental GerontologyIschemic preconditioning increases antioxidants in the brain and peripheral organs after cerebral ischemia
2005, Experimental Neurology
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Present address: Department of Neurology - Los Angeles County & University of Southern California Medical Center, 1200 N. State Street, Unit 1, Room 5641, Los Angeles, CA 90033, USA.
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Present address: Department of Microbiology and Immunology, Temple University School of Medicine, Kresge Hall, Room 503, Philadelphia, PA 19140, USA.