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(1) Background: The role of uric acid in stroke outcomes remains inconclusive. (2) Methods: We retrospectively enrolled 3370 patients with acute ischemic stroke. (3) Results: Uric acid level was higher in men than in women. Univariate analyses revealed that the rates of hyperuricemia were higher in all patients and in women for unfavorable outcomes. For death, the hyperuricemia rates were higher in all patients including men and women, and the uric acid levels were also higher in all patients and in women. A J-shaped curve was observed between uric acid and the discharge-modified Rankin Scale score. Patients within Quartiles 1 (6.5 mg/dL) of uric acid had higher rates of unfavorable outcomes and death than patients within Quartiles 2 (4.1–5.1 mg/dL) and 3 (5.1–6.2 mg/dL). Multivariable analyses for unfavorable outcomes revealed that Quartile 1 of uric acid was a significant factor in all patients and in men. In men, a significant factor for death was being in Quartile 1 of uric acid. In women, higher levels of uric acid or hyperuricemia (>6.6 mg/dL) were significant factors for death. (4) Conclusions: Lower uric acid levels are a predictor for unfavorable outcomes and death in men, and higher uric acid levels are a predictor for death in women.

Prion diseases, including Creutzfeldt–Jakob disease, are mediated by transmissible proteinaceous pathogens. Pathological changes indicative of neuro-degeneration have been observed in the brains of affected patients. Simultaneously, microglial activation, along with the upregulation of pro-inflammatory cytokines, including IL-1 or TNF-α, have also been observed in brain tissue of these patients. Consequently, pro-inflammatory cytokines are thought to be involved in the pathogenesis of these diseases. Accelerated prion infections have been seen in interleukin-10 knockout mice, and type 1 interferons have been found to be protective against these diseases. Since interleukin-10 and type 1 interferons are key mediators of the antiviral THαβ immunological pathway, protective host immunity against prion diseases may be regulated via THαβ immunity. Currently no effective treatment strategies exist for prion disease; however, drugs that target the regulation of IL-10, IFN-alpha, or IFN-β, and consequently modulate the THαβ immunological pathway, may prove to be effective therapeutic options.