Mostrando 2,701 - 2,720 Resultados de 3,294 Para Buscar '"gout"', tiempo de consulta: 0.20s Limitar resultados
  1. 2701
    “…SHP deficiency results in increased secretion of proinflammatory cytokines IL-1β and IL-18, and excessive pathologic responses typically observed in mouse models of kidney tubular necrosis and peritoneal gout. Notably, the loss of SHP results in accumulation of damaged mitochondria and a sustained interaction between NLRP3 and ASC in the endoplasmic reticulum. …”
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  2. 2702
    por Prasad Sah, Om Shankar, Qing, Yu Xue
    Publicado 2015
    “…For recurring bouts of hyperuricemia or gout, patients should have a blood test and joint fluid test to determine whether the medication taken is effective. …”
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  3. 2703
  4. 2704
    “…In the acute phase the patient usually presents with edema, redness and increased temperature of the foot, which can suggest many other diagnoses including bacterial infection, gout, venous thrombosis or trauma. Because of its non specific clinical presentation and unsufficient awareness of the specificity of the diabetic foot syndrome among health professionals and the patients the diagnosis of this process is in many cases delayed. …”
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  5. 2705
    “…Besides traditionally used for dropsy, anemia, arthritis, gout, asthma, ulcer, piles, and urinary problems, it is also used in treating gastric problems, body pain, and rheumatic pains of joints. …”
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  6. 2706
    “…These small molecules suppressed LPS-induced TNF production, alleviated collagen-induced arthritis, and blocked gout formation in mouse models. IRAK4 inhibition promoted killing of ABC DLBCL lines harboring MYD88 L265P, by down-modulating survival signals, including NF-κB and autocrine IL-6/IL-10 engagement of the JAK–STAT3 pathway. …”
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  7. 2707
    por Park, Bo-Kyung, Cho, Mi-Sook
    Publicado 2016
    “…The Korean taste education program was adapted from "Les classes du goût" by J. Puisais and modified to suit a Korean education environment. …”
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  8. 2708
    “…Case Presentation: We describe a case of a 76-year-old female with past medical history of chronic kidney disease (baseline serum creatinine was 1.5-2.5 mg/dL), hypertension, gout and psoriatic arthritis, who was admitted for evaluation of elevated creatinine, peaking at 5.40 mg/dL. …”
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  9. 2709
    “…The activity of urate oxidase was lost during hominoid evolution, resulting in high susceptibility to hyperuricemia and gout in humans. In order to develop a more “human-like” uricase for therapeutic use, exon replacement/restoration and site-directed mutagenesis were performed to obtain porcine–human uricase with higher homology to deduced human uricase (dHU) and increased uricolytic activity. …”
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  10. 2710
    “…Elevated serum urate, which is regulated at multiple levels including genetic variants, is a risk factor for gout and other metabolic diseases. This study aimed to investigate the association between UCP2 variants and serum urate as well as hyperuricemia in a Chinese population. …”
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  11. 2711
    por Sayan, Mutlay, Mossman, Brooke T.
    Publicado 2016
    “…Although classically studied in models of gout, Type II diabetes, Alzheimer’s disease, and multiple sclerosis, the importance and mechanisms of action of inflammasome priming and activation have recently been elucidated in cells of the respiratory tract where they modulate the responses to a number of inhaled pathogenic particles and fibres. …”
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  12. 2712
    “…The effects of nonadherence to OAM on the risk of ESRD were significant for patients without hypertension, without gout, without chronic kidney disease, undergoing OAM polytherapy, and undergoing metformin polytherapy (HR [95% CIs], 1.18 [1.00–1.39], 1.13 [1.02–1.26], 1.17 [1.03–1.33], 1.22 [1.08–1.38], and 1.13 [1.02–1.25], respectively). …”
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  13. 2713
    por Kapoor, Neha, Saxena, Sanjai
    Publicado 2016
    “…Xanthine oxidase is a key enzyme responsible for hyperuricemia, a pre-disposing factor for Gout and oxidative stress-related diseases. Only two clinically approved xanthine oxidase inhibitors Allopurinol and Febuxostat are currently used for treatment of hyperuricemia. …”
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  14. 2714
    “…Acinetobacter pittii 44551 was recovered from a patient with gout combined with tuberculosis and was found to harbor the carbapenemase genes bla(NDM-1) and bla(OXA-58) on two different plasmids pNDM-44551 and pOXA58-44551, respectively. pNDM-44551 displayed high self-transferability across multiple bacterial species, while pOXA58-44551 was likely co-transferable with pNDM-44551 into A. baumannii receipts. pNDM-44551 was a close variant of the previously characterized pNDM-BJ01, and the bla(NDM-1) gene cluster was arranged sequentially as orfA, ISAba14, aphA6, ISAba125, bla(NDM-1), ble(MBL), ΔtrpF, dsbC, tnpR, and zeta. pOXA58-44551 was a repAci9-containing plasmid, and bla(OXA-58) was embedded in a 372F-ISAba3-like-bla(OXA-58)-ISAba3 structure. …”
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  15. 2715
    “…Background: Hyperuricemia (HUA) contributes to gout and many other diseases. Many hyperuricemia-related risk factors have been discovered, which provided the possibility for building the hyperuricemia prediction model. …”
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  16. 2716
    “…These data have implications for the treatment of hyperuricemia and gout, the pharmacology of tranilast, and the structure‐function analysis of urate transport.…”
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  17. 2717
    “…Mutations in UMOD, the gene encoding uromodulin, cause autosomal dominant tubulointerstitial kidney disease uromodulin-related (ADTKD-UMOD), characterised by hyperuricemia, gout and progressive loss of renal function. While the primary effect of UMOD mutations, retention in the endoplasmic reticulum (ER), is well established, its downstream effects are still largely unknown. …”
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  18. 2718
    “…Arthrosis was the dominant cause of inflammatory type pain, followed by rheumatoid arthritis and gout. NSAIDs (74.5%) were the most frequently prescribed analgesics followed by paracetamol (49.5%), weak opioids (23%) and corticosteroids (12.25%). …”
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  19. 2719
    “…It is used to treat hyperuricemia and gout, and also in a diagnostic kit. In this study, error-prone polymerase chain reaction and staggered extension process was used to generate a mutant urate oxidase with improved enzyme activity from Bacillus subtilis. …”
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  20. 2720
    “…CONCLUSIONS: These results indicate that the transmembrane region of ABCG2 is sensitive to amino acid substitution and that patients harboring these ABCG2 variant forms could suffer from unexpected pharmacokinetic events of ABCG2 substrate drugs or have an increased risk for diseases such as gout where ABCG2 is implicated. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (doi:10.1007/s11095-017-2127-1) contains supplementary material, which is available to authorized users.…”
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