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Background: The prevalence of hyperuricemia has increased dramatically during the past several decades. Studies indicating uric acid is an independent risk factor for hypertension did not sufficiently control for other known risk factors. We explored this relationship in a comprehensive Chinese senior dynamic cohort.Methods: To investigate the relationship between serum uric acid (SUA) levels and hypertension, we carried out a 6-year retrospective study (2006-2011) in a dynamic cohort with 3591 subjects free of hypertension. The first occasion of documented hypertension per subject was the index event. A Cox proportional hazards model assessed the relationship between SUA and hypertension. Kaplan-Meier survival analysis compared incidence of hypertension among individuals with each SUA quartile. Receiver operating characteristic curves were generated to obtain the area under the curve as a prediction of hypertension from SUA levels.Results: The cumulative prevalence of hypertension in our cohort was 20.7 %. The prevalence of hyperuricemia was 17.5 %. Cox regression analysis showed that, compared with the lowest SUA quartile (<4.69 mg/dl), the 4.69-5.58, 5.58-6.52, and ≥6.52 mg/dl quartiles yielded hazard ratios (95 % confidence intervals) for hypertension of 1.652 (1.265-2.156), 2.195 (1.705-2.825), and 3.058 (2.399-3.899), respectively. Cumulative incidence of hypertension was consistently higher among individuals with hyperuricemia than among those with normal SUA levels. A Kaplan-Meier survival analysis showed that hyperuricemia predicted higher incidences of hypertension in a dose-dependent manner: hypertension onset significantly differed across SUA quartiles. SUA levels were significantly and independently associated with incidence of hypertension in our cohort.Conclusions: Our results, controlling for known risk factors, suggest that SUA level is an independent risk factor for hypertension and could be a useful indicator of hypertension. [ABSTRACT FROM AUTHOR]

The underlying molecular pathogenesis of hepatocellular carcinoma (HCC) remains poorly understood. Mitogen-activated protein kinase kinase 3 (MKK3), has been reported as a novel tumor suppressor in breast cancer. However, its potential suppressive role in HCC has not been evaluated. In the current study, the biologic functions of MKK3 in HCC were investigated and a previously unreported cell cycle regulation mechanism was observed. MKK3 overexpression suppressed HepG2 and PLC‑PRF‑5 cell proliferation and induced cell cycle arrest in the two cell lines. In addition, MKK3 overexpression upregulated the cyclin-dependent kinase inhibitors, p16 INK4A and p15 INK4B in HCC cells. Their negative regulator, Bim‑1, was downregulated following MKK3 overexpression. Moreover, MKK3 activated p38 in HCC cells and SB203580, a p38 inhibitor, reversed the tumor suppressive effect of MKK3. In conclusion, the results identify MKK3 as a tumor suppressor and highlighted the significance of p38 pathway aberration in HCC.