We examined the association of serum uric acid (SUA) with development of hypertension (blood pressure > or = 140/90 mmHg and/or medication for hypertension) and impaired fasting glucose (IFG) (a fasting plasma glucose level 6.1-6.9 mmol/l) or Type II (non-insulin-dependent) diabetes (a fasting plasma glucose level > or = 7.0 mmol/l and/or medication for diabetes) over a 6-year follow-up among 2310 Japanese male office workers aged 35-59 years who did not have hypertension, IFG, Type II diabetes, or past history of cardiovascular disease at study entry. After controlling for potential predictors of hypertension and diabetes, the relative risk for hypertension compared with quintile 1 of SUA level was 1.27 [95% confidence interval (CI): 1.00-1.62] for quintile 2, 1.34 (95% CI: 1.08-1.74) for quintile 3, 1.48 (95% CI: 1.18-1.89) for quintile 4, and 1.58 (95% CI: 1.26-1.99) for quintile 5 (p for trend <0.001). The respective multivariate-adjusted relative risks for IFG or Type II diabetes compared with quintile 1 of SUA level were 1.55 (95% CI: 0.95-2.63), 1.62 (95% CI: 0.98-2.67), 1.61 (95% CI: 1.01-2.58), and 1.78 (95% CI: 1.11-2.85) (p for trend = 0.030). The association between SUA level and risk for hypertension and IFG or Type II diabetes was stronger among men with a body mass index (BMI) <24.2 kg/m2 than among men with a BMI > or = 24.2 kg/m2, although the absolute risk was greater in more obese men. These results indicate that SUA level is closely associated with an increased risk for hypertension and IFG or Type II diabetes.
RIG-I-mediated type I interferon (IFN) production and nuclease-mediated viral RNA degradation are essential for antiviral innate immune responses. DDX60 is an IFN-inducible cytoplasmic helicase. Here, we report that DDX60 is a sentinel for both RIG-I activation and viral RNA degradation. We show that DDX60 is an upstream factor of RIG-I that activates RIG-I signaling in a ligand-specific manner. DDX60 knockout attenuates RIG-I signaling and significantly reduces virus-induced type I IFN production in vivo. In addition, we show that DDX60 is involved in RIG-I-independent viral RNA degradation. DDX60 and RIG-I adaptor MAVS double-knockout mice reveal a role for DDX60-dependent RNA degradation in antiviral responses. Several viruses induced DDX60 phosphorylation via epidermal growth factor receptor (EGFR), leading to attenuation of the DDX60 antiviral activities. Our results define DDX60 as a sentinel for cytoplasmic antiviral response, which is counteracted by virus-mediated EGF receptor activation.
The association of cigarette smoking with development of hearing impairment (loss of 30 dB at 1000 Hz and 40 dB at 4000 Hz) over a 5-year follow-up was studied in 1554 non-hearing-impaired Japanese male office workers who ranged in age from 30 to 59 years. After controlling for potential predictors of hearing impairment, the relative risk for low-frequency hearing impairment compared with never smokers was 1.12 (95% confidence interval [CI], 0.57 to 2.17) for ever-smokers, 1.21 (95% CI, 0.65 to 2.25) for current smokers of 1 to 20 cigarettes/day, 1.35 (95% CI, 0.70 to 2.61) for current smokers of 21 to 30 cigarettes/day, and 1.82 (95% CI, 0.98 to 3.38) for current smokers of 31 or more cigarettes/day (P for trend = 0.063). The respective multivariate-adjusted relative risks for high-frequency hearing impairment compared with never smokers were 1.70 (95% CI, 0.85 to 3.40), 1.82 (95% CI, 0.92 to 3.59), 2.00 (95% CI, 0.98 to 4.08), and 2.20 (95% CI, 1.09 to 4.42) (P for trend = 0.025). As the number of pack-years of exposure increased, the risk for high-frequency hearing impairment increased in a dose-dependent manner (P for trend = 0.011), but the risk for low-frequency hearing impairment did not (P for trend = 0.172). Our results indicate that cigarette smoking is highly associated with development of high-frequency hearing impairment in Japanese male office workers.
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