OBJECTIVE: The dietary intake of fructose-rich sugar-sweetened beverages (SSB) may have a significant role in raising serum uric acid (SUA) levels as well as the risk of contracting gout and cardiovascular risk factors. Our objective was to investigate the impact of SSB intake on SUA, body mass index (BMI) and systolic blood pressure (SBP) among adolescents in Taiwan. METHODS: We evaluated data from 2727 representative adolescents who were multistage sampled from 36 Junior High schools in Taiwan. We cross-sectionally collected demographic, physical, dietary and anthropometric variables, and prospectively measured clinical outcomes. Data were analyzed using multiple regression and logistic models adjusted for covariates. RESULTS: We found that 87.7% of adolescents were SSB drinkers, with 25.1% drinking 4500 ml per day of such beverages. Increased SSB intake was associated with increased waist and hip circumferences, body fat, BMI, SBP and SUA. As compared with non-drinkers, SSB drinkers had a 3.2-4.9 elevated risk of obesity. The prevalence of hyperuricemia in heavy SSB users (40.2-49.4%) was appreciably greater than that for non-users (24.2%). Adolescents who consumed 4500 ml per day of heavy high-fructose corn syrup (HFCS) containing beverages had a 0.42 mg dl À 1 higher SUA level and a 2.0-2.1 increased risk of developing hyperuricemia than non-drinkers. The consumption of HFCS-rich beverages was also found to interact with obesity in determining higher levels of SUA (2.2-2.4 mg dl À 1 increases). CONCLUSION: High SSB consumption has a notable effect on increased levels of BMI and SUA. The intake of HFCS-rich beverages and BMI were likely to interactively strengthen SUA levels among obese adolescents.

Head and neck squamous cell carcinoma (HNSCC) is a world-wide malignancy. This study aimed to identify differential gene expression associated with the progression of disease from primary to metastatic HNSCC. Microdissection retrieved pure epithelial cells from paired primary tumours and cervical lymph node metastasis. cDNA microarray analysis and algorithm grouping identified differential mRNA expression of 301 genes. Quantitative reverse transcription-polymerase chain reaction analysis clarified the up-regulation of CCL19, CR2, EGR2, FUCA1, RGS1, and SELL, as well as the down-regulation of IGFBP6 and KLK8 in nodal metastasis compared to primary tumours. Immunohistochemistry confirmed the up-regulation of SELL and down-regulation of IGFBP6 in nodal metastasis relative to primary tumours. Interestingly, primary tumours exhibiting higher FUCA1 and SELL expression were associated with significantly worse patient survival. In OECM-1 HNSCC cells, inhibition of proliferation, migration, and anchorage-independent growth was noted following knockdown of SELL expression. In SAS HNSCC cells, expression of exogenous SELL resulted in increased invasion, anchorage-independent growth, and xenographic tumourigenesis in nude mice. Knockdown of FUCA1 and treatment with IGFBP6 inhibited the migration of OECM-1 cells. Knockdown of RGS1 inhibited the anchorage-independent growth of SAS cells. Our results provide a useful gene signature profile describing the factors underlying the metastasis of HNSCC to cervical lymph nodes, which may be beneficial for the treatment of HNSCC metastasis.

Hepatoma cells are known to be highly resistant to chemotherapy. Previously, we have found differential Taxol resistance in human and murine hepatoma cells. The aim of this study was to examine the effect of a multidrug resistance inhibitor, cyclosporin A in combination with Taxol on hepatoma in vitro and in vivo, and to identify the possible mechanism involved in Taxol resistance. Simultaneous treatment of cyclosporin A (0 -10 mM) and Taxol (0.1 mM) inhibited cell growth in vitro. Cyclosporin A interfered with Taxol (0.1 mM)-induced AKT activation and BAD phosphorylation. Cyclosporin A combined with Taxol treatment augments caspase-9, -3 activation and loss of mitochondrial membrane potential in HepG2 cells. PI3 kinase inhibitor, wortmannin, or a dominantnegative AKT1 expression vector treatment partially enhanced Taxol-induced apoptosis indicating that PI3 kinase-AKT pathway was involved in Taxol-resistance pathway. Moreover, combination treatment reduced tumour growth in SCID and C57BL/6 mice as compared to either Taxol or cyclosporin A treatment. Our results indicate that the combination of cyclosporin A and Taxol is effective in the reversal of Taxol resistance through the inhibition of PI3 kinase-AKT1 pathway.