Ruixia Sun

OBJECTIVE: To demonstrate the prevalence of hyperuricemia and gout associated with dietary and lifestyle changes and evaluate the implication of metabolic disorders to the development of hyperuricemia. METHODS: Data collected from 5,003 subjects randomly recruited from 5 coastal cities (Qingdao, Rizhao, Yantai, Weihai, and Dongying) of Shandong province in Eastern China were analyzed. RESULTS: Overall, the prevalence for hyperuricemia and gout in the studied populations was 13.19% and 1.14%, respectively. The prevalence was significantly higher in men as compared to women (18.32% vs 8.56% for hyperuricemia, 1.94% vs 0.42% for gout). Hyperuricemia was more common in men over age 30 and in women over age 50. A significant steady increase for the prevalence was noted as compared to the previous published data. Urban residents showed much higher prevalence of hyperuricemia as compared to rural residents (14.9% vs 10.1%, p = 0.004). Similarly, higher prevalence was noted in the developed city compared to the less developed city (18.02 vs 5.3%). These discrepancies were highly correlated with economic development as manifested by the increase of daily consumption of meat and seafood. Additionally, alcohol, overweight or obesity, hypertension, and abnormal triglycerides were highly associated with higher prevalence of hyperuricemia. Moreover, hyperuricemia is likely a risk factor for the development of diabetes mellitus. CONCLUSION: There was a remarkable increase for the prevalence of hyperuricemia and gout, which is highly correlated with the development of the economy as manifested by dietary and lifestyle changes.

PURPOSE: Hepatocellular carcinoma (HCC) is an aggressive malignancy and is a devastating clinical complication of chronic liver disease. Therapeutic options are limited mainly because the genetic and biochemical understanding of this disease remains fragmented. We intended to study the role of signal transducer and activator of transcription 3 (STAT3) aberrant signaling in HCC malignancy, and the therapeutic potential of inhibition of STAT3 expression for HCC. EXPERIMENTAL DESIGN: A 2'-O-methoxyethylribose-modified phosphorothioate antisense oligonucleotide (ASO) was used to knock down STAT3 expression in different human HCC cell lines, including the highly metastatic HCCLM3 derived from orthotopic implantation and subsequent lung metastasis in athymic mice. The effects of STAT3 ASO treatment on HCC cells, metastasis, and animal survival following HCCLM3 orthotopic implantation were evaluated. RESULTS: Specific suppression of phosphorylated STAT3 reduced its DNA-binding activity, inhibited the expression of vascular endothelial growth factor, survivin, matrix metalloproteinases 2 and 9, reduced cell proliferation and migratory potential, induced apoptosis in vitro, and inhibited intradermal angiogenesis and s.c. tumorigenesis upon injection in mice. In mice bearing orthotopically implanted HCCLM3, STAT3 inhibition following therapeutic treatment with STAT3 ASO reduced circulating vascular endothelial growth factor and basic fibroblast growth factor, decreased intratumor CD34-positive microvessel density, intrahepatic and intraperitoneal transmission, and lung metastasis. HCC tumor volume and weight were reduced and the survival time of mice bearing orthotopically xenografted HCC was approximately doubled in STAT3 ASO-treated mice (P < 0.05). CONCLUSIONS: Constitutively activated STAT3 is essential for the growth, survival, and metastasis of HCC, suggesting that STAT3-targeted therapy may have utility for HCC.

The effects and possible mechanisms of adipose-derived stem cells (ASC) infusion on type 2 diabetic rats were investigated in this study. Twenty normal male Sprague-Dawley rats were included in normal control group, and 40 male diabetic rats were randomly divided into diabetic control group and ASC group (which received ASC infusion). After therapy, levels of fasting plasma glucose (FPG), HbA1c, serum insulin and C-peptide, recovery of islet cells, inflammatory cytokines, and insulin sensitivity were analyzed. After ASC infusion, compared with diabetic control group, hyperglycemia in ASC group was ameliorated in 2 weeks and maintained for about 6 weeks, and plasma concentrations of insulin and C-peptide were significantly improved (P<0.01). Number of islet β cells and concentration of vWF in islets in ASC group increased, while activity of caspase-3 in islets was reduced. Moreover, concentrations of TNF-α, IL-6 and IL-1β in ASC group obviously decreased (P<0.05). The expression of GLUT4, INSR, and phosphorylation of insulin signaling molecules in insulin target tissues were effectively improved. ASC infusion could aid in T2DM through recovery of islet β cells and improvement of insulin sensitivity. Autologous ASC infusion might be an effective method for T2DM.