2014 Vol. 27, No. 3
Methods We used life tables, cause-elimination life tables, and age decomposition of LE with corrected mortality data from the National Disease Surveillance System in 2010.
Results LE at birth of Chinese people was 73.24 years in 2010. Women had a longer LE than men, and urban population had a longer LE than rural population. CVD deaths resulted in a 4.79-year LE loss and premature deaths in people aged 25 to 64 years were responsible for a substantial part of LE loss from CVD. Death from ischemic heart disease and cerebrovascular diseases accounted for 69.2%of LE loss from CVD deaths and death from cerebrovascular diseases was the largest contributor. In rural men, 51.1% LE loss from CVD deaths was caused by cerebrovascular diseases. If there were no changes in mortality rates for all other diseases, a 27.4%reduction in CVD mortality would increase LE by 1 year in Chinese population.
Conclusion There is a considerable impact of CVD deaths on LE. A 1-year LE increase in the future requires at least a 27.4% reduction in CVD mortality from the current level. Targeting the rural population and tackling cerebrovascular diseases are important for reaching the national goal of health improvement.
Methods LE and cause-eliminated LE were calculated by using standard life tables which used adjusted mortality data from the Death Surveillance Data Sets in 2005 and 2010 from the National Disease Surveillance System. Decomposition was used to quantitate the impact of cerebrovascular disease in different age groups.
Results LE in China was 73.24 years in 2010, which was higher in women and urban residents compared with men and rural residents. The loss of LE caused by cerebrovascular disease mortality was 2.26 years, which was higher in men and rural residents compared with women and urban residents. More than 30%of the loss of LE were attributed to premature death from cerebrovascular disease in people aged <65 years. Compared with 2005, LE in 2010 increased by 0.92 years. The reduction of cerebrovascular disease mortality in urban residents contributed 0.45 years to the increase of LE, but the increase of cerebrovascular disease mortality caused a 0.12-year loss of LE in rural residents.
Conclusion Cerebrovascular disease mortality had a major impact on LE in China, with a significant difference between urban and rural residents. LE is likely to be further increased by reducing cerebrovascular disease mortality, and special attention should be paid to reducing premature deaths in people aged<65 years.
Methods A community-based cross-sectional survey was conducted in a Chinese Han population. BMI, soybean food intake, and single nucleotide polymorphisms of rs599839, rs3846662, rs3846663, rs12916, rs174547, rs174570, rs4938303, and rs1558861 were measured in 944 subjects. A multivariate logistic regression was used to analyze the association of the studied polymorphisms with BMIs. The expectation-maximization algorithm was employed to evaluate the extent of linkage disequilibrium between pairwise polymorphisms. The gene-environment interaction was assessed in the general multifactor dimensionality reduction model.
Results The polymorphisms of rs3846662 and rs3846663 were associated with 10% highest BMIs when comparing to the 10% lowest values both in individuals and haplotype-based association tests. Although no statistically significant gene-environment interactions were found, people with the haplotype composed of C allele in rs3846662 and T allele in rs3846663 and low frequency of soybean intake had significantly higher risk to overweight and obesity as compared with those with the haplotype consisting of T allele in rs3846662 and C allele in rs3846663 and highly frequent soybean food intake, with an odds ratio of 1.64 (95%confidence interval: 1.15-2.34, P<0.01) after adjusting for the common confounders.
Conclusion Our study has suggested that rs3846662 and rs3846663 may be the potential candidate polymorphisms for obesity, and their effect on the pathogenesis could be mediated by the frequency of soybean food intake.
Methods 30 Senescence-accelerated mice prone 8 (SAMP8) mice were divided into three groups and treated with normal diet, blueberry extracts (200 mg/kg·bw/day) and cyaniding-3-O-galactoside (Cy-3-GAL) (50 mg/kg·bw/day) from blueberry for 8 weeks. 10 SAMR1 mice were set as control group. The capacity of spatial memory was assessed by Passive avoidance task and Morris water maze. Histological analyses on hippocampus were completed. Malondialdehyde (MDA) levels, Superoxide Dismutase (SOD) activity and the expression of ERK were detected.
Results Both Cy-3-GAL and blueberry extracts were shown effective functions to relieve cellular injury, improve hippocampal neurons survival and inhibit the pyramidal cell layer damage. Cy-3-GAL and blueberry extracts also increased SOD activity and reduced MDA content in brain tissues and plasma, and increased hippocampal phosphorylated ERK (p-ERK) expression in SAMP8 mice. Further more, the passive avoidance task test showed that both the latency time and the number of errors were improved by Cy-3-GAL treatment, and the Morris Water Maze test showed significant decreases of latency were detected by Cy-3-GAL and blueberry extracts treatment on day 4.
Conclusion Blueberry extracts may reverse the declines of cognitive and behavioral function in the ageing process through several pathways, including enhancing the capacity of antioxidation, altering stress signaling. Cy-3-GAL may be an important active ingredient for these biological effects.
Methods After the HCT116 cells were pretreated with specific ERK inhibitor (U0126) or specific siRNA and exposed to 10 mmol/L sodium butyrate (NaBT) for 24 h, their apoptosis was detected by flow cytometry, levels of SphK2 and ERK protein were measured by Western blot, and translocation of SphK2 was assayed by immunofluorescence microscopy.
Results The U0126 and siRNAs specific for SphK2 blocked the export of SphK2 from nuclei to cytoplasm and increased the apoptosis of HCT116 cells following NaBT exposure. Over-expression of PKD decreased NaBT-induced apoptosis of HCT116 cells, which was reversed by U0126. Furthermore, transfection of HCT116 cells with constitutively activated PKD plasmids recovered the U0126-blocked export of SphK2.
Conclusion ERK regulates the export of SphK2 and apoptosis of HCT116 cells by modulating PKD. Modulation of these molecules may help increase the sensitivity of colon cancer cells to the physiologic anti-colon cancer agent, NaBT.