Data-Driven Dietary Patterns,Nutrient Intake and Body Weight Status in a Cross-Section of Singaporean Children Aged 6–12 Years

Pattern analysis of children’s diet may provide insights into chronic disease risk in adolescence and adulthood. This study aimed to assess dietary patterns of young Singaporean children using cluster analysis. An existing dataset included 15,820 items consumed by 561 participants (aged 6–12 years) over 2 days of dietary recall. Thirty-seven food groups were defined and expressed as a percentage contribution of total energy. Dietary patterns were identified using k-means cluster analysis. Three clusters were identified, “Western”, “Convenience” and “Local/hawker”, none of which were defined by more prudent dietary choices. The “Convenience” cluster group had the lowest total energy intake (mean 85.8 ± SD 25.3% of Average Requirement for Energy) compared to the other groups (95.4 ± 25.9% for “Western” and 93.4 ± 25.3% for “Local/hawker”, p < 0.001) but also had the lowest calcium intake (66.3 ± 34.7% of Recommended Dietary Allowance), similar to intake in the “Local/hawker” group (69.5 ± 38.9%) but less than the “Western” group (82.8 ± 36.1%, p < 0.001). These findings highlight the need for longitudinal analysis of dietary habit in younger Singaporeans in order to better define public health messaging targeted at reducing risk of major noncommunicable disease.     

脾内血管的应用解剖学研究盐酸喹那普利治疗原发性高血压的临床应用观察

目的　探讨盐酸喹那普利 (QuinaprilHydrochloride)治疗轻、中度原发性高血压的有效性和安全性。方法　全国 6家医院参加的一项多中心、随机、双盲、平行组间对照研究。结果　 113例原发性高血压病人治疗 8周后 ,总有效率达 85 84% ,统计学有显著性差异。盐酸喹那普利副反应较轻 ,对肾脏、肝脏、造血系统和心脏未见有害作用。结论　盐酸喹那普利是一种安全、疗效好、副反应小的治疗轻、中度原发性高血压的有效药物。     

Histone deacetylase inhibitor induces DNA damage,which normal but not transformed cells can repair

Histone deacetylase inhibitors (HDACi) developed as anti-cancer agents have a high degree of selectivity for killing cancer cells. HDACi induce acetylation of histones and nonhistone proteins, which affect gene expression, cell cycle progression, cell migration, and cell death. The mechanism of the tumor selective action of HDACi is unclear. Here, we show that the HDACi, vorinostat (Suberoylanilide hydroxamic acid, SAHA), induces DNA double-strand breaks (DSBs) in normal (HFS) and cancer (LNCaP, A549) cells. Normal cells in contrast to cancer cells repair the DSBs despite continued culture with vorinostat. In transformed cells, phosphorylated H2AX (γH2AX), a marker of DNA DSBs, levels increased with continued culture with vorinostat, whereas in normal cells, this marker decreased with time. Vorinostat induced the accumulation of acetylated histones within 30 min, which could alter chromatin structure-exposing DNA to damage. After a 24-h culture of cells with vorinostat, and reculture without the HDACi, γH2AX was undetectable by 2 h in normal cells, while persisting in transformed cells for the duration of culture. Further, we found that vorinostat suppressed DNA DSB repair proteins, e.g., RAD50, MRE11, in cancer but not normal cells. Thus, the HDACi, vorinostat, induces DNA damage which normal but not cancer cells can repair. This DNA damage is associated with cancer cell death. These findings can explain, in part, the selectivity of vorinostat in causing cancer cell death at concentrations that cause little or no normal cell death.