ABSTRACT
Vitamin D deficiency in children can have adverse health consequences, such as growth failure and rickets. In 2008,the American Academy of Pediatrics increased its recommended daily intake of vitamin D in infants, children, and adolescents to 400 IU. Infants who are breastfed and children and adolescents who consume less than 1 L of vitamin D-fortified milk per day will likely need supplementation to reach 400 IU of vitamin D per day. This recommendation is based on expert opinion and recent clinical trials measuring biomarkers of vitamin D status. It is also based on the precedent of preventing and treating rickets with 400 IU of vitamin D. In addition to dietary sources, exposure to ultraviolet B sunlight provides children and adults with additional vitamin D. Although the American Academy of Pediatrics recommends keeping infants out of direct sunlight, decreased sunlight exposure may increase children's risk of vitamin D deficiency. No randomized controlled trials assessing patient-oriented outcomes have been performed on universal vitamin D supplementation. However, vitamin D may reduce the risk of certain infections and chronic diseases. Physicians should help parents choose the appropriate vitamin D supplement for their child.
Subject(s)
Dietary Supplements , Vitamin D Deficiency/therapy , Vitamin D/administration & dosage , Vitamins/administration & dosage , Adolescent , Breast Feeding , Child , Child, Preschool , Humans , Infant , Practice Guidelines as Topic , Vitamin D Deficiency/complications , Vitamin D Deficiency/diagnosisABSTRACT
Farnesyltransferase inhibitors (FTIs) are being developed to block Ras-mediated actions, but current data suggest that the FTIs act through other non-Ras pathways. A new agent, farnesylthiosalicylic acid (FTS), blocks the binding of Ras to membrane acceptor sites and causes a marked reduction in Ras levels. Accordingly, FTS could be a useful new agent for the treatment of hormone-dependent breast cancer. We examined the dose-response effects of FTS on the growth of MCF-7 breast cancer cells in vitro and in vivo. Further, we dissected out its specific effects on cell proliferation and apoptosis by measuring BrdU incorporation into DNA and by using an ELISA assay to quantitate the magnitude of apoptosis. FTS and its solubilized conjoiner FTS-cyclodextrin markedly inhibited cell growth in MCF-7 breast cancer cells in culture and in xenografts. This agent exerted dual effects to reduce cell proliferation as assessed by BrdU incorporation and to enhance apoptosis as quantitated by ELISA assay. These data suggest that FTS is a promising agent to be developed for treatment of hormone-dependent breast cancer.
