Prevalence of peanut allergy in primary-school children in Montreal, Canada

BACKGROUND: Peanut allergy is receiving increasing attention. Only one study has estimated the prevalence in North America, but it did not corroborate history with diagnostic testing. OBJECTIVE: We estimated the prevalence of peanut allergy in Montreal by administering questionnaires regarding peanut ingestion to children in kindergarten through grade 3 in randomly selected schools. METHODS: Respondents were stratified as follows: (1). peanut tolerant, (2). never-rarely ingest peanut, (3). convincing history of peanut allergy, and (4). uncertain history of peanut allergy. Groups 2, 3, and 4 underwent peanut skin prick tests (SPTs), and if the responses were positive in groups 2 or 4, measurement of peanut-specific IgE were undertaken. Children in group 3 with a positive SPT response were considered allergic to peanut without further testing. Children in groups 2 and 4 with peanut-specific IgE levels of less than 15 kU/L underwent oral peanut challenges. RESULTS: Of the 7768 children surveyed, 4339 responded, 94.6% in group 1. The prevalence of peanut allergy was 1.50% (95% CI, 1.16%-1.92%). When multiple imputation was used to incorporate data on those responding to the questionnaire but withdrawing before testing, the estimated prevalence increased to 1.76% (95% CI, 1.38%-2.21%). When data regarding the peanut allergy status of nonresponders (as declared to the school before the study) were also incorporated, the estimated prevalence was 1.34% (95% CI, 1.08%-1.64%). CONCLUSION: Our prevalence study is the first in North America to corroborate history with confirmatory testing and the largest worldwide to incorporate these techniques. We have shown that, even with conservative assumptions, prevalence exceeds 1.0%.     

Welfare reform and child care options for low-income families

For the changes under welfare reform to positively affect children, the gains that mothers make from employment must lead to improvements in children's daily settings at home, in child care, at school, or in the community. This article focuses on the role child care can play in promoting the development of, and life opportunities for, low-income children. Key observations include: Total federal and state funding for child care for welfare and working poor families has increased dramatically since welfare reform, from $2.8 billion in 1995 to $8.0 billion in 2000. The majority of welfare mothers tend to rely on informal child care arrangements when first participating in welfare-to-work programs, but as they move off welfare and into more stable jobs, they are more likely to choose a center or a family child care home. Although children from poor households stand to benefit the most from high-quality care, they are less likely to be enrolled in high-quality programs than are children from affluent families, partly due to uneven access to high-quality options in their neighborhoods. Less than one-quarter of all eligible families use child care subsidies, and usage varies widely across states and local areas reflecting various barriers to access and scarcity of quality center-based care. The authors conclude that to achieve welfare reform's ultimate goal of breaking the cycle of intergenerational poverty and dependence on government benefits, welfare-to-work programs should promote learning and development among children in welfare and working poor families by increasing access to high-quality child care in low-income neighborhoods.     

Complex regulation of the fibroblast growth factor-binding protein in MDA- MB-468 breast cancer cells by CCAAT/enhancer-binding protein beta

The fibroblast growth factor-binding protein (FGF-BP) binds and activates fibroblast growth factors in the extracellular matrix, and can have a rate-limiting role in tumor angiogenesis. Here we demonstrate high levels of FGF-BP expression in invasive human breast cancer, relative to normal breast and in situ carcinoma, and in MDA-MB-468 human breast cancer cells. In these cells, FGF-BP was up-regulated by treatment with epidermal growth factor (EGF), dependent on protein kinase C and p38 mitogen-activated protein kinase signaling. Mutational analysis revealed that the activator protein 1 and CCAAT/enhancer binding protein (C/EBP) sites on the FGF-BP gene promoter were required for the EGF effect, whereas deletion of the C/EBP site resulted in a significant increase in promoter basal activity indicating a basal repressive control mechanism. These data suggest that the C/EBP site is a central regulatory element for the regulation of FGF-BP promoter activity in MDA-MB-468 cells. We found that MDA-MB-468 cells express high endogenous levels of both the activating (LAP) and repressive (LIP) isoforms of C/EBPbeta. Overexpression of C/EBPbeta-LAP in MDA-MB-468 cells resulted in a large 80-fold increase in FGF-BP promoter basal activity, which was reversed by coexpression of LIP. Gel-shift analysis revealed that four LIP- and LAP-containing complexes (a-d) bind to the C/EBP site. DNA binding of the LIP and LAP-containing c complex and the b complex in the presence of EGF was modulated by inhibition of p38 mitogen-activated protein kinase, suggesting a role for these complexes in the EGF induction of the FGF-BP promoter. This study suggests that along with its well-defined role in mammary gland development, C/EBPbeta may well play a role in the pathology of breast cancer, in particular in the control of angiogenesis in the invasive phenotype.     

Modulation of redox signal transduction pathways in the treatment of cancer

Reactive oxygen species (ROS)-mediated damage to DNA is associated with induction of stress-activated protein kinases leading to secondary and tertiary effects on the nuclear matrix, cytoplasmic transport mechanisms, and altered mitochondrial and cell membranes. The cellular defenses against ROS damage are associated with up-regulation of gene products that can significantly alter cell biology, including antiapoptotic Bax family proteins and inflammatory proteins. Altered cell integrity can occur either directly or by indirect paracrine and juxtacrine interactions within tissues. Previous approaches toward therapeutic intervention against ROS damage have included administration of radical scavenger compounds, use of novel drugs that increase cellular production of constitutive antioxidants, or pharmacologic agents that modify the intracellular transport of antioxidants. Strategies to modify the cellular effects of ROS in hyperbaric oxygen injury to the lung, reperfusion injury to transplanted organs, and cancer have led to novel approaches of gene therapy in which the transgenes for antioxidant proteins can be expressed in specific tissues. Reducing tissue-damaging effects of ROS may have relevance to cancer patients by ameliorating normal tissue damage from ionizing irradiation therapy, photodynamic therapy, and cancer chemotherapy.