Annual bluegrass is a problematic weed in bermudagrass and other intensively maintained turfgrasses. Flumioxazin is reported to control annual bluegrass both PRE and POST; however, as a contact herbicide, flumioxazin injures actively growing bermudagrass. Research was conducted in Alabama and California to evaluate optimal flumioxazin application timing for annual bluegrass control, bermudagrass response, and overall sward quality in the field, and to assess annual bluegrass control at various growth stages in the greenhouse. November and December application timings resulted in the best balance of the three parameters. When bermudagrass was not dormant at application, treatment resulted in necrosis of green tissues and thus induced dormancy. The herbicide-induced dormancy resulted in better sward quality due to more uniform and therefore more aesthetically pleasing dormant turfgrass relative to natural dormancy. Flumioxazin at 0.43 kg ai ha−1 resulted in better annual bluegrass control and improved sward quality relative to 0.21 kg ha−1. Incomplete POST annual bluegrass control from later applications was attributed to larger weed size, limiting the effectiveness of this contact herbicide. Greenhouse data corroborated field results and indicated that flumioxazin at 0.43 kg ha−1 controlled ≥ 95% of annual bluegrass up to two tillers. Flumioxazin can be utilized for PRE and POST annual bluegrass control, but utilization of this herbicide is limited to dormant bermudagrass unless induced dormancy can be tolerated, and POST control is limited to annual bluegrass plants ≤ two tillers in size.

Human selenium (Se) requirements are currently based on biochemical markers of Se status. In rats, tissue glutathione peroxidase-1 (Gpx1) mRNA levels can be used effectively to determine Se requirements; blood Gpx1 mRNA levels decrease in Se-deficient rats, so molecular biology-based markers have potential for human nutrition assessment. To study the efficacy of molecular biology markers for assessing Se status in humans, we conducted a longitudinal study on 39 subjects (age 45 ± 11) in Reading, UK. Diet diaries (5 day) and blood were obtained from each subject at 2, 8, 17 and 23 weeks, and plasma Se, glutathione peroxidase (Gpx3) enzyme activity, and selenoprotein mRNA levels were determined. There were no significant longitudinal effects on Se biomarkers. Se intake averaged 48 ± 14 μg/d. Plasma Se concentrations averaged 1·13 ± 0·16 μmol/l. Plasma Se v. energy-corrected Se intake (ng Se/kJ/d) was significantly correlated, but neither Gpx3 activity v. Se intake (ng Se/kJ/d) nor Gpx3 activity v. plasma Se was significantly correlated. Collectively, this indicates that subjects were on the plateaus of the response curves. Selenoprotein mRNAs were quantitated in total RNA isolated from whole blood, but mRNA levels for Gpx1, selenoprotein H, and selenoprotein W (all highly regulated by Se in rodents), as well selenoprotein P, Gpx3, and phospholipid hydroperoxide glutathione peroxidase were also not significantly correlated with plasma Se. Thus selenoprotein molecular biomarkers, as well as traditional biochemical markers, are unable to further distinguish differences in Se status in these Se replete subjects. The efficacy of molecular biomarkers to detect Se deficiency needs to be tested in Se-deficient populations.

Nutrigenomics is the study of how constituents of the diet interact with genes, and their products, to alter phenotype and, conversely, how genes and their products metabolise these constituents into nutrients, antinutrients, and bioactive compounds. Results from molecular and genetic epidemiological studies indicate that dietary unbalance can alter gene–nutrient interactions in ways that increase the risk of developing chronic disease. The interplay of human genetic variation and environmental factors will make identifying causative genes and nutrients a formidable, but not intractable, challenge. We provide specific recommendations for how to best meet this challenge and discuss the need for new methodologies and the use of comprehensive analyses of nutrient–genotype interactions involving large and diverse populations. The objective of the present paper is to stimulate discourse and collaboration among nutrigenomic researchers and stakeholders, a process that will lead to an increase in global health and wellness by reducing health disparities in developed and developing countries.