Do COX-2 inhibitors worsen renal function?

No, COX-2 inhibitors, as a class, do not worsen renal function for those without renal disease. Celecoxib is the only COX-2 inhibitor available, and it is associated with a lower risk of renal dysfunction and hypertension when compared with controls. Available data do not allow for adjusted risk assessment for patients with preexisting renal disease on COX-2 inhibitors (strength of recommendation [SOR]: A, based on meta-analysis)

Characterization of transposon insertion mutants in desulfovibrio vulgaris hilderborough by sequencing genomic DNA [abstract]

Abstract only availableTn5 transposon mutagenesis occurs by a mechanism in which a segment of DNA (transposon) encoded in a plasmid is inserted into genomic DNA (the target) by a conservative (cut-and-paste) mechanism. When the insertion position is in a coding sequence or regulatory region of DNA, the insertion results in a mutation. The plasmid pRL27 encodes a mini-Tn5 transposon, Tn5 transposase, and kanamycin resistance, (Metcalf, William W. et al, 2002 Arch Microbiol 178 :193-201) and was used to transform Desulfovibrio vulgaris Hildenborough by electroporation. Transposon insertion mutants were identified by their ability to grow in the presence of kanamycin. To identify the insertion sites of the transposons, in theory one should be able to sequence from the transposon into chromosomal DNA and identify the mutation site by comparison with the known genome. Unlike sequencing of plasmid DNA or PCR products, direct genomic sequencing has a limited success rate. Direct genomic sequencing is sensitive to DNA quality, interference of secondary DNA structures, salt concentration, and the availability of primer binding sites. Because of these difficulties, in our attempts to identify insertion sites of mini-Tn5, we examined template DNA quality as well as modifying sequencing reaction conditions. Our objective is to develop an effective, reliable method for sequencing genomic DNA to identify where transposon insertion sites have occurred in each mutant.Department of Energy Genomics: Genomes to Life Progra

Dietary intake and food sources of EPA, DPA and DHA in Australian children

Secondary analysis of the 2007 Australian National Children\u27s Nutrition and Physical Activity survey was undertaken to assess the intake and food sources of EPA, DPA and DHA (excluding supplements) in 4,487 children aged 2-16 years. An average of two 24-h dietary recalls was analysed for each child and food sources of EPA, DPA and DHA were assessed using the Australian nutrient composition database called AUSNUT 2007. Median (inter quartile range, IQR) for EPA, DPA and DHA intakes (mg/day) for 2-3, 4-8, 9-13, 14-16 year were: EPA 5.3 (1.5-14), 6.7 (1.8-18), 8.7 (2.6-23), 9.8 (2.7-28) respectively; DPA 6.2 (2.2-14), 8.2 (3.3-18), 10.8 (4.3-24), 12.2 (5-29) respectively; and DHA 3.9 (0.6-24), 5.1 (0.9-26), 6.8 (1.1-27), 7.8 (1.5-33) respectively. Energy-adjusted intakes of EPA, DPA and DHA in children who ate fish were 7.5, 2 and 16-fold higher, respectively (P \u3c 0.001) compared to those who did not eat fish during the 2 days of the survey. Intake of total long chain n-3 PUFA was compared to the energy adjusted suggested dietary target (SDT) for Australian children and 20 % of children who ate fish during the 2 days of the survey met the SDT. Fish and seafood products were the largest contributors to DHA (76 %) and EPA (59 %) intake, while meat, poultry and game contributed to 56 % DPA. Meat consumption was 8.5 times greater than that for fish/seafood. Australian children do not consume the recommended amounts of long chain omega-3 fatty acids, especially DHA, which could be explained by low fish consumption