Only unbiased estimates of end-stage renal disease (ESRD) incidence and trends are useful for disease control-identification of risk factors and measuring the effect of intervention.
Adoption of optimal dietary habits during adolescence is associated with better health outcomes later in life. However, the associations between a pattern of healthy dietary habits encapsulated in an index and sociodemographic and nutrient intake have not been examined among adolescents. This study aimed to develop a behavior-based diet index and examine its validity in relation to sociodemographic factors, nutrient intakes, and biomarkers in a representative sample of New Zealand (NZ) adolescents aged 15-18 y (n = 694). A 17-item Healthy Dietary Habits Score for Adolescents (HDHS-A) was developed based on dietary habits information from the 2008/2009 NZ Adult Nutrition Survey. Post hoc trend analyses were used to identify the associations between HDHS-A score and nutrient intakes estimated by single 24-h diet recalls and selected nutritional biomarkers. Being female, not of Maori or Pacific ethnicity, and living in the least-deprived socioeconomic quintile were associated with a higher HDHS-A score (all P < 0.001). HDHS-A tertile was associated positively with intake of protein, dietary fiber, polyunsaturated fatty acid, and lactose and negatively with sucrose. Associations in the expected directions were also found with most micronutrients (P < 0.05), urinary sodium (P < 0.001), whole blood (P < 0.05), serum (P < 0.01), and RBC folate (P < 0.05) concentrations. This suggests that the HDHS-A is a valid indicator of diet quality among NZ adolescents.
The EphA4 receptor tyrosine kinase is involved in numerous cell-signalling activities during embryonic development. EphA4 has the ability to bind to both types of ephrin ligands, the ephrinAs and ephrinBs. The C57BL/6J-Epha4rb-2J/GrsrJ strain, denoted Epha4(rb-2J/rb-2J), is a spontaneous mouse mutant that arose at The Jackson Laboratory. These mutants exhibited a synchronous hind limb locomotion defect or "hopping gait" phenotype, which is also characteristic of EphA4 null mice. Genetic complementation experiments suggested that Epha4(rb-2J) corresponds to an allele of EphA4, but details of the genomic defect in this mouse mutant are currently unavailable. We found a single base-pair deletion in exon 9 resulting in a frame shift mutation that subsequently resulted in a premature stop codon. Analysis of the predicted structure of the truncated protein suggests that both the kinase and sterile α motif (SAM) domains are absent. Definitive determination of genotype is needed for experimental studies of mice carrying the Epha4(rb-2J) allele, and we have also developed a method to ease detection of the mutation through RFLP. Eph-ephrin family members are reportedly expressed as numerous isoforms. Hence, delineation of the specific mutation in EphA4 in this strain is important for further functional studies, such as protein-protein interactions, immunostaining and gene compensatory studies, investigating the mechanism underlying the effects of altered function of Eph family of receptor tyrosine kinases on phenotype.