12 research outputs found

    Marker development for quality protein maize breeding and an interaction study between Opaque-2 and Ask2 genes

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    Quality Protein Maize (QPM) kernels contain twice the amounts of lysine and tryptophan compared to normal corn kernels. Although the opaque-2 (o2) mutation is the underlying cause of this beneficial change, other genes such as Aspartate kinase-2 (Ask2) affect the amino acid content in the endosperm to a lesser degree. To date, reports on the interaction between both loci are scarce and there are no high-throughput assays for the identification of the alleles of these genes. The objectives of this research were: 1) to study the interaction between the o2 and Ask2 genes with respect to the accumulation of amino acids in the endosperm in an F2 population, 2) to identify conserved SNPs into the o2 gene that can be used as markers, 3) to estimate the frequency of an SNP of Ask2 associated with the accumulation of lysine in the endosperm in CIMMYT germplasm, and 4) to develop high-throughput marker assays for these SNPs. The interaction study showed a preponderant effect of o2 on the accumulation of 11 amino acids (P ≤ 0.01). Ask2 appeared only to act with o2 to enhance marginally lysine, histidine and methionine levels in the double recessive homozygotes. Sequencing of amplicons at the o2 locus led to the identification of an SNP in exon 1 that discriminated all QPM (C) genotypes from non-QPM (T) genotypes. Validation of this SNP through KASP™ assays indicated that it was 92 % assertive in differentiating the o2 genotypes. In contrast, the frequency of the Ask2 SNP in CIMMYT QPM germplasm was low; however, an SSCP marker developed using this SNP detected five variants indicating that other unknown base changes may confer positive lysine-increasing responses. These markers could aid the marker-assisted selection of QPM cultivars

    A biopsychosocial model of normative and problematic pediatric feeding

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    A comprehensive model is presented that (a) highlights factors that have been implicated in the development and maintenance of feeding problems in both normal and clinical populations; and (b) provides a framework for the prevention, management, and treatment of feeding problems across the range of physically healthy children to children with acute and chronic illnesses. Relevant literatures and feeding models were synthesized to present a comprehensive unified biopsychosocial model that may aid in the prediction and synthesis of information about feeding and eating in both normal and clinical populations and provide a framework for interdisciplinary research and intervention

    Patterns of medical and developmental comorbidities among children presenting with feeding problems: A latent class analysis

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    OBJECTIVE: Children with feeding problems often have multiple co-occurring medical and developmental conditions; however, it is unknown whether patterns of comorbidity exist and whether they relate to important feeding-related health outcomes. The main objective of this study was to examine (1) the relationship between the number of medical and developmental comorbidities and important feeding-related health outcomes; (2) how various comorbidities interact and form empirically derived patterns; and (3) how empirically derived patterns of comorbidity relate to weight status, nutritional variety, and child and parent mealtime behavior problems. METHODS: The medical records of 286 children (mean age = 35.56 months) seen at an outpatient feeding disorders clinic were reviewed. Child weight status, nutritional variety, and child and parent mealtime behavior problems were assessed using standardized measures. The lifetime occurrence of medical and developmental conditions was reliably coded. Empirically derived patterns of comorbidity were generated via latent class analyses. RESULTS: Latent class analyses generated 3 comorbidity patterns: Behavioral (58% of cases), Developmentally Delayed (37%), and Autism Spectrum Disorder (ASD, 5%). The Autism Spectrum Disorder group was found to have less nutritional variety compared to the Behavioral and Developmentally Delayed groups. No differences were found between groups in terms of percent ideal body weight, or severity of child or parent mealtime behavior problems. CONCLUSION: Multiple co-occurring conditions of children with feeding problems were empirically reduced to 3 patterns of comorbidities. Comorbidity patterns were largely unrelated to weight status and child or parent mealtime behavior problems. This suggests that medical and developmental conditions confer general, rather than specific, risk for feeding problems in children. Copyright © 2011 Lippincott Williams & Wilkins
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