Positive Possibilities for Child and Family Welfare: Options for Expanding the Anglo-American Child Protection Paradigm

The creation of the ‘problem of child maltreatment’ and how we deal with it are best understood as particular discourses which grow out of specific histories and social configurations. The Anglo-American child protection paradigm can be viewed as a particular configuration rooted in our vision for children, families, community, and society. However, other settings have constructed quite different responses reflecting their own priorities and desired outcomes. This paper is an effort to understand the choices made in Ontario’s child protection system by examining its history and the underlying beliefs and values which have fostered its development. In addition, the paper is an attempt to counteract the sense of inevitability of this child protection approach. By discussing the many different ways in which other countries and settings work with, and think about, families and children, we will uncover a spectrum of positive possibilities which exist outside our current conceptions of child and family welfare systems

Positive Possibilities for Child and Family Welfare: Options for Expanding the Anglo-American Child Protection Paradigm

The creation of the ‘problem of child maltreatment’ and how we deal with it are best understood as particular discourses which grow out of specific histories and social configurations. The Anglo-American child protection paradigm can be viewed as a particular configuration rooted in our vision for children, families, community, and society. However, other settings have constructed quite different responses reflecting their own priorities and desired outcomes. This paper is an effort to understand the choices made in Ontario’s child protection system by examining its history and the underlying beliefs and values which have fostered its development. In addition, the paper is an attempt to counteract the sense of inevitability of this child protection approach. By discussing the many different ways in which other countries and settings work with, and think about, families and children, we will uncover a spectrum of positive possibilities which exist outside our current conceptions of child and family welfare systems

Mucus plugging, air trapping, and bronchiectasis are important outcome measures in assessing progressive childhood cystic fibrosis lung disease

Objective: To determine which outcome measures could detect early progression of disease in school-age children with mild cystic fibrosis (CF) lung disease over a two-year time interval utilizing chest computed tomography (CT) scores, quantitative CT air trapping (QAT), and spirometric measurements. Methods: Thirty-six school-age children with mild CF lung disease (median [interquartile range] age 12 [3.7] years; percent predicted forced expiratory volume in 1 second (ppFEV1) 99 [12.5]) were evaluated by serial spirometer-controlled chest CT scans and spirometry at baseline, 3-month, 1- and 2-years. Results: No significant changes were noted at 3-month for any variable except for decreased ppFEV1. Mucus plugging score (MPS) and QATA1andA2 increased at 1- and 2-years. The bronchiectasis score (BS), and total score (TS) were increased at 2-year. All variables tested with the exception of bronchial wall thickness score, parenchymal score (PS), and ppFEV1, were consistent with longitudinal worsening of lung disease. Multivariate analysis revealed baseline PS, baseline TS, and 1-year changes in BS and air trapping score were predictive of 2-year changes in BS. Conclusions: MPS and QATA1-A2 were the most sensitive indicators of progressive childhood CF lung disease. The 1-year change in the bronchiectasis score had the most positive predictive power for 2-year change in bronchiectasis

Defining the role of common variation in the genomic and biological architecture of adult human height

Using genome-wide data from 253,288 individuals, we identified 697 variants at genome-wide significance that together explained one-fifth of the heritability for adult height. By testing different numbers of variants in independent studies, we show that the most strongly associated ∼2,000, ∼3,700 and ∼9,500 SNPs explained ∼21%, ∼24% and ∼29% of phenotypic variance. Furthermore, all common variants together captured 60% of heritability. The 697 variants clustered in 423 loci were enriched for genes, pathways and tissue types known to be involved in growth and together implicated genes and pathways not highlighted in earlier efforts, such as signaling by fibroblast growth factors, WNT/β-catenin and chondroitin sulfate-related genes. We identified several genes and pathways not previously connected with human skeletal growth, including mTOR, osteoglycin and binding of hyaluronic acid. Our results indicate a genetic architecture for human height that is characterized by a very large but finite number (thousands) of causal variants