Reframing the Issue: Child Care Advocacy in Alberta

This article focuses on the organization, strategies, and motivations of the contemporary child care movement in Alberta. The concept of framing is used to explore the ways in which child care advocates negotiate the gap between their desires for policy change and their knowledge of what advances are feasible given the political realities of the province. In particular, the article emphasizes advocates’ use of gender-neutral, child-centred frames that focus on the developmental and economic benefits of child care, rather than feminist-informed frames that emphasize the need for public, universal child care. This has implications for the scope of policy reforms on the political agenda and for women’s equality in Alberta.Cet article s’intéresse à l’organisation, aux stratégies et aux mobiles du mouvement contemporain de la garde des enfants en Alberta. On utilise le concept d’élaboration afin d’explorer les méthodes employées par les militants de la garde d’enfants, pour négocier l’écart entre leur désir de changement de politique et leur connaissance sur les avancées qui sont faisables, compte tenu des réalités de la province. Cet article met particulièrement l’emphase sur l’utilisation des termes « élaborations de genres neutres» et « élaborations centrées sur les enfants » par les militants, afin de porter une attention particulière sur les avantages développementaux et économiques de la garde d’enfants, plutôt que sur des élaborations d’information féministes, qui mettent l’emphase sur une garde d’enfant universelle et publique. Cela a un impact sur la place des réformes politiques et sur l’égalité

Comparing Child Care Policy in the Canadian Provinces

The ten Canadian provinces offer a rich site for comparative analysis of child care policy. To utilize this, we construct a framework that uses quantitative measures to assess the variation in child care arrangements across the ten provinces. Our framework suggests that provincial child care variation is multi-dimensional and often involves trade-offs or compromises. This finding challenges some of the assumptions of regime theory, which suggests that social policy arrangements are logical and cohesive. We argue that while regime theory is useful for understanding broad differences in social policy arrangements, including differences between Canada and other industrialized democracies, empirical comparative analysis of the kind we have undertaken is important for uncovering the more complex and nuanced variation apparent in real-world policy arrangements at the provincial level

New mutations at the imprinted Gnas cluster show gene dosage effects of Gsα in postnatal growth and implicate XLαs in bone and fat metabolism, but not in suckling

The imprinted Gnas cluster is involved in obesity, energy metabolism, feeding behavior, and viability. Relative contribution of paternally expressed proteins XLαs, XLN1, and ALEX or a double dose of maternally expressed Gsα to phenotype has not been established. In this study, we have generated two new mutants (Ex1A-T-CON and Ex1A-T) at the Gnas cluster. Paternal inheritance of Ex1A-T-CON leads to loss of imprinting of Gsα, resulting in preweaning growth retardation followed by catch-up growth. Paternal inheritance of Ex1A-T leads to loss of imprinting of Gsα and loss of expression of XLαs and XLN1. These mice have severe preweaning growth retardation and incomplete catch-up growth. They are fully viable probably because suckling is unimpaired, unlike mutants in which the expression of all the known paternally expressed Gnasxl proteins (XLαs, XLN1 and ALEX) is compromised. We suggest that loss of ALEX is most likely responsible for the suckling defects previously observed. In adults, paternal inheritance of Ex1A-T results in an increased metabolic rate and reductions in fat mass, leptin, and bone mineral density attributable to loss of XLαs. This is, to our knowledge, the first report describing a role for XLαs in bone metabolism. We propose that XLαs is involved in the regulation of bone and adipocyte metabolism

Postnatal Changes in the Expression Pattern of the Imprinted Signalling Protein XLαs Underlie the Changing Phenotype of Deficient Mice

The alternatively spliced trimeric G-protein subunit XLαs, which is involved in cAMP signalling, is encoded by the Gnasxl transcript of the imprinted Gnas locus. XLαs deficient mice show neonatal feeding problems, leanness, inertia and a high mortality rate. Mutants that survive to weaning age develop into healthy and fertile adults, which remain lean despite elevated food intake. The adult metabolic phenotype can be attributed to increased energy expenditure, which appears to be caused by elevated sympathetic nervous system activity. To better understand the changing phenotype of Gnasxl deficient mice, we compared XLαs expression in neonatal versus adult tissues, analysed its co-localisation with neural markers and characterised changes in the nutrient-sensing mTOR1-S6K pathway in the hypothalamus. Using a newly generated conditional Gnasxl lacZ gene trap line and immunohistochemistry we identified various types of muscle, including smooth muscle cells of blood vessels, as the major peripheral sites of expression in neonates. Expression in all muscle tissues was silenced in adults. While Gnasxl expression in the central nervous system was also developmentally silenced in some midbrain nuclei, it was upregulated in the preoptic area, the medial amygdala, several hypothalamic nuclei (e.g. arcuate, dorsomedial, lateral and paraventricular nuclei) and the nucleus of the solitary tract. Furthermore, expression was detected in the ventral medulla as well as in motoneurons and a subset of sympathetic preganglionic neurons of the spinal cord. In the arcuate nucleus of Gnasxl-deficient mice we found reduced activity of the nutrient sensing mTOR1-S6K signalling pathway, which concurs with their metabolic status. The expression in these brain regions and the hypermetabolic phenotype of adult Gnasxl-deficient mice imply an inhibitory function of XLαs in energy expenditure and sympathetic outflow. By contrast, the neonatal phenotype of mutant mice appears to be due to a transient role of XLαs in muscle tissues

A Mouse Model for Osseous Heteroplasia

GNAS/Gnas encodes Gsa that is mainly biallelically expressed but shows imprinted expression in some tissues. In Albright Hereditary Osteodystrophy (AHO) heterozygous loss of function mutations of GNAS can result in ectopic ossification that tends to be superficial and attributable to haploinsufficiency of biallelically expressed Gsa. Oed-Sml is a point missense mutation in exon 6 of the orthologous mouse locus Gnas. We report here both the late onset ossification and occurrence of benign cutaneous fibroepithelial polyps in Oed-Sml. These phenotypes are seen on both maternal and paternal inheritance of the mutant allele and are therefore due to an effect on biallelically expressed Gsa. The ossification is confined to subcutaneous tissues and so resembles the ossification observed with AHO. Our mouse model is the first with both subcutaneous ossification and fibroepithelial polyps related to Gsa deficiency. It is also the first mouse model described with a clinically relevant phenotype associated with a point mutation in Gsa and may be useful in investigations of the mechanisms of heterotopic bone formation. Together with earlier results, our findings indicate that Gsa signalling pathways play a vital role in repressing ectopic bone formation

Clarifying the complexity: rethinking studies of variation in child care policy

Bibliography: p. 106-112Includes copy of ethics approval. Original copy with original Partial Copyright Licence.This thesis argues that existing accounts of variation in child care policy fail to systematically address, define, and measure the ways in which child care policy arrangements vary from jurisdiction to jurisdiction. Comparative studies of child care policy rely on broad or general descriptions of variation in child care policy that fail to provide a systematic comparative framework for understanding the extent, nature, and complexity of this variation. Drawing on comparative data measuring child care in the Canadian provinces, and a qualitative case study of child care policy in Alberta, I argue that child care policy arrangements display many inconsistencies and conflicting ideas that cannot be easily described and classified. This finding has important implications for the methods and theories used to describe and understand variation in child care policy

Policy legacies and child care politics in Australia and Canada

Thesis: S.M., Massachusetts Institute of Technology, Department of Political Science, 2015."September 2015." Cataloged from PDF version of thesis.Includes bibliographical references (pages 58-63).This study explores the puzzle of why Australia and Canada have followed significantly different paths in national-level child care policy despite their otherwise similar welfare state structures. Australia has developed a relatively generous system of public subsidies to support the provision of care for young children, while at the same time relying increasingly on the market to deliver child care. In contrast, Canada has extremely low levels of public spending and service provision, resulting in a less expansive system of regulated child care. I trace these divergent outcomes to the impact of post-WWII child care policy legacies in these countries and the way that these legacies interact with the changing politics of the welfare state to produce variation. In Canada, child care policy was first established within a social assistance framework as a service intended to combat poverty, while in Australia, child care was introduced as an economic policy to facilitate women's workforce participation. The differences in the intended goals of these policies affected the subsequent patterns of child care politics and policy development in these two countries, leading to the divergent outcomes observed today.by Kelly E. Pasolli.S.M

Transgenic Overexpression of the Extra-Large Gsα Variant XLαs Enhances Gsα-Mediated Responses in the Mouse Renal Proximal Tubule in Vivo

Targeting XLαs expression to the mouse renal proximal tubule augments Gsα-mediated responses and mitigates the PTH-resistance phenotype observed in mice with maternal Gsα ablation