2,211 research outputs found

    From Anthroposophy to non-confessional preparation for spirituality? Could common schools learn from spiritual education in Steiner schools?

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    It has been suggested common schools might have something to learn from spiritual education in Steiner schools. This arguably assumes practice in Steiner schools to be compatible with the aims of spiritual education in common schools. I question this by considering whether the former is confessional, as the latter should not be. I begin by highlighting how my concern about the potentially confessional nature of Steiner spiritual education arose. I argue for a nuanced understanding of confessional education, which distinguishes between ‘weak’ and ‘strong’ confessional education, as well as between confessional education as intentional and as defined by outcome. I then argue that spiritual education in common schools should prepare pupils for spirituality, without being confessional. I consider whether Steiner schools are confessional by drawing upon findings from research conducted at six Steiner schools. I conclude that spiritual education in Steiner schools is weakly confessional in an intentional sense. I further conclude that practices which might contribute to preparation for spirituality and which can be implemented in a non-confessional manner are worthy of consideration for transfer to common schools. Common schools committed to preparation for spirituality as an educational aim could learn from spiritual education in Steiner schools

    Uncovering regulatory pathways that affect hematopoietic stem cell function using 'genetical genomics'

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    We combined large-scale mRNA expression analysis and gene mapping to identify genes and loci that control hematopoietic stem cell (HSC) function. We measured mRNA expression levels in purified HSCs isolated from a panel of densely genotyped recombinant inbred mouse strains. We mapped quantitative trait loci (QTLs) associated with variation in expression of thousands of transcripts. By comparing the physical transcript position with the location of the controlling QTL, we identified polymorphic cis-acting stem cell genes. We also identified multiple trans-acting control loci that modify expression of large numbers of genes. These groups of coregulated transcripts identify pathways that specify variation in stem cells. We illustrate this concept with the identification of candidate genes involved with HSC turnover. We compared expression QTLs in HSCs and brain from the same mice and identified both shared and tissue-specific QTLs. Our data are accessible through WebQTL, a web-based interface that allows custom genetic linkage analysis and identification of coregulated transcripts.

    Epigenetic regulation of cyclooxygenase-2 by methylation of c8orf4 in pulmonary fibrosis

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    Fibroblasts derived from the lungs of patients with idiopathic pulmonary fibrosis (IPF) and systemic sclerosis (SSc) produce low levels of prostaglandin (PG) E(2), due to a limited capacity to up-regulate cyclooxygenase-2 (COX-2). This deficiency contributes functionally to the fibroproliferative state, however the mechanisms responsible are incompletely understood. In the present study, we examined whether the reduced level of COX-2 mRNA expression observed in fibrotic lung fibroblasts is regulated epigenetically. The DNA methylation inhibitor, 5-aza-2′-deoxycytidine (5AZA) restored COX-2 mRNA expression by fibrotic lung fibroblasts dose dependently. Functionally, this resulted in normalization of fibroblast phenotype in terms of PGE(2) production, collagen mRNA expression and sensitivity to apoptosis. COX-2 methylation assessed by bisulfite sequencing and methylation microarrays was not different in fibrotic fibroblasts compared with controls. However, further analysis of the methylation array data identified a transcriptional regulator, chromosome 8 open reading frame 4 (thyroid cancer protein 1, TC-1) (c8orf4), which is hypermethylated and down-regulated in fibrotic fibroblasts compared with controls. siRNA knockdown of c8orf4 in control fibroblasts down-regulated COX-2 and PGE(2) production generating a phenotype similar to that observed in fibrotic lung fibroblasts. Chromatin immunoprecipitation demonstrated that c8orf4 regulates COX-2 expression in lung fibroblasts through binding of the proximal promoter. We conclude that the decreased capacity of fibrotic lung fibroblasts to up-regulate COX-2 expression and COX-2-derived PGE(2) synthesis is due to an indirect epigenetic mechanism involving hypermethylation of the transcriptional regulator, c8orf4
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