Child agency and therapy in primary school

The article reports on, and analyses, qualitative research involving children’s therapy in two primary school contexts in England. It aims to explore the potentials of how agency as a concept can contribute to a challenge to existing theory, research and ways of working concerning therapy in primary school contexts. The article addresses how this challenge can be theorised: drawing on a critical review of how the fields of health, therapy, education and child rights connect to concepts of agency. Themes within this review include different disciplinary paradigms of childhood; how concepts of agency relate to those of child rights and voice; how a field such as therapy, created around concepts of welfare, can shift to acknowledge the presence of a child rights framework; and the complexities of child agency in therapy within primary school contexts. Data are included from the authors’ research projects that access children’s views of their therapy and that engages with them through a questionnaire, a member checking group and as co-researchers into their experiences of therapy. The analysis of the data reveals the challenges, potentials and advantages of recognising and listening to children as ‘active agents’ and ‘experts’ in relation to their therapy

Low cost, low tech SNP genotyping tools for resource-limited areas: Plague in Madagascar as a model

Genetic analysis of pathogenic organisms is a useful tool for linking human cases together and/or to potential environmental sources. The resulting data can also provide information on evolutionary patterns within a targeted species and phenotypic traits. However, the instruments often used to generate genotyping data, such as single nucleotide polymorphisms (SNPs), can be expensive and sometimes require advanced technologies to implement. This places many genotyping tools out of reach for laboratories that do not specialize in genetic studies and/or lack the requisite financial and technological resources. To address this issue, we developed a low cost and low tech genotyping system, termed agarose-MAMA, which combines traditional PCR and agarose gel electrophoresis to target phylogenetically informative SNPs

Oceanography of Cowichan Bay: A background view for early marine survival of Chinook and Coho salmon

Early Marine Survival (EMS) of Chinook and Coho salmon in the Salish Sea has plummeted over the past decades, and both bottom-up and top-down mechanisms for decline have been proposed. As a background for an ecosystem-based assessment of EMS, a pilot study on the basic oceanography of a small sub-component of the system was launched in spring and early summer, 2013. A repeat sampling grid covering Cowichan Bay and immediately connected waters was established, and then sampled on weekly intervals for temperature, salinity, chlorophyll fluorescence, nutrients and zooplankton. Oceanographic studies were carried out concurrently with fisheries assessments. A longer section was carried out at monthly intervals, with the purpose of connecting Cowichan Bay to the Strait of Georgia. This talk will present findings from this study, identify key shortcoming and suggest an approach to expand the pilot study to the scale of the Salish Sea

Intragenic DNA methylation: implications of this epigenetic mechanism for cancer research

Epigenetics is the study of all mechanisms that regulate gene transcription and genome stability that are maintained throughout the cell division, but do not include the DNA sequence itself. The best-studied epigenetic mechanism to date is DNA methylation, where methyl groups are added to the cytosine base within cytosine–guanine dinucleotides (CpG sites). CpGs are frequently clustered in high density (CpG islands (CGIs)) at the promoter of over half of all genes. Current knowledge of transcriptional regulation by DNA methylation centres on its role at the promoter where unmethylated CGIs are present at most actively transcribed genes, whereas hypermethylation of the promoter results in gene repression. Over the last 5 years, research has gradually incorporated a broader understanding that methylation patterns across the gene (so-called intragenic or gene body methylation) may have a role in transcriptional regulation and efficiency. Numerous genome-wide DNA methylation profiling studies now support this notion, although whether DNA methylation patterns are a cause or consequence of other regulatory mechanisms is not yet clear. This review will examine the evidence for the function of intragenic methylation in gene transcription, and discuss the significance of this in carcinogenesis and for the future use of therapies targeted against DNA methylation

Defending the genome from the enemy within:mechanisms of retrotransposon suppression in the mouse germline

The viability of any species requires that the genome is kept stable as it is transmitted from generation to generation by the germ cells. One of the challenges to transgenerational genome stability is the potential mutagenic activity of transposable genetic elements, particularly retrotransposons. There are many different types of retrotransposon in mammalian genomes, and these target different points in germline development to amplify and integrate into new genomic locations. Germ cells, and their pluripotent developmental precursors, have evolved a variety of genome defence mechanisms that suppress retrotransposon activity and maintain genome stability across the generations. Here, we review recent advances in understanding how retrotransposon activity is suppressed in the mammalian germline, how genes involved in germline genome defence mechanisms are regulated, and the consequences of mutating these genome defence genes for the developing germline

Computational Micromodel for Epigenetic Mechanisms

Characterization of the epigenetic profile of humans since the initial breakthrough on the human genome project has strongly established the key role of histone modifications and DNA methylation. These dynamic elements interact to determine the normal level of expression or methylation status of the constituent genes in the genome. Recently, considerable evidence has been put forward to demonstrate that environmental stress implicitly alters epigenetic patterns causing imbalance that can lead to cancer initiation. This chain of consequences has motivated attempts to computationally model the influence of histone modification and DNA methylation in gene expression and investigate their intrinsic interdependency. In this paper, we explore the relation between DNA methylation and transcription and characterize in detail the histone modifications for specific DNA methylation levels using a stochastic approach

Ca2+ influx and phosphoinositide signalling are essential for the establishment and maintenance of cell polarity in monospores from the red alga Porphyra yezoensis

The asymmetrical distribution of F-actin directed by cell polarity has been observed during the migration of monospores from the red alga Porphyra yezoensis. The significance of Ca2+ influx and phosphoinositide signalling during the formation of cell polarity in migrating monospores was analysed pharmacologically. The results indicate that the inhibition of the establishment of cell polarity, as judged by the ability of F-actin to localize asymmetrically, cell wall synthesis, and development into germlings, occurred when monospores were treated with inhibitors of the Ca2+ permeable channel, phospholipase C (PLC), diacylglycerol kinase, and inositol-1,4,5-trisphosphate receptor. Moreover, it was also found that light triggered the establishment of cell polarity via photosynthetic activity but not its direction, indicating that the Ca2+ influx and PLC activation required for the establishment of cell polarity are light dependent. By contrast, inhibition of phospholipase D (PLD) prevented the migration of monospores but not the asymmetrical localization of F-actin. Taken together, these findings suggest that there is functional diversity between the PLC and PLD signalling systems in terms of the formation of cell polarity; the former being critical for the light-dependent establishment of cell polarity and the latter playing a role in the maintenance of established cell polarity

Predicting genome-wide DNA methylation using methylation marks, genomic position, and DNA regulatory elements

Background: Recent assays for individual-specific genome-wide DNA methylation profiles have enabled epigenome-wide association studies to identify specific CpG sites associated with a phenotype. Computational prediction of CpG site-specific methylation levels is important, but current approaches tackle average methylation within a genomic locus and are often limited to specific genomic regions. Results: We characterize genome-wide DNA methylation patterns, and show that correlation among CpG sites decays rapidly, making predictions solely based on neighboring sites challenging. We built a random forest classifier to predict CpG site methylation levels using as features neighboring CpG site methylation levels and genomic distance, and co-localization with coding regions, CGIs, and regulatory elements from the ENCODE project, among others. Our approach achieves 91% -- 94% prediction accuracy of genome-wide methylation levels at single CpG site precision. The accuracy increases to 98% when restricted to CpG sites within CGIs. Our classifier outperforms state-of-the-art methylation classifiers and identifies features that contribute to prediction accuracy: neighboring CpG site methylation status, CpG island status, co-localized DNase I hypersensitive sites, and specific transcription factor binding sites were found to be most predictive of methylation levels. Conclusions: Our observations of DNA methylation patterns led us to develop a classifier to predict site-specific methylation levels that achieves the best DNA methylation predictive accuracy to date. Furthermore, our method identified genomic features that interact with DNA methylation, elucidating mechanisms involved in DNA methylation modification and regulation, and linking different epigenetic processes