45 research outputs found

    A Justice-Oriented Conceptual and Analytical Framework for Decolonising and Desecularising the Field of Educational Technology

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    Education systems globally are increasingly being shaped by the logics, assumptions and pedagogical underpinnings of educational technology (EdTech) products, services, programmes, policies, and systems. These often promote rationalistic, secular, universal, objectivist, (post)modernist, written, behaviourist, and individualistic ways of being, marginalising religious, spiritual, oral, subjective, critical, and communitarian ways of being. Given that technological ways of being have been propagated globally, these logics are no longer predominantly promoted by those in the Global North, but by techno-solutionists globally, although the core-to-periphery flows of ideology and funding are still prominent. This article develops a conceptual and analytical framework for decolonising and desecularising the field of EdTech. Concepts are drawn from various discourses: the desecularisation of knowledge to set the ontological framing; embodied cognition to set the epistemological framing; and social justice and decolonial discourses to set the axiological framing. From this, the article develops the Dimensions of Human Injustice Analytical Framework—covering material, ontological and epistemic, and (geo)political injustices—to assist policymakers, educators, EdTech developers, and international development practitioners in identifying and confronting coloniality in their EdTech. Acknowledging the complexity and contentions within decolonial thought, this article does not claim a unified stance on achieving justice but aims to offer a tool for deconstructing and questioning injustices

    Decolonising educational technology

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    © 2024 by the authors. Published by MDPI under a Creative Commons licence. This is a Reprint of the Special Issue Decolonising Educational Technology that was published in Education Sciences. https://doi.org/10.3390/books978-3-7258-2335-2This important volume brings together some key thinkers in various fields such as educational technology (EdTech), decolonisation, colonialism, neocolonialism, higher education, international education, and social justice. EdTech can be seen as both ubiquitous and hegemonic. At the same time, it can be seen as neocolonial and represents another example of how Western thought, languages, and technology pervade global educational contexts. The authors in this Special Issue explore whether EdTech can be used to overcome the issues inherent in each of their respective contexts without necessarily promulgating 'Global Northern' thought and practice. Thought-provoking and timely, this Reprint seeks to stimulate further debate and discourse around these issues

    Digital neocolonialism and massive open online courses (MOOCs): colonial pasts and neoliberal futures

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    Through evaluating dominant MOOC platforms created by Western universities, I argue that MOOCs on such platforms tend to embed Western-centric epistemologies and propagate this without questioning their global relevance. Consequently, such MOOCs can be detrimental when educating diverse and complex participants as they erode local and indigenous knowledge systems. Arguing that the digital divide is an exacerbation of historical inequalities, I draw parallels between colonial education, specifically across Sub-Saharan Africa, and ‘digital neocolonialism’ through Western MOOC platforms. I analyse similarities in ideology, assumptions, and methods of control. Highlighting evolving forms of coloniality, I include contemporary problems created by neoliberal techno-capitalist agendas, such as the commodification of education. Balance is needed between the opportunities offered through MOOCs and the harms they cause through overshadowing marginalised knowledges and framing disruptive technologies as the saviour. While recommending solutions for inclusion of marginalised voices, further problems such as adverse incorporation are raised

    Genome-wide association analysis within The Manitoba Personalized Lifestyle Research study

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    Overall Abstract Background: Obesity is a major public health challenge worldwide and in Manitoba. An estimated 40-70% of obesity is heritable; however, these genetic associations are poorly investigated in the Manitoban adult population using the “gold standard” Dual Energy X-Ray Absorptiometry (DXA) to assess obesity phenotypes. The Manitoba Personalized Lifestyle Research (TMPLR) project enabled a genetic association study in middle-aged Manitobans. Obesity phenotypes considered are total, gynoid, android, arms, legs, and trunk fat mass. Objectives: 1. Perform a systematic review to determine genes associated with obesity phenotypes assessed by DXA in middle-aged cohorts. 2. Develop a “pipeline” to conduct Genome-Wide Association Studies (GWAS) within the TMPLR. 3. Conduct a GWAS on obesity phenotypes within TMPLR. 4. Compare the genes from the systematic review to those from TMPLR data analysis. Methods: The Covidence platform was used for the systematic review. Publications up to July 2023 sourced from Embase and Medline. The methods for the TMPLR project have been published. A GWAS pipeline was established using the Biodata Catalyst bioinformatics platform and the Seven Bridges R studio version 4.1. Results: Out of 94 and 25 studies obtained from Medline and Embase respectively, 14 studies met the eligibility criteria and 13 genes were identified that are associated with obesity-related phenotypes. No significant genome-wide association with obesity was established in the TMPLR cohort. However, 23 loci have had suggestive associations with the obesity phenotypes. Conclusion: There is a lack of high-quality genetic studies that use DXA data and adult populations. No genome-wide associations were reported in TMPLR, likely due to the limited sample size of the cohort. However, a bioinformatics pipeline to analyze genome-wide associations in TMPLR cohort is established and can be used for larger cohorts, such as UK biobanks.Biodata Catalyst Pilot FundsFebruary 202

    Is there Learning Continuity during the COVID-19 Pandemic? A Synthesis of the Emerging Evidence

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    Since the onset of COVID-19, governments have launched technology-supported education interventions to ensure children learn. This paper offers a narrative synthesis of emerging evidence on technology-based education to understand the current experiences of learners, teachers and families. Studies find that few students in low- and middle-income countries have access to technology-supported learning with the most marginalised children appearing to have the least educational opportunities. As such, the education response to COVID-19 could widen existing inequalities

    Methodological insights for decolonising research and EdTech

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    © 2024 The Authors. Published by MDPI. This is an open access article available under a Creative Commons licence. The published version can be accessed at the following link on the publisher’s website: https://doi.org/10.3390/educsci14060580Published onlin

    Metformin alleviates neuronal and renal related stress signals in diabetic C57BL/6 mice.

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    Doctoral Degree. University of KwaZulu-Natal, Durban.In recent years, diabetes has become more prevalent due to modern, demanding, and sedentary lifestyle patterns. This disease is characterised by insulin resistance and associated molecular complications. Metformin (MF) is a popular antidiabetic agent that has effects beyond glycaemic control such as regulation of metabolic molecular pathways. However, the exact mechanisms against hyperglycaemic induced end organ damage remain elusive. This study aimed to investigate the protective effects of MF in the brain and kidney in vivo, by exploring dysregulated pathways related to mitochondrial function, oxidative stress, ER stress, inflammation, and apoptosis. This study established a diabetic mouse (C57BL/6) model (Ethics no: AREC/057/016) through intraperitoneal multiple low-dose STZ (50 mg/kg BW) injections (10 days). Blood sugar levels of 7-16mmol/L were considered diabetic, and the 15 day treatment period (MF, 20 mg/kg BW per day, oral gavage) was inducted thereafter. Fasting (12 hr) plasma OGTT revealed MF significantly lowered blood glucose levels in diabetic mice. All mice experiments were performed by Dr. N. Naicker. Post-sacrifice (isoflurane), the investigator (author) of the work in the presented in this thesis assisted in harvesting Whole brain and kidney tissue and performed all downstream protein and mRNA analyses. Diabetic mice exhibited heightened oxidative stress by protein carbonylation, and diminished antioxidant responses in both the brain and kidney compared to normoglycaemic mice. Metformin significantly reduced protein carbonylation, increased GSTA4 expression in the brain; and Nrf2 and GPx mRNA levels in the kidney, alleviating oxidative stress. Further, MF improved mt activity, and decreased the HIF-1 expression in the kidney through upregulation of AMPK, and Sirt1 expression. In addition, MF induced epigenetic changes in mice brain through miR-148a repression and concomitant increases in PGC-1α, Sirt1, and Sirt3 protein and gene expressions, thus regulating mt biogenesis. Mitochondrial chaperone proteins HSP60, HSP70 and LonP1 in diabetic mice brain were upregulated through a MF-induced miR-132 repression mechanism. Regulation of the UPR by PERK-eIF2α inhibition after MF-treatment attenuated ER stress in diabetic mice brain and kidney tissue. Moreover, renal injury associated with diabetes was attenuated by MF through decreased CHOP expression, downstream to ER stress. This finding was supplemented by inhibition of Bax, cyt-c, and ultimately the intrinsic apoptotic pathway. MiR-141 modulates expression of PP2A, a phosphoesterase that regulates phosphorylation of tau protein. In hyperglycaemic mice there was increased miR-141 expression with concomitant PP2A downregulation in the brain. Treatment with MF exerted epigenetic regulation by downregulating miR-141 expression, concomitantly increasing PP2A and subsequent downregulation of tau protein phosphorylation at Ser396. Additionally, MF inhibited proinflammatory NLRP3 inflammasome and related components by regulation of the PP2A/ NF-κB cascade. Neuroplasticity was increased by increased BDNF overexpression by MF in diabetic mice. Herein we show that MF exerts protective mechanistic effects in the brain and kidney over an acute experimental period. We highlight that anti-oxidant and Sirt1 modulation are at the forefront of renal cell defence to metabolic stress. Neuroinflammatory and epigenetic therapeutic targets of MF are revealed through miRNA regulatory mechanisms, integrating the mechanisms of diabetic neuronal and renal damage
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