The covid-19 learning crisis as a challenge and an opportunity for schools: An evidence review and conceptual synthesis of research-based tools for sustainable change

This paper advances our understanding of how schools can become change agents capable of transforming local practice to address the challenges arising from the Covid-19 pandemic. It presents a novel application of cultural-historical activity theory to reinterpret evidence on widespread learning loss and increasing educational inequities resulting from the pandemic, and to identify scalable transformative learning opportunities through reframing the crisis as a double stimulation. By reviewing evidence of the emerging educational landscape, we first develop a picture of the new ‘problem space’ upon which schools must act. We develop a problem space map to serve as the first stimulus to articulate local challenges. Integrating this problem space with research on professional change, we identify conceptual tools to capture learning gaps and implement pedagogic interventions at scale, in order to enhance schools’ agency in directly addressing the crisis. These tools can act as the second stimulus, enabling educators to address local challenges. We conclude by discussing the Covid-19 educational crisis as a unique stimulus for professional learning and outline the potential for durable shifts in educational thinking and practice beyond the pandemic. We argue that this unprecedented historic disruption can be harnessed as a transformative professional learning opportunity. In particular, we consider how research on professional change offers local, scalable interventions and tools that can support educators in preventing the new insights from ‘slipping away’ post-pandemic. Utilising the notions of boundaries and tool-mediated professional change, we examine the ways in which this disruption generates opportunities to envision alternative futures for equitable learning in school.Author 1: The epiSTEMe project [grant number RES-179-25-0003, PI Prof. K. Ruthven] The TEACh project [ES/M005445/1, PI Prof. P. Rose] ESRC Impact Acceleration Grant, University of Cambridge [PI Dr. R. Hofmann] Cambridge University Health Partners Commonwealth Education Trust (PI. Prof. S. Hennessy) Authors 2-8: (2) Faculty of Education, University of Cambridge, PhD scholarship (3) Economic and Social Research Council PhD scholarship [ES/P000738/1] (4) Agencia Nacional de Investigación y Desarrollo (ANID), Cambridge Trust, PhD scholarship (5) Economic and Social Research Council [ES/P000738/1] and MRC Epidemiology Unit PhD scholarship (6) Yayasan Khazanah, Cambridge Trust, PhD scholarship (7) Guy’s and St Thomas’ Charity, UK [TCF180902] PhD scholarship (8) The LEGO Foundatio

Bayesian approach to determining penetrance of pathogenic SDH variants.

BACKGROUND: Until recently, determining penetrance required large observational cohort studies. Data from the Exome Aggregate Consortium (ExAC) allows a Bayesian approach to calculate penetrance, in that population frequencies of pathogenic germline variants should be inversely proportional to their penetrance for disease. We tested this hypothesis using data from two cohorts for succinate dehydrogenase subunits A, B and C (SDHA-C) genetic variants associated with hereditary pheochromocytoma/paraganglioma (PC/PGL). METHODS: Two cohorts were 575 unrelated Australian subjects and 1240 unrelated UK subjects, respectively, with PC/PGL in whom genetic testing had been performed. Penetrance of pathogenic SDHA-C variants was calculated by comparing allelic frequencies in cases versus controls from ExAC (removing those variants contributed by The Cancer Genome Atlas). RESULTS: Pathogenic SDHA-C variants were identified in 106 subjects (18.4%) in cohort 1 and 317 subjects (25.6%) in cohort 2. Of 94 different pathogenic variants from both cohorts (seven in SDHA, 75 in SDHB and 12 in SDHC), 13 are reported in ExAC (two in SDHA, nine in SDHB and two in SDHC) accounting for 21% of subjects with SDHA-C variants. Combining data from both cohorts, estimated lifetime disease penetrance was 22.0% (95% CI 15.2% to 30.9%) for SDHB variants, 8.3% (95% CI 3.5% to 18.5%) for SDHC variants and 1.7% (95% CI 0.8% to 3.8%) for SDHA variants. CONCLUSION: Pathogenic variants in SDHB are more penetrant than those in SDHC and SDHA. Our findings have important implications for counselling and surveillance of subjects carrying these pathogenic variants

Bayesian approach to determining penetrance of pathogenic SDH variants

Background: Until recently, determining penetrance required large observational cohort studies. Data from the Exome Aggregate Consortium (ExAC) allows a Bayesian approach to calculate penetrance, in that population frequencies of pathogenic germline variants should be inversely proportional to their penetrance for disease. We tested this hypothesis using data from two cohorts for succinate dehydrogenase subunits A, B and C (SDHA–C) genetic variants associated with hereditary pheochromocytoma/paraganglioma (PC/PGL).Methods: Two cohorts were 575 unrelated Australian subjects and 1240 unrelated UK subjects, respectively, with PC/PGL in whom genetic testing had been performed. Penetrance of pathogenic SDHA–C variants was calculated by comparing allelic frequencies in cases versus controls from ExAC (removing those variants contributed by The Cancer Genome Atlas).Results: Pathogenic SDHA–C variants were identified in 106 subjects (18.4%) in cohort 1 and 317 subjects (25.6%) in cohort 2. Of 94 different pathogenic variants from both cohorts (seven in SDHA, 75 in SDHB and 12 in SDHC), 13 are reported in ExAC (two in SDHA, nine in SDHB and two in SDHC) accounting for 21% of subjects with SDHA–C variants. Combining data from both cohorts, estimated lifetime disease penetrance was 22.0% (95% CI 15.2% to 30.9%) for SDHB variants, 8.3% (95% CI 3.5% to 18.5%) for SDHC variants and 1.7% (95% CI 0.8% to 3.8%) for SDHA variants.Conclusion: Pathogenic variants in SDHB are more penetrant than those in SDHC and SDHA. Our findings have important implications for counselling and surveillance of subjects carrying these pathogenic variants