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Silence is traditionally understood as a power deficit; yet, it creates spaces in which power works unobtrusively. In this article, I report the findings of a qualitative study examining silence in school relationships. Based on nine conceptual discussions and 33 interviews with teachers and students in a secondary school in the UK, I assert that uses of silence in relationships between students and teachers revolve around two conceptions of power: a stronghold of respect and a refuge for dignity.

This article presents a conceptualisation of children’s participation rights based on Miranda Fricker’s epistemic injustice. Drawing on research conducted in a secondary school in the UK, the article applies Fricker’s framework, in particular her concepts of testimonial and hermeneutical injustice, to explain some of the reasons for adults’ disquiet around children’s participation rights. Fricker’s concept of testimonial injustice explains how prejudice about a social group results in deflated attributions of credibility to their views and opinions. Hermeneutical injustice occurs when a social group struggles to make sense of their social experiences because of insufficient interpretive resources in the collective social imagination. By applying these concepts to children, I highlight the role of silence in conceptualising children’s right to be heard and to freedom of expression. I present a conceptual framework of participation, informed by epistemic injustice and based on empirical research, in order to bolster children’s participation rights.

Silence infuses all aspects of our daily communications: what we say and what remains unspoken; those to whom we speak, and those we ignore; those we trust and respect, and those we do not. In the school environment, interactions between students and teachers lie at the heart of pedagogy. This relationship is also marked by its silences, and the concept of ‘student voice’ arose out of these silences on matters that affect students. However, the role of silence in such interactions has yet to receive comprehensive attention. This article presents the findings of a study on the uses and experiences of silence in the classroom with secondary school students aged 14–15 years and their teachers. Drawing on nine group discussions and 33 interviews with 20 teachers and 35 students, respectively, I argue that an oversight of silence in the student voice discipline has obscured the power dimensions of student voice, and the injustices that become visible when different forms of silence are illuminated. I argue that there are two core ideas which emerge from the findings: firstly, that silent practices manifest in two distinct paradigms of productivity and listening which function as expectations of teaching and learning; secondly, that the conflation of the listening paradigm with respect demonstrates the capacity of silent practices to reinforce the division between teaching and learning to become mediums of injustice. I conclude that this dichotomous relationship between pedagogy and student voice requires a pedagogy based on a critical examination of respect.

International audience; Purpose: Malignant hyperthermia (MH) is a pharmacogenetic disorder arising from uncontrolled muscle calcium release due to an abnormality in the sarcoplasmic reticulum (SR) calcium-release mechanism triggered by halogenated inhalational anesthetics. However, the molecular mechanisms involved are still incomplete.Methods: We aimed to identify transient receptor potential vanilloid 1 (TRPV1) variants within the entire coding sequence in patients who developed sensitivity to MH of unknown etiology. In vitro and in vivo functional studies were performed in heterologous expression system, trpv1−/− mice, and a murine model of human MH.Results: We identified TRPV1 variants in two patients and their heterologous expression in muscles of trpv1−/− mice strongly enhanced calcium release from SR upon halogenated anesthetic stimulation, suggesting they could be responsible for the MHphenotype. We confirmed the in vivo significance by using mice with a knock-in mutation (Y524S) in the type I ryanodine receptor (Ryr1), a mutation analogous to the Y522S mutation associated with MH in humans. We showed that the TRPV1 antagonist capsazepine slows the heat-induced hypermetabolic response in this model.Conclusion: We propose that TRPV1 contributes to MH and could represent an actionable therapeutic target for prevention of the pathology and also be responsible for MH sensitivity when mutated.Genetics in Medicine (2019) 21:441–450; https://doi.org/10.1038/s41436- 018-0066-9Keywords:TRP channel; TRPV1; Calcium; Hereditary disease; Malignant hyperthermia