Governments worldwide are committing more funding for scientific research in the face of the ongoing pandemic and climate crises. However, the funding process must be restructured to remove the barriers arising from conscious and unconscious biases experienced by minoritized groups, including women, and particularly women of colour.
This article is a response to ‘Losing Sight of Women's Rights: The Unregulated Introduction of Gender Self-Identification as a Case Study of Policy Capture in Scotland’ by Kath Murray, Lucy Hunter Blackburn and Lisa MacKenzie, published in Scottish Affairs 28(3). Murray et al. sought to explore the legal status of women, particularly with regard to discrimination legislation, and concluded that the interests of trans women had begun to systematically erode the interests of non-trans women in Scotland. In this response, we aim to correct some of the erroneous statements made by Murray et al. about legal definitions of sex and gender, and about discrimination law. In critically engaging with Murray et al..’s argument we aim to build a much-needed clearer understanding of law and policy on sex and gender in Scotland, particularly as it relates to the application of the Equality Act 2010. We argue that, in that claiming that there has been policy capture in Scotland, Murray et al.. have neglected to contextualise ongoing debates about sex and gender in law against the backdrop of over two decades of clear legal and policy shifts across the UK. We call for researchers and others – in Scotland and elsewhere – to take care, particularly in interpreting and applying the law, especially as it applies to marginalised minority populations, so that we do not further obfuscate or mislead on important legal and social issues.
Delaying the decline in skeletal muscle function will be critical to better maintenance of an active lifestyle in old age. The skeletal muscle ryanodine receptor, the major intracellular membrane channel through which calcium ions pass to elicit muscle contraction, is central to calcium ion balance and is hypothesized to be a significant factor for age-related decline in muscle function. The nematode Caenorhabditis elegans is a key model system for the study of human aging, and strains were generated with modified C. elegans ryanodine receptors corresponding to human myopathic variants linked with malignant hyperthermia and related conditions. The altered response of these strains to pharmacological agents reflected results of human diagnostic tests for individuals with these pathogenic variants. Involvement of nerve cells in the C. elegans responses may relate to rare medical symptoms concerning the central nervous system that have been associated with ryanodine receptor variants. These single amino acid modifications in C. elegans also conferred a reduction in lifespan and an accelerated decline in muscle integrity with age, supporting the significance of ryanodine receptor function for human aging. KEYWORDSCaenorhabditis elegans aging ryanodine receptor malignant hyperthermia muscleTo improve the health of the world's aging population we need a better understanding of the aging processes, and age-related decline of skeletal muscle function is of key importance. Defective excitation-contraction coupling (Payne and Delbono 2004) and reduced capacity of Ca 2+ homeostasis (Weisleder et al. 2006;Zhao et al. 2008) have been suggested to contribute to the human muscle contractile dysfunction that occurs with age. The ryanodine receptor isoform 1 (RyR1) is the channel through which Ca 2+ is released from the skeletal muscle sarcoplasmic reticulum to elicit contraction. In the mouse there is an age-related increase in the ryanodine receptor "leakiness" (Anderson et al. 2011) and age-related decrease in both the number of RyR1s and their degree of coupling to regulatory proteins (Ryan et al. 2000). Single-point variants in the human RYR1 gene have been associated with the impairment of calcium handling in malignant hyperthermia (MH) (Robinson et al.
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