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Non-therapeutic medical interventions on the bodies of children born with disorders of sex development (DSD)/intersex variations have been subject to increasing critical scrutiny. In response to recent criticism directed at the United Kingdom, and early moves to consider reform, we report on a freedom of information exercise that sought to evaluate whether National Health Service England is meeting international standards on optimal clinical management of DSD/intersex variations. The study explored what medical protocols are being followed to help inform potential reform, particularly with regard to non-therapeutic surgery. While the exercise revealed limited examples of promising practice, current protocols in the majority of Trusts appear unlikely to meet the complex needs of these children. We identify areas where significant improvement is needed, including data management, consistency in guideline use, composition of multidisciplinary teams and addressing disciplinary hierarchies within teams. These concerns sharpen criticisms of the lack of recognition of children’s rights in this context.

This chapter seeks to develop our model of ‘embodied integrity’ by addressing its capacity to protect profoundly disabled children from irreversible non-therapeutic bodily interventions and to frame a more appropriate ethico-legal response to their care. Specifically, we suggest that the decision-making process in the controversial case of Ashley X, and much subsequent academic commentary, was impoverished and served to reify understandings of severely disabled children as frozen in a state of perpetual childhood and reducible to their bodies. In contrast, the conception of embodied integrity that we flesh out in this chapter takes account of these children’s corporeality while also recognising that they are entangled in institutional and familial contexts. Responding to evidence of a growing demand for growth attenuation and shaping surgeries we argue that our embodied understanding of integrity promotes the immediate and future interests of children, including those who are profoundly disabled.

Female genital cutting (FGC) is generally understood as a gendered harm, abusive cultural practice and human rights violation. By contrast, male genital cutting (MGC) is held to be minimally invasive, an expression of religious identity and a legitimate parental choice. Yet scholars increasingly problematize this dichotomy, arguing that male and female genital cutting can occasion comparable levels of harm. In 2015 this academic critique received judicial endorsement, with Sir James Munby's acknowledgement that all genital cutting can cause 'significant harm'. This article investigates the harm occasioned by MGC. It is informed by a Freedom of Information (FoI) study which provides some empirical evidence of the nature and frequency of physical harm caused by MGC in U.K. hospitals. While acknowledging the challenges and limitations of FoI research, we outline important lessons that this preliminary study contains for medical ethics, law and policy. It provides some empirical evidence to support claims regarding the risks which accompany the procedure and the obligation of health professionals to disclose them, and reveals the paucity of measures in place to ensure that harms are recorded, disclosed and monitored.

Changes in gene expression are associated with switching to an autoprotected phenotype in response to environmental and physiological stress. Ubiquitous molecular chaperones from the heat shock protein (HSP) superfamily confer neuronal protection that can be blocked by antibodies. Recent research has focused on the interactions between the molecular sensors that affect the increased expression of neuroprotective HSPs above constitutive levels. An examination of the conditions under which the expression of heat shock protein 70 (Hsp70) was up regulated in a hypoxia and anoxia tolerant tropical species, the epaulette shark (Hemiscyllium ocellatum), revealed that up-regulation was dependent on exceeding a stimulus threshold for an oxidative stressor. While hypoxic-preconditioning confers neuroprotective changes, there was no increase in the level of Hsp70 indicating that its increased expression was not associated with achieving a neuroprotected state in response to hypoxia in the epaulette shark. Conversely, there was a significant increase in Hsp70 in response to anoxic-preconditioning, highlighting the presence of a stimulus threshold barrier and raising the possibility that, in this species, Hsp70 contributes to the neuroprotective response to extreme crises, such as oxidative stress. Interestingly, there was a synergistic effect of coincident stressors on Hsp70 expression, which was revealed when metabolic stress was superimposed upon oxidative stress. Brain energy charge was significantly lower when adenosine receptor blockade, provided by treatment with aminophylline, was present prior to the final anoxic episode, under these circumstances, the level of Hsp70 induced was significantly higher than in the pair-matched saline treated controls. An understanding of the molecular and metabolic basis for neuroprotective switches, which result in an up-regulation of neuroprotective Hsp70 expression in the brain, is needed so that intervention strategies can be devised to manage CNS pathologies and minimise damage caused by ischemia and trauma. In addition, the current findings indicate that measurements of HSP expression per se may provide a useful correlate of the level of neuroprotection achieved in the switch to an autoprotected phenotype.