Climate change and infectious disease: time for a new normal?

At present, there is a clarion call for action on climate change across the global health landscape. At the recent WHO-sponsored conference on health and climate (held in Geneva, Switzerland, on Aug 27–29, 2014) and the UN Climate Summit (New York, USA, on Sept 23, 2014), participants were encouraged to act decisively to change the current trajectory of climate disruption. Health inequalities, including those related to infectious diseases, have now been pushed to centre stage. This approach represents a step-change in thinking. But as we are urged toward collective action, is it time to rethink our approach to research, especially in relation to climate change and infectious disease?

Big data: a normal accident waiting to happen?

Widespread commercial use of the internet has significantly increased the volume and scope of data being collected by organisations. ‘Big data’ has emerged as a term to encapsulate both the technical and commercial aspects of this growing data collection activity. To date, much of the discussion of big data has centred upon its transformational potential for innovation and efficiency, yet there has been less reflection on its wider implications beyond commercial value creation. This paper builds upon normal accident theory (NAT) to analyse the broader ethical implications of big data. It argues that the strategies behind big data require organisational systems that leave them vulnerable to normal accidents, that is to say some form of accident or disaster that is both unanticipated and inevitable. Whilst NAT has previously focused on the consequences of physical accidents, this paper suggests a new form of system accident that we label data accidents. These have distinct, less tangible and more complex characteristics and raise significant questions over the role of individual privacy in a ‘data society’. The paper concludes by considering the ways in which the risks of such data accidents might be managed or mitigated.

Dystrophin immunoreactivity in normal and Duchenne human fetal neurons in culture.

Dystrophin, the protein product defective in Duchenne muscular dystrophy (DMD), is present in all types of muscle and in the brain. The function of the protein is unknown and its role in the brain is unclear, although 30% of DMD patients show nonprogressive mental retardation. We have therefore studied the localisation of dystrophin in cultures of normal and DMD human fetal neurons using antibodies raised to different regions of the protein. Dystrophin immunoreactivity was demonstrated in the soma and axon hillock of normal neurons and appeared to be associated with the inner part of the cell membrane, although some intracellular staining was also observed. Positive dystrophin staining was present only in cells with fully developed neuronal features, although not all the neurons were positive. Glial cells were always negative for the antigen. Immunostaining with antibodies to the brain spectrins indicate that the dystrophin antibodies did not crossreact with these proteins. The possibility of cross-reactivity with other proteins is discussed. Studies of cells cultured from a DMD fetus also showed specific dystrophin immunostaining in neurons, although the muscle was generally negative for dystrophin. However, the localisation of dystrophin immunostaining and that of the brain spectrins and neurofilaments appeared abnormal, as did the overall morphology of the cells. This suggests that dystrophin may play a role during brain development and dystrophin deficiency results in abnormal neuronal features. This would be consistent with the nonprogressive nature of the mental retardation observed in DMD patients.

Dystrophin-related protein, utrophin, in normal and dystrophic human fetal skeletal muscle.

Dystrophin is the product of the Duchenne muscular dystrophy (DMD) gene. Dystrophin-related protein (utrophin), an autosomal homologue of dystrophin, was studied in skeletal muscle from normal fetuses aged 9-26 weeks and one stillbirth of 41 weeks' gestation, and compared with low- and high-risk DMD fetuses aged 9-20 weeks. Utrophin was present at the sarcolemma from before 9 weeks' gestation, although there was variability in intensity both within and between myotubes. Sarcolemmal immunolabelling became more uniform, and levels of utrophin increased to a maximum at approximately 17-18 weeks. Levels then declined, until by 26 weeks sarcolemmal labelling was negligible and levels were similar to adult control muscle. By 41 weeks there was virtually no sarcolemmal labelling, although immunolabelling of capillaries was bright. Similar results were obtained with normal and DMD fetal muscle. Utrophin is therefore expressed in the presence and absence of dystrophin and down-regulated before birth in normal fetal muscle fibres. Samples were not available to determine whether or when, utrophin levels decline in DMD fetal muscle. On Western blots, utrophin was shown to have a smaller relative molecular mass than adult dystrophin, but similar to the fetal isoform. Blood vessels were brightly immunolabelled at all ages, although utrophin immunolabelling of peripheral nerves increased with gestational age.