Maternal mortality in low- and middle-income countries continues to remain high. The Ugandan Ministry of Health’s Strategic Plan suggests that little, if any, progress has been made in Uganda in terms of improvements in Maternal Health [Millennium Development Goal (MDG) 5] and, more specifically, in reducing maternal mortality. Furthermore, the UNDP report on the MDGs describes Uganda’s progress as ‘stagnant’. The importance of understanding the impact of delays on maternal and neonatal outcomes in low resource settings has been established for some time. Indeed, the ‘3-delays’ model has exposed the need for holistic multi-disciplinary approaches focused on systems change as much as clinical input. The model exposes the contribution of social factors shaping individual agency and care-seeking behaviour. It also identifies complex access issues which, when combined with the lack of timely and adequate care at referral facilities, contributes to extensive and damaging delays. It would be hard to find a piece of research on this topic that does not reference human resource factors or ‘staff shortages’ as a key component of this ‘puzzle’. Having said that, it is rare indeed to see these human resource factors explored in any detail. In the absence of detailed critique (implicit) ‘common sense’ presumptions prevail: namely that the economic conditions at national level lead to inadequacies in the supply of suitably qualified health professionals exacerbated by losses to international emigration. Eight years’ experience of action-research interventions in Uganda combining a range of methods has lead us to a rather stark conclusion: the single most important factor contributing to delays and associated adverse outcomes for mothers and babies in Uganda is the failure of doctors to be present at work during contracted hours. Failure to acknowledge and respond to this sensitive problem will ultimately undermine all other interventions including professional voluntarism which relies on local ‘co-presence’ to be effective. Important steps forward could be achieved within the current resource framework, if the political will existed. International NGOs have exacerbated this problem encouraging forms of internal ‘brain drain’ particularly among doctors. Arguably the system as it is rewards doctors for non-compliance resulting in massive resource inefficiencies.

Gonadotropin-releasing hormone (GnRH) neurons regulate puberty onset and sexual reproduction by secreting GnRH to activate and maintain the hypothalamic-pituitary-gonadal axis. During embryonic development, GnRH neurons migrate along olfactory and vomeronasal axons through the nose into the brain, where they project to the median eminence to release GnRH. The secreted glycoprotein SEMA3A binds its receptors neuropilin (NRP) 1 or NRP2 to position these axons for correct GnRH neuron migration, with an additional role for the NRP co-receptor PLXNA1. Accordingly, mutations in SEMA3A, NRP1, NRP2 and PLXNA1 have been linked to defective GnRH neuron development in mice and inherited GnRH deficiency in humans. Here, we show that only the combined loss of PLXNA1 and PLXNA3 phenocopied the full spectrum of nasal axon and GnRH neuron defects of SEMA3A knockout mice. Together with Plxna1, the human orthologue of Plxna3 should therefore be investigated as a candidate gene for inherited GnRH deficiency.

Key content Myocardial infarction is a rare but life‐threatening medical condition during pregnancy. If unrecognised and not managed appropriately, the associated mortality and morbidity are high. A high index of suspicion, early diagnosis and treatment are essential. Multidisciplinary management involving the obstetric physician, cardiologist, anaesthetists and obstetrician is key to improving outcomes. Learning objectives To revise the physiological cardiovascular changes in pregnancy. To recognise the pathophysiology of myocardial infarction during pregnancy. Identify risks factors for myocardial infarction. Recognise symptoms and signs of myocardial infarction. To learn the general management principles of myocardial infarction in pregnancy. Ethical issues Should asymptomatic pregnant women with multiple risk factors be screened for coronary heart disease?

Alzheimer's disease (AD) is a multifactorial progressive neurodegenerative disease. Despite decades of research, no disease modifying therapy is available and a change of research objectives and/or development of novel research tools may be required. Much AD research has been based on experimental models using animals with a short lifespan that have been extensively genetically manipulated and do not represent the full spectrum of late-onset AD, which make up the majority of cases. The aetiology of AD is heterogeneous and involves multiple factors associated with the late-onset of the disease like disturbances in brain insulin, oxidative stress, neuroinflammation, metabolic syndrome, retinal degeneration and sleep disturbances which are all progressive abnormalities that could account for many molecular, biochemical and histopathological lesions found in brain from patients dying from AD. This review is based on the long-lived rodent Octodon degus (degu) which is a small diurnal rodent native to South America that can spontaneously develop cognitive decline with concomitant phospho-tau, β-amyloid pathology and neuroinflammation in brain. In addition, the degu can also develop several other conditions like type 2 diabetes, macular and retinal degeneration and atherosclerosis, conditions that are often associated with aging and are often comorbid with AD. Long-lived animals like the degu may provide a more realistic model to study late onset AD.