Human suffering arising out of disaster or conflict includes death and disability from noncommunicable diseases, including diabetes, which have largely been neglected in humanitarian crises. The objectives of this paper were to examine the evidence on the burden of diabetes, utilization of health services, and access to care for people with diabetes among populations affected by humanitarian crises in low-and middle-income countries and identify research gaps for future studies We performed a review of the literature on this topic published between 1992 and 2018. The results highlight that the burden of diabetes in humanitarian settings is not being captured, clinical guidance is lacking, and suggest diabetes is not being adequately addressed. Crisis-affected populations with diabetes face enormous constraints in accessing care, primarily due to high medical costs. Further research is needed to characterize the epidemiology of diabetes in humanitarian settings and develop simplified, cost-effective models of care to improve the delivery of diabetes care in the wake of global disasters.

Purpose: There are often high rates of mental disorders in low-and middle-income countries during humanitarian crises but the prevalence of somatic distress (SD) is underreported in existing health services research. We aim to examine patterns of SD among internally displaced persons (IDPs) in Ukraine, who were forcibly displaced due to the ongoing conflict in the country's eastern region. Methods: The study design was a cross-sectional survey of 2203 adult IDPs throughout Ukraine. The survey collected data on sociodemographic characteristics, traumatic life events (Life Events Checklist), utilisation of mental health care services, and self-reported outcomes of SD (Patient Health Questionnaire 15), anxiety (Generalised Anxiety Disorder 7), depression (Patient Health Questionnaire 9), and post-traumatic stress (PTSD Checklist). Descriptive and multivariate regression analyses were used. Results: Over half of respondents (n=1142, 55%) were identified as being at risk of SD (PHQ-15 score≥6) and the prevalence of moderate (n=377, 18%) and high severity SD risk (n=275, 13%) was substantial. There were significant associations (p<0.05) between SD and age, female gender, economic status, self-reported depression and post-traumatic stress, and multiple trauma exposures. Being at risk of SD was also significantly associated with increased functional disability. Use of mental health care services was low across this population and only high SD risk seemed to be a reliable predictor of care-seeking behaviour. Conclusions: There is a significant risk of SD among IDPs in Ukraine. Our results illustrate the need for targeted health services research and regional programs to ensure that mental health needs are appropriately met.

The placenta, a tissue that is metabolically active and rich in mitochondria, forms a critical interface between the mother and developing fetus. Oxidative stress within this tissue, derived from the dysregulation of reactive oxygen species (ROS), has been linked to a number of adverse fetal outcomes. While such outcomes have been associated with mitochondrial dysfunction, the causal role of mitochondrial dysfunction and mitochondrially generated ROS in altering the process of placentation remains unclear. In this study, mitochondrial complex I activity was attenuated using 10 nM rotenone to induce cellular oxidative stress by increasing mitochondrial ROS production in the BeWo choriocarcinoma cell line. Increased mitochondrial ROS resulted in a significant decrease in the transcripts which encode for proteins associated with fusion (GCM1, ERVW-1, and ERVFRD-1) resulting in a 5-fold decrease in the percentage of BeWo fusion. This outcome was associated with increased indicators of mitochondrial fragmentation, as determined by decreased expression of MFN2 and OPA1 along with an increase in a marker of mitochondrial fission (DRP1). Importantly, increased mitochondrial ROS also resulted in a 5.0-fold reduction of human placental lactogen (PL) and a 4.4-fold reduction of insulin like growth factor 2 (IGF2) transcripts; hormones which play an important role in regulating fetal growth. The pre-treatment of rotenone-exposed cells with 5 mM N-acetyl cysteine (NAC) resulted in the prevention of these ROS mediated changes in BeWo function and supports a central role for mitochondrial ROS signaling in the maintenance and function of the materno-fetal interface.

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