05). When compared with the most common haplotypes of each gene, haplotype GAAG in CYP17A1 was associated with a 1.44-fold increased risk of progesterone elevation (95% confidence interval [CI] 1.22-1.69, PFDR less then 0.001), while haplotypes of the following genes showed a decreased risk of progesterone elevation haplotype CC in FSHR and LHCGR (0.66-fold, PFDR = 0.020, and 0.64-fold, PFDR less then 0.001, respectively), CA in ESR1 (0.90-fold, PFDR less then 0.001), TCTGG in ESR2 (0.92-fold, PFDR = 0.007) and GAACC in HSD3B1 (0.42-fold, PFDR less then 0.001). CONCLUSIONS Polymorphism in genes involved in enzymes or hormone receptors in the progesterone synthesis pathway may have a role in modifying risk of serum progesterone elevation. BACKGROUND We developed a culturally-adapted program (WE Stop the Bleed) to increase bleeding control knowledge and self-efficacy among Somali individuals, and to build trust between Somali individuals and first responders. METHODS WE Stop the Bleed was piloted in the Seattle Somali community with first responders as skills coaches. The program included 1) adapted ACS Stop the Bleed program; 2) cultural exchange. We evaluated knowledge, self-efficacy, and trust between Somali participants and first responders using a pre/post survey. RESULTS Attendance exceeded a priori goals (27 community participants, 13 first responders). 96% of participants would recommend the training. Knowledge and self-efficacy improved pre/post (62%-72%, 65%-93% respectively). First responders indicated increased comfort with Somali individuals, and participants reported positive changes in perceptions of first responders.  https://www.selleckchem.com/products/hg106.html  CONCLUSIONS WE Stop the Bleed is a feasible and acceptable program to increase bleeding control knowledge and self-efficacy among participants and build trust between participants and first responders. Experiencing poverty in childhood has been associated with increased risk for physical and mental health difficulties later in life. An emerging body of evidence suggests that brain development may be one mediator of this relation. In this chapter, we discuss evidence for an association between childhood poverty and brain structure/function. First, we examine the association from a lifespan perspective discussing studies at multiple developmental stages from the prenatal period to late adulthood. Second, we examine existing studies that link childhood poverty, brain development, and physical and mental health outcomes. Third, we discuss studies linking childhood poverty and environmental risks and protective factors. Lastly, we discuss suggestions for future studies including advances in network neuroscience, population neuroscience, using multiple imaging modalities, and the use of longitudinal neuroimaging studies. Overall, associations between childhood poverty, brain development, and development over the life course may help to both better understand and eventually reveal salient intervention strategies to mitigate social disparities in health. © 2020 Elsevier Inc. All rights reserved.Adverse experiences during childhood can have long-lasting impacts on physical and mental health. At the heart of most theories of how these effects are transduced into health impacts is the activity of stress-mediating systems, most notably the hypothalamic-pituitary-adrenocortical (HPA) axis. Here we review the anatomy and physiology of the axis, models of stress and development, the development of the axis prenatally through adolescence, the role of experience and sensitive periods in shaping its regulation, the social regulation of the axis at different points in development, and finally conclude with suggestions for future research. We conclude that it is clear that early adversity sculpts the stress system, but we do not understand which dimensions have the most impact and at what points in early development. It is equally clear that secure attachment relationships buffer the developing stress system; however, the mechanisms of social buffering and how these may change with development are not yet clear. Another critical issue that is not understood is when and for whom adversity will result in hypo- vs hyperactivity of stress-mediating systems. These and other issues are important for advancing our understanding of how early adversity "gets under the skin" and shapes human physical and mental health. © 2020 Elsevier Inc. All rights reserved.Stress leads to ill-health and disease, and with today's fast-pace western society, engaging in strategies to relieve stress is crucial for good health across the life-course. Activities such as focusing on positive characteristics, art/music therapies, mindfulness, yoga and engaging with nature and/or physical activity have been shown to reduce stress and enhance well-being. It is thought that patterns of cortisol secretion, which are regulated by the brain, are a key mediator of stress-disease and well-being-health links. Measurement of cortisol in saliva is a non-invasive and ecologically valid tool for detecting early changes in brain health, as well as evaluating the effectiveness of strategies in relieving stress and improving brain health as well as monitoring stress-related brain changes. This chapter will review the evidence that engaging in stress-relieving strategies promotes regulation and/or restoration of patterns of cortisol secretion. If such strategies are found to be effective in healthy populations, they could potentially inform ways of promoting brain health and the prevention or delay of clinical disorders involving disorders in the brain (e.g., Parkinson's disease) and symptoms experienced with such disorders. To inform this field of research, recommendations are provided for the use of salivary cortisol as a marker of early monitoring of brain health and effectiveness of stress-alleviating interventions. © 2020 Elsevier Inc. All rights reserved.There is evidence that stress-induced disruption of the circadian rhythm of cortisol secretion, has negative consequences for brain health. The cortisol awakening response (CAR) is the most prominent and dynamic aspect of this rhythm. It has complex regulatory mechanisms making it distinct from the rest of the cortisol circadian rhythm, and is frequently investigated as a biomarker of stress and potential intermediary between stress and impaired brain function. Despite this, the precise function of the CAR within the healthy cortisol circadian rhythm remains poorly understood. Cortisol is a powerful hormone known to influence cognition in multiple and complex ways. Studies of the CAR and cognitive function have used varied methodological approaches which have produced similarly varied findings. The present review considers the accumulating evidence linking stress, attenuation of the CAR and reduced cognitive function, and seeks to contextualize the many findings to study populations, cognitive measures, and CAR methodologies employed.