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A new generation of satellites for Earth observation and telecommunications are being designed and built with off the shelf components. This is driving down costs and permitting the launch of large satellite swarms with unprecedented spatial and temporal coverage. On-orbit maneuvers are commonly performed using ion thrusters. Mercury is one of the cheapest and easiest to store propellants for electric propulsion. While some mercury released in Low Earth Orbit may escape Earth’s gravitational field, mercury emissions originating from many common orbital maneuvers will return to Earth. The environmental and human health implications of such releases have not been evaluated. Using an atmospheric chemical transport model, we simulate global deposition of mercury released from satellite propulsion systems. We estimate that 75% of the mercury falling back to Earth will be deposited in the world’s oceans, with potentially negative implications for commercial fish and other marine life. Understanding the scale of this novel mercury source in a post-Minamata Convention world is necessary to limit ecosystem exposure to mercury contamination.

A new generation of satellites for Earth observation and telecommunications are being designed and built with off the shelf components. This is driving down costs and permitting the launch of large satellite swarms with unprecedented spatial and temporal coverage. On-orbit maneuvers are commonly performed using ion thrusters. Mercury is one of the cheapest and easiest to store propellants for electric propulsion. While some mercury released in Low Earth Orbit may escape Earth's gravitational field, mercury emissions originating from many common orbital maneuvers will return to Earth. The environmental and human health implications of such releases have not been evaluated. Using an atmospheric chemical transport model, we simulate global deposition of mercury released from satellite propulsion systems. We estimate that 75% of the mercury falling back to Earth will be deposited in the world's oceans, with potentially negative implications for commercial fish and other marine life. Understanding the scale of this novel mercury source in a post-Minamata Convention world is necessary to limit ecosystem exposure to mercury contamination.

Behavioral studies indicate that adverse childhood experiences (ACE) are associated with altered empathic responding, but the neural mechanisms underlying this relationship remain unclear. Given the significance of empathy in contexts marred by historical conflict and systemic inequality, work on these mechanisms is particularly important in such contexts. The current study extends previous work by (1) examining associations of different dimensions of ACE with volumetric change in empathy-related circuitry, (2) distinguishing between trait and state empathy, and (3) including perceived discrimination as an additional psychosocial stressor. Thirty-nine healthy South African adults from the general population ( M age  = 40.6 years) underwent 3 T MRI. FreeSurfer v6.0 was used to extract predefined volumes subserving empathy. Results showed that childhood abuse and perceived discrimination were associated with reduced state empathic concern, whereas childhood neglect was associated with reduced trait cognitive empathy. Childhood abuse was furthermore associated with volumetric increases in frontolimbic (hippocampus, anterior cingulate cortex (ACC)) and neocortical (superior frontal and temporal) regions subserving affective and cognitive empathy, and uniquely mediated the relationship between ACC volume and perceived discrimination. The association of ACE with altered empathic responding may thus be underpinned by specific circuitry reflective of adversity type, with childhood abuse contributing to heightened responsivity to socioemotional cues.

There is extensive evidence of an association between early adversity and enduring neural changes that impact socioemotional processing throughout life. Yet little is known about the effects of on-going social discrimination on socioemotional functioning. Here we examined how cumulative experiences of social discrimination impact brain response during empathic responding—a crucial issue in South Africa, given its historical apartheid context and continuing legacies. White and Black South Africans completed measures of social adversity (early adversity and social discrimination), and underwent fMRI while viewing video clips depicting victims and perpetrators of apartheid crimes. Increased neural response was detected in brain regions associated with cognitive rather than affective empathy, and greater social adversity was associated with reduced reported compassion across participants. Notably, social discrimination (due to income level, weight, gender) in White participants was associated with increased amygdala reactivity, whereas social discrimination (due to race) in Black participants mediated the negative associations of temporoparietal junction and inferior frontal gyrus activation with compassion during emotionally provocative conditions. These findings suggest that (i) social discrimination has comparable associations at the neural level as other psychosocial stressors, and that (ii) the mechanisms underlying empathic responding vary as a function of the type of social discrimination experienced.

Moral emotions elicited in response to others’ suffering are mediated by empathy and affect how we respond to their pain. South Africa provides a unique opportunity to study group processes given its racially divided past. The present study seeks insights into aspects of the moral brain by investigating behavioral and functional MRI responses of White and Black South Africans who lived through apartheid to in- and out-group physical and social pain. Whereas the physical pain task featured faces expressing dynamic suffering, the social pain task featured victims of apartheid violence from the South African Truth and Reconciliation Commission to elicit heartfelt emotion. Black participants’ behavioral responses were suggestive of in-group favoritism, whereas White participants’ responses were apparently egalitarian. However, all participants showed significant in-group biases in activation in the amygdala (physical pain), as well as areas involved in mental state representation, including the precuneus, temporoparietal junction (TPJ) and frontal pole (physical and social pain). Additionally, Black participants reacted with heightened moral indignation to own-race suffering, whereas White participants reacted with heightened shame to Black suffering, which was associated with blunted neural empathic responding. These findings provide ecologically valid insights into some behavioral and brain processes involved in complex moral situations.

H3Africa is developing capacity for health-related genomics research in Africa Our understanding of genome biology, genomics, and disease, and even human history, has advanced tremendously with the completion of the Human Genome Project. Technological advances coupled with significant cost reductions in genomic research have yielded novel insights into disease etiology, diagnosis, and therapy for some of the world's most intractable and devastating diseases—including malaria, HIV/AIDS, tuberculosis, cancer, and diabetes. Yet, despite the burden of infectious diseases and, more recently, noncommunicable diseases (NCDs) in Africa, Africans have only participated minimally in genomics research. Of the thousands of genome-wide association studies (GWASs) that have been conducted globally, only seven (for HIV susceptibility, malaria, tuberculosis, and podoconiosis) have been conducted exclusively on African participants; four others (for prostate cancer, obsessive compulsive disorder, and anthropometry) included some African participants ( www.genome.gov/gwastudies/ ). As discussed in 2011 ( www.h3africa.org ), if the dearth of genomics research involving Africans persists, the potential health and economic benefits emanating from genomic science may elude an entire continent.

Background & Aims. Intestinal barrier alterations are associated with fatty liver (FL) and metabolic syndrome (MetS), but microRNA (miR) signaling pathways in MetS-FL pathogenesis remain unclear. This study investigates an epithelial-focused miR network in colorectal cell models based on the previously reported MetS-FL miR trio of hsa-miR-142-3p, hsa-miR-18b, and hsa-miR-890. Methods. Each miR mimic construct of MetS-FL miR trio was transfected into human colorectal cells, CRL-1790 or Caco-2. Global miRNome changes posttransfection were profiled (nCounter® Human v3 miRNA, NanoString Technologies). Changes in barrier (transepithelial electrical resistance, TEER) and epithelial cell junction structure (Occludin and Zona Occludens-1/ZO-1 immunofluorescence staining-confocal microscopy) were examined pre- and posttransfection in Caco-2 cell monolayers. A signaling network was constructed from the MetS-FL miR trio, MetS-FL miR-induced colorectal miRNome changes, ZO-1, and Occludin. Results. Transfection of CRL-1790 cells with each MetS-FL miR mimic led to global changes in the cellular miRNome profile, with 288 miRs being altered in expression by more than twofold. Eleven miRs with known cytoskeletal and metabolic roles were commonly altered in expression by all three miR mimics. Transfection of Caco-2 cell monolayers with each MetS-FL miR mimic induced barrier-associated TEER variations and led to structural modifications of ZO-1 and Occludin within epithelial cell junctions. Pathway analysis incorporating the MetS-FL miR trio, eleven common target miRs, ZO-1, and Occludin revealed a signaling network centered on TNF and AKT2, which highlights injury, inflammation, and hyperplasia. Conclusions. Colon-specific changes in epithelial barriers, cell junction structure, and a miRNome signaling network are described from functional studies of a MetS-FL miR trio signature.