Purpose

South Sudan is embroiled in a conflict that erupted in December 2013. This study examines what people in South Sudan think is necessary to achieve reconciliation and how trauma exposure and PTSD are associated with those beliefs.

Methods

1525 participants (51.0% female) were selected using random and purposive sampling in six states and Abyei. Participants reported on traumatic events, PTSD symptoms, and attitudes towards reconciliation mechanisms.

Results

Results indicated that 40.7% met symptom criteria for probable PTSD. Most participants thought reconciliation was not possible without prosecuting perpetrators or compensating victims and did not support amnesty. Participants with probable PTSD were more likely to endorse confessions (OR 2.42 [1.75, 3.35]), apologies (OR 2.04 [1.46, 2.83]), and amnesty (OR 1.58 [1.21, 2.08]), and to report that compensation (OR 2.32 [1.80, 3.00]) and prosecution (OR 1.47 [1.15, 1.89]) were not necessary for reconciliation. The more traumatic events people experienced, the more they endorsed criminal punishment for perpetrators (OR 1.07 [1.04, 1.10]) and the less they endorsed confessions (OR 0.97 [0.95, 0.99]).

Conclusions

People with PTSD may prioritize ending violence via opportunities for reconciliation, while those with more trauma exposure may support more punitive mechanisms. Policy makers should take mental health treatment and trauma into account when designing conflict mitigation, peace building, and justice mechanisms.

Mineral-respiring bacteria use a process called extracellular electron transfer to route their respiratory electron transport chain to insoluble electron acceptors on the exterior of the cell. We recently characterized a flavin-based extracellular electron transfer system that is present in the foodborne pathogen Listeria monocytogenes, as well as many other Gram-positive bacteria, and which highlights a more generalized role for extracellular electron transfer in microbial metabolism. Here we identify a family of putative extracellular reductases that possess a conserved posttranslational flavinylation modification. Phylogenetic analyses suggest that divergent flavinylated extracellular reductase subfamilies possess distinct and often unidentified substrate specificities. We show that flavinylation of a member of the fumarate reductase subfamily allows this enzyme to receive electrons from the extracellular electron transfer system and support L. monocytogenes growth. We demonstrate that this represents a generalizable mechanism by finding that a L. monocytogenes strain engineered to express a flavinylated extracellular urocanate reductase uses urocanate by a related mechanism and to a similar effect. These studies thus identify an enzyme family that exploits a modular flavin-based electron transfer strategy to reduce distinct extracellular substrates and support a multifunctional view of the role of extracellular electron transfer activities in microbial physiology.

Rationale

It is unknown whether every ventricular myocyte expresses all 5 of the cardiac adrenergic receptors (ARs), β1, β2, β3, α1A, and α1B. The β1 and β2 are thought to be the dominant myocyte ARs.

Objective

Quantify the 5 cardiac ARs in individual ventricular myocytes.

Methods and results

We studied ventricular myocytes from wild-type mice, mice with α1A and α1B knockin reporters, and β1 and β2 knockout mice. Using individual isolated cells, we measured knockin reporters, mRNAs, signaling (phosphorylation of extracellular signal-regulated kinase and phospholamban), and contraction. We found that the β1 and α1B were present in all myocytes. The α1A was present in 60%, with high levels in 20%. The β2 and β3 were detected in only ≈5% of myocytes, mostly in different cells. In intact heart, 30% of total β-ARs were β2 and 20% were β3, both mainly in nonmyocytes.

Conclusion

The dominant ventricular myocyte ARs present in all cells are the β1 and α1B. The β2 and β3 are mostly absent in myocytes but are abundant in nonmyocytes. The α1A is in just over half of cells, but only 20% have high levels. Four distinct myocyte AR phenotypes are defined: 30% of cells with β1 and α1B only; 60% that also have the α1A; and 5% each that also have the β2 or β3. The results raise cautions in experimental design, such as receptor overexpression in myocytes that do not express the AR normally. The data suggest new paradigms in cardiac adrenergic signaling mechanisms.

Cellular respiration is essential for multiple bacterial pathogens and a validated antibiotic target. In addition to driving oxidative phosphorylation, bacterial respiration has a variety of ancillary functions that obscure its contribution to pathogenesis. We find here that the intracellular pathogen Listeria monocytogenes encodes two respiratory pathways which are partially functionally redundant and indispensable for pathogenesis. Loss of respiration decreased NAD⁺ regeneration, but this could be specifically reversed by heterologous expression of a water-forming NADH oxidase (NOX). NOX expression fully rescued intracellular growth defects and increased L. monocytogenes loads >1000-fold in a mouse infection model. Consistent with NAD⁺ regeneration maintaining L. monocytogenes viability and enabling immune evasion, a respiration-deficient strain exhibited elevated bacteriolysis within the host cytosol and NOX expression rescued this phenotype. These studies show that NAD⁺ regeneration represents a major role of L. monocytogenes respiration and highlight the nuanced relationship between bacterial metabolism, physiology, and pathogenesis.