Short-term and long-term effects of United Nations peace operations

Earlier studies have shown that United Nations peace operations make a positive contribution to peacebuilding efforts after civil wars. But do these effects carry over to the period after the peacekeepers leave? And how do the effects of UN peace operations interact with other determinants of peacebuilding in the long run? The author addresses these questions using a revised version of the Doyle and Sambanis dataset and applying different estimation methods to estimate the short-term and long-term effects of UN peace missions. He finds that UN missions have robust, positive effects on peacebuilding in the short term. UN missions can help parties implement peace agreements but the UN cannot fight wars, and UN operations contribute more to the quality of the peace where peace is based on participation, than to the longevity of the peace, where peace is simply the absence of war. The effects of UN missions are also felt in the long run, but they dissipate over time. What is missing in UN peacebuilding is a strategy to foster the self-sustaining economic growth that could connect increased participation with sustainable peace.Post Conflict Reintegration,Peace&Peacekeeping,International Affairs,Post Conflict Reconstruction,Politics and Government

Error blindness and motivational significance: Shifts in networks centering on anterior insula co-vary with error awareness and pupil dilation

This investigation aims to further our understanding of the brain mechanisms underlying the awareness of one's erroneous actions. While all errors are registered as such in the rostral cingulate zone, errors enter awareness only when the anterior insula cortex is activated. Aware but not unaware errors elicit autonomic nervous system reactivity. Our aim is to investigate the hypothesis that activation in the insula during error awareness is related to autonomic arousal and to inter-regional interactions with other areas of the brain. To examine the role of the anterior insula in error awareness, we assessed its functional connectivity to other brain regions along with autonomic nervous system reactivity in young healthy participants who underwent simultaneous pupil-diameter and functional magnetic resonance imaging measurements while performing a complex and error-prone task. Error blindness was associated with failures to engage sufficient autonomic reactivity. During aware errors increased pupil-diameter along with increased task-related activation within, and increased connectivity between anterior insula and task-related networks suggested an increased capacity for action-control information transfer. Increased pupil-diameter during aware errors was furthermore associated with decreased activation of the default-mode network along with decreased insular connectivity with regions of the default mode system, possibly reflecting decreased task-irrelevant information processing. This shifting mechanism may be relevant to a better understanding of how the brain and the autonomic nervous system interact to enable efficient adaptive behavior during cognitive challenge

Conscious perception of errors and its relation to the anterior insula

To detect erroneous action outcomes is necessary for flexible adjustments and therefore a prerequisite of adaptive, goal-directed behavior. While performance monitoring has been studied intensively over two decades and a vast amount of knowledge on its functional neuroanatomy has been gathered, much less is known about conscious error perception, often referred to as error awareness. Here, we review and discuss the conditions under which error awareness occurs, its neural correlates and underlying functional neuroanatomy. We focus specifically on the anterior insula, which has been shown to be (a) reliably activated during performance monitoring and (b) modulated by error awareness. Anterior insular activity appears to be closely related to autonomic responses associated with consciously perceived errors, although the causality and directions of these relationships still needs to be unraveled. We discuss the role of the anterior insula in generating versus perceiving autonomic responses and as a key player in balancing effortful task-related and resting-state activity. We suggest that errors elicit reactions highly reminiscent of an orienting response and may thus induce the autonomic arousal needed to recruit the required mental and physical resources. We discuss the role of norepinephrine activity in eliciting sufficiently strong central and autonomic nervous responses enabling the necessary adaptation as well as conscious error perception

Acute D3 Antagonist GSK598809 Selectively Enhances Neural Response During Monetary Reward Anticipation in Drug and Alcohol Dependence.

Evidence suggests that disturbances in neurobiological mechanisms of reward and inhibitory control maintain addiction and provoke relapse during abstinence. Abnormalities within the dopamine system may contribute to these disturbances and pharmacologically targeting the D3 dopamine receptor (DRD3) is therefore of significant clinical interest. We used functional magnetic resonance imaging to investigate the acute effects of the DRD3 antagonist GSK598809 on anticipatory reward processing, using the monetary incentive delay task (MIDT), and response inhibition using the Go/No-Go task (GNGT). A double-blind, placebo-controlled, crossover design approach was used in abstinent alcohol dependent, abstinent poly-drug dependent and healthy control volunteers. For the MIDT, there was evidence of blunted ventral striatal response to reward in the poly-drug-dependent group under placebo. GSK598809 normalized ventral striatal reward response and enhanced response in the DRD3-rich regions of the ventral pallidum and substantia nigra. Exploratory investigations suggested that the effects of GSK598809 were mainly driven by those with primary dependence on alcohol but not on opiates. Taken together, these findings suggest that GSK598809 may remediate reward deficits in substance dependence. For the GNGT, enhanced response in the inferior frontal cortex of the poly-drug group was found. However, there were no effects of GSK598809 on the neural network underlying response inhibition nor were there any behavioral drug effects on response inhibition. GSK598809 modulated the neural network underlying reward anticipation but not response inhibition, suggesting that DRD3 antagonists may restore reward deficits in addiction.The research was carried out at the NIHR/Wellcome Trust Imperial Clinical Research Facility, the NIHR/Wellcome Trust Cambridge Research Facility and Clinical Trials Unit at Salford Royal NHS Foundation Trust, and is supported by the North West London, Eastern and Greater Manchester NIHR Clinical Research Networks

Error awareness and salience processing in the oddball task: shared neural mechanisms

A body of work suggests similarities in the way we become aware of an error and process motivationally salient events. Yet, evidence for a shared neural mechanism has not been provided. A within subject investigation of the brain regions involved in error awareness and salience processing has not been reported. While the neural response to motivationally salient events is classically studied during target detection after longer target-to-target intervals in an oddball task and engages a widespread insula-thalamo-cortical brain network, error awareness has recently been linked to, most prominently, anterior insula cortex. Here we explore whether the anterior insula activation for error awareness is related to salience processing, by testing for activation overlap in subjects undergoing two different task settings. Using a within subjects design, we show activation overlap in six major brain areas during aware errors in an antisaccade task and during target detection after longer target-to-target intervals in an oddball task: anterior insula, anterior cingulate, supplementary motor area, thalamus, brainstem, and parietal lobe. Within subject analyses shows that the insula is engaged in both error awareness and the processing of salience, and that the anterior insula is more involved in both processes than the posterior insula. The results of a fine-grained spatial pattern overlap analysis between active clusters in the same subjects indicates that even if the anterior insula is activated for both error awareness and salience processing, the two types of processes might tend to activate non-identical neural ensembles on a finer-grained spatial level. Together, these outcomes suggest a similar functional phenomenon in the two different task settings. Error awareness and salience processing share a functional anatomy, with a tendency toward subregional dorsal and ventral specialization within the anterior insula

The complex interactions of Chs5p, the ChAPs and the cargo Chs3p

The exomer complex is a putative vesicle coat required for the direct transport of a subset of cargoes from the trans-Golgi network (TGN) to the plasma membrane. Exomer comprises Chs5p as well as the ChAPs family of proteins (Chs6p, Bud7p, Bch1p and Bch2p), which are thought to act as cargo receptors, and in particular Chs6p is required for the transport of the chitin synthase Chs3p to the bud neck. However, how the ChAPs associate with Chs5p and recognize cargo is not well understood. Using domain-switch chimeras of Chs6p and Bch2p we show that four tetratricopeptide repeats (TPRs) are involved in interaction with Chs5p. Since these roles are conserved between the ChAPs, the TPRs are interchangeable between different ChAP proteins. In contrast, the N-terminal and the central parts of the ChAPs contribute to cargo specificity. While the entire N-terminal domain of Chs6p is required for Chs3p export at all cell cycle stages, the central part seems to predominantly favor Chs3p export in small-budded cells. The cargo Chs3p probably also uses a complex motif for the interaction with Chs6, as the C-terminus of Chs3p interacts with Chs6p and is necessary, but not sufficient, for TGN export

Vps10p Cycles between the TGN and the Late Endosome via the Plasma Membrane in Clathrin Mutants

Clathrin-coated vesicles mediate the transport of the soluble vacuolar protein CPY from the TGN to the endosomal/prevacuolar compartment. Surprisingly, CPY sorting is not affected in clathrin deletion mutant cells. Here, we have investigated the clathrin-independent pathway that allows CPY transport to the vacuole. We find that CPY transport is mediated by the endosome and requires normal trafficking of its sorting receptor, Vps10p, the steady state distribution of which is not altered in chc1 cells. In contrast, Vps10p accumulates at the cell surface in a chc1/end3 double mutant, suggesting that Vps10p is rerouted to the cell surface in the absence of clathrin. We used a chimeric protein containing the first 50 amino acids of CPY fused to a green fluorescent protein (CPY-GFP) to mimic CPY transport in chc1. In the absence of clathrin, CPY-GFP resides in the lumen of the vacuole as in wild-type cells. However, in chc1/sec6 double mutants, CPY-GFP is present in internal structures, possibly endosomal membranes, that do not colocalize with the vacuole. We propose that Vps10p must be transported to and retrieved from the plasma membrane to mediate CPY sorting to the vacuole in the absence of clathrin-coated vesicles. In this circumstance, precursor CPY may be captured by retrieved Vps10p in an early or late endosome, rather than as it normally is in the trans-Golgi, and delivered to the vacuole by the normal VPS gene-dependent process. Once relieved of cargo protein, Vps10p would be recycled to the trans-Golgi and then to the cell surface for further rounds of sorting