Intersubject correlations in reward and mentalizing brain circuits separately predict persuasiveness of two types of ISIS video propaganda.

The Islamist group ISIS has been particularly successful at recruiting Westerners as terrorists. A hypothesized explanation is their simultaneous use of two types of propaganda: Heroic narratives, emphasizing individual glory, alongside Social narratives, which emphasize oppression against Islamic communities. In the current study, functional MRI was used to measure brain responses to short ISIS propaganda videos distributed online. Participants were shown 4 Heroic and 4 Social videos categorized as such by another independent group of subjects. Persuasiveness was measured using post-scan predictions of recruitment effectiveness. Inter-subject correlation (ISC) was used to measure commonality of brain activity time courses across individuals. ISCs in ventral striatum predicted rated persuasiveness for Heroic videos, while ISCs in mentalizing and default networks, especially in dmPFC, predicted rated persuasiveness for Social videos. This work builds on past findings that engagement of the reward circuit and of mentalizing brain regions predicts preferences and persuasion. The observed dissociation as a function of stimulus type is novel, as is the finding that intersubject synchrony in ventral striatum predicts rated persuasiveness. These exploratory results identify possible neural mechanisms by which political extremists successfully recruit prospective members and specifically support the hypothesized distinction between Heroic and Social narratives for ISIS propaganda.

EEG distinguishes heroic narratives in ISIS online video propaganda.

The Islamic State (ISIS) was uniquely effective among extremist groups in the Middle East at recruiting Westerners. A major way ISIS accomplished this was by adopting Hollywood-style narrative structures for their propaganda videos. In particular, ISIS utilized a heroic martyr narrative, which focuses on an individual's personal glory and empowerment, in addition to traditional social martyr narratives, which emphasize duty to kindred and religion. The current work presented adult participants (n = 238) video clips from ISIS propaganda which utilized either heroic or social martyr narratives and collected behavioral measures of appeal, narrative transportation, and psychological dispositions (egoism and empathy) associated with attraction to terrorism. Narrative transportation and the interaction between egoism and empathy predicted video recruitment appeal. A subset of adults (n = 80) underwent electroencephalographic (EEG) measurements while watching a subset of the video-clips. Complementary univariate and multivariate techniques characterized spectral power density differences when perceiving the different types of narratives. Heroic videos show increased beta power over frontal sites, and globally increased alpha. In contrast, social narratives showed greater frontal theta, an index of negative feedback and emotion regulation. The results provide strong evidence that ISIS heroic narratives are specifically processed, and appeal to psychological predispositions distinctly from other recruitment narratives.

A multilevel social neuroscience perspective on radicalization and terrorism.

Why are some people capable of sympathizing with and/or committing acts of political violence, such as attacks aimed at innocent targets? Attempts to construct terrorist profiles based on individual and situational factors, such as clinical, psychological, ethnic, and socio-demographic variables, have largely failed. Although individual and situational factors must be at work, it is clear that they alone cannot explain how certain individuals are radicalized. In this paper, we propose that a comprehensive understanding of radicalization and of how it may lead to political violence requires the integration of information across multiple levels of analysis and interdisciplinary perspectives from evolutionary theory, social, personality and cognitive psychology, political science and neuroscience. Characterization of the structural-functional relationships between neural mechanisms and the cognitive and affective psychological processes that underpin group dynamics, interpersonal processes, values and narratives, as well as micro-sociological processes may reveal latent drivers of radicalization and explain why some people turn to extreme political violence. These drivers may not be observable within a single individual level of scientific enquiry. The integrative, multilevel approach that characterizes social neuroscience has the potential to provide theoretical and empirical clarity regarding the antecedents of radicalization and support for extreme violence.

Description and Ecology of A New Cavernicolous, Arachnophilous Thread- legged Bug (Hemiptera: Reduviidae: Emesini) from Kartchner Caverns, Cochise County, Arizona.

A new cavernicolous, arachnophilous thread-legged bug (Phasmatocoris labyrinthicus sp. nov.; Reduviidae: Emesini) is described from Kartchner Caverns, a limestone cavern in Kartchner Caverns State Park near Benson, Arizona, USA. Cavernicolous emesines are recorded from caves in many parts of the world and are distributed across several genera, but are generally uncommon. P. labyrinthicus shows no obvious troglomorphy but ecological evidence suggests it is, at minimum, a cave-limited troglophile. The species seems to be low-humidity intolerant, due to its occurrence in a cave within a desert region, effectively confines the population to the cave, and the species may thus actually be troglobitic by default. Arachnophily in emesines is more common, including in Phasmatocoris Breddin, but has been previously documented in only a single cavernicolous species, Bagauda cavernicola Paiva, reported from India, Malaysia and Sri Lanka. However, unlike P. labyrinthicus, B. cavernicola is apparently not morphologically adapted for its arachnophilous association. P. labyrinthicus is the only known troglophilic emesine that is also a morphologically adapted and behaviorally functional arachnophile. The only other known cavernicolous Phasmatocoris (P. xavieri Gil-Santana, Alves, Barrett and Costa) is recorded from a sandstone cave in Brazil. P. xavieri exhibits morphological features indicative of a potentially arachnophilous habit, but its ecology has not been studied. Adults of P. labyrinthicus share characteristics with the species Phasmatocoris praecellens Bergroth, P. minor McAtee and Malloch, P. xavieri, P. spectrum Breddin, and P. rapax McAtee and Malloch. Phasmatocoris is primarily a Neotropical genus and the discovery of P. labyrinthicus represents a significant range extension for the genus, being the first Nearctic species identified, with its geographically nearest relative an undescribed species from Mazatlan, Mexico, over 1,000 km to the south.

Thrombin receptors in vascular smooth muscle cells - function and regulation by vasodilatory prostaglandins.

The vast majority of thrombin (>95%) is generated after clotting is completed, suggesting that thrombin formation serves purposes beyond coagulation, such as tissue repair after vessel injury. Two types of vascular thrombin binding sites exist: protease-activated receptors (PARs) and thrombomodulin (TM). Their expression is low in contractile vascular smooth muscle cells (SMC), the dominating subendothelial cell population, but becomes markedly up-regulated upon injury. In human SMC, PAR-1, PAR-3, and PAR-4 mediate thrombin-induced proliferation, migration and matrix biosynthesis as well as generation of inflammatory and growth-promoting mediators. Thrombin-responsive PARs are transcriptionally down-regulated in human vascular SMC by vasodilatory prostaglandins (PGI2/PGE2). For PAR-1 and PAR-3 this mechanism involves cAMP-dependent inactivation of the transcription factor NFAT. The human PAR-4 promoter does not possess NFAT recognition motifs suggesting involvement of other cAMP-regulated effectors. Unlike PARs, TM is induced in SMC exposed to vasodilatory prostaglandins. Enhanced thrombin binding to TM might ameliorate PAR-mediated SMC stimulation. Also expressed in human SMC is the endothelial protein C receptor (EPCR), which serves as an anchor to facilitate generation of activated protein C (aPC) by TM-bound thrombin. Whether prostaglandins affect aPC-generation is not known. In SMC, thrombin and aPC act synergistically via PAR-1 to modify tissue remodelling, in contrast to their antagonistic interaction in the coagulation pathways. Overall, this will contribute to plaque stability and wound healing. The processes outlined here are likely to become clinically relevant after up-regulation of vascular cyclooxygenase2, the rate limiting step in vascular PGE2/PGI2 biosynthesis, such as in advanced atherosclerosis and acute coronary syndromes.

Transcriptional inhibition of protease-activated receptor-1 expression by prostacyclin in human vascular smooth muscle cells.

OBJECTIVE: Stimulation of protease-activated receptor-1 (PAR-1) by thrombin causes vascular smooth muscle cell (SMC) mitogenesis and has been implicated in the vascular response to injury. Vascular injury is also associated with enhanced formation of PGE2 and PGI2 (prostacyclin). This study investigates whether PGI2 and PGE2 modify the expression of PAR-1 and the cellular response to thrombin in human SMC. METHODS AND RESULTS: The PGI2-mimetic iloprost (1 to 100 nmol/L) attenuated mRNA, total protein, and cell surface expression of PAR-1. This was associated with inhibition of thrombin-induced mitogenesis and migration. Comparable inhibition of PAR-1 expression was observed with the selective IP-receptor agonist cicaprost, the adenylyl cyclase activator forskolin, the phosphodiesterase inhibitor isobutylmethylxanthine and the PKA activator dibutyryl-cAMP. Similar effects of PGE2 required micromolar concentrations. The specific PKA-inhibitor Myr-PKI prevented PAR-1 downregulation by iloprost. The potential role of Rho family GTPases in PAR-1 regulation was also investigated. Iloprost decreased Rac1 mRNA and the Rac1 inhibitor NSC23766 mimicked the inhibitory effects of iloprost on PAR-1 protein--but not mRNA. The Rho kinase inhibitor Y27632 did not influence PAR-1 expression. CONCLUSIONS: IP-receptor agonists may limit the mitogenic actions of thrombin in human SMC by downregulating PAR-1 via modulation of cAMP-/PKA- and Rac1-dependent signaling pathways.

Human vascular smooth muscle cells express functionally active endothelial cell protein C receptor.

The endothelial cell protein C receptor (EPCR) is expressed on endothelial cells and regulates the protein C anticoagulant pathway via the thrombin-thrombomodulin complex. Independent of its anticoagulant activity, activated protein C (APC) can directly signal to endothelial cells and upregulate antiapoptotic and antiinflammatory genes. Here we show that vascular smooth muscle cells (SMCs) also express EPCR. EPCR protein on SMCs was detected by flow cytometry and Western blotting. EPCR mRNA was identified by quantitative RT-PCR. To examine the functionality of EPCR, intracellular signaling in APC-stimulated SMCs was analyzed by determination of intracellular free calcium transients using confocal laser scanning microscopy. Phosphorylation of extracellular signal-regulated kinases 1 and 2 (ERK-1/2) was detected by immunoblotting. APC-induced ERK-1/2 phosphorylation was inhibited by an anti-EPCR antibody and by a cleavage site blocking anti-PAR-1 antibody, indicating that binding of APC to EPCR and cleavage of protease-activated receptor-1 (PAR-1) were involved. APC elicited an increase in [(3)H]-thymidine incorporation. The mitogenic effect of APC was significantly enhanced in the presence of thrombin. EPCR expression was also detected in SMCs in the fibrous cap of human carotid artery plaques. The present data demonstrate functionally active EPCR in SMCs and suggest that EPCR-bound APC might modulate PAR-1-mediated responses of SMCs to vascular injury.

Regulation of thrombomodulin expression in human vascular smooth muscle cells by COX-2-derived prostaglandins.

There is concern that cyclooxygenase (COX)-2 inhibitors may promote atherothrombosis by inhibiting vascular formation of prostacyclin (PGI2) and an increased thrombotic risk of COX-2 inhibitors has been reported. It is widely accepted that the prothrombotic effects of COX-2 inhibitors can be explained by the removal of platelet-inhibitory PGI2. Using microarray chip technology, we have previously demonstrated that thrombomodulin (TM) mRNA is upregulated in cultured human coronary artery smooth muscle cells by the stable prostacyclin mimetic iloprost. This study is the first to demonstrate a stimulation of the expression of functionally active thrombomodulin in human smooth muscle cells by prostaglandins, endogenously formed via the COX-2 pathway. Because TM is an important inhibitor of blood coagulation, these findings provide a novel platelet-independent mechanism to explain the prothrombotic effects of COX-2 inhibitors. The full text of this article is available online at http://circres.ahajournals.org.