The Ascent of Man: Theoretical and Empirical Evidence for Blatant Dehumanization

Dehumanization is a central concept in the study of intergroup relations. Yet although theoretical and methodological advances in subtle, “everyday” dehumanization have progressed rapidly, blatant dehumanization remains understudied. The present research attempts to refocus theoretical and empirical attention on blatant dehumanization, examining when and why it provides explanatory power beyond subtle dehumanization. To accomplish this, we introduce and validate a blatant measure of dehumanization based on the popular depiction of evolutionary progress in the “Ascent of Man.” We compare blatant dehumanization to established conceptualizations of subtle and implicit dehumanization, including infrahumanization, perceptions of human nature and human uniqueness, and implicit associations between ingroup–outgroup and human–animal concepts. Across 7 studies conducted in 3 countries, we demonstrate that blatant dehumanization is (a) more strongly associated with individual differences in support for hierarchy than subtle or implicit dehumanization, (b) uniquely predictive of numerous consequential attitudes and behaviors toward multiple outgroup targets, (c) predictive above prejudice, and (d) reliable over time. Finally, we show that blatant—but not subtle—dehumanization spikes immediately after incidents of real intergroup violence and strongly predicts support for aggressive actions like torture and retaliatory violence (after the Boston Marathon bombings and Woolwich attacks in England). This research extends theory on the role of dehumanization in intergroup relations and intergroup conflict and provides an intuitive, validated empirical tool to reliably measure blatant dehumanization

Interaction entre l’effet différentiel du sexe et l’effet modérateur du soutien social perçu sur la santé mentale des travailleurs en Protection de la Jeunesse victimes de violence au travail

Contexte. La violence au travail (VAT) fait partie de la réalité de nombreux travailleurs en Protection de la Jeunesse (PJ) en raison de la clientèle desservie. L’exposition à la VAT est associée à plusieurs conséquences psychologiques, notamment le trouble de stress post-traumatique (TSPT), l’anxiété et la dépression. Parmi les facteurs pouvant influencer le développement des différents symptômes de santé mentale, le soutien social (SS) ressort comme l’un des plus forts prédicteurs du TSPT. Les études plus récentes indiquent qu’au-delà de la quantité de SS, la qualité perçue de celui-ci peut influencer lien entre VAT et conséquences psychologiques. Finalement, certaines études notent des variations entre ces associations en fonction du sexe des participants. Objectif. L’objectif principal est de suivre l’évolution des symptômes de TSPT, d’anxiété et de dépression selon la qualité du SS perçu. Un deuxième objectif consiste à vérifier si les effets du SS varient en fonction du sexe des participants. Méthode. Un échantillon de 150 travailleurs en PJ ont rempli une série de questionnaires à quatre temps de mesure suite à un évènement de VAT. Des modèles linéaires mixtes ont été utilisés afin de suivre l’évolution des différentes conséquences psychologiques en fonction de la qualité du SS et du sexe des participants. Résultats. D’abord, pour le SS positif, une association significative négative est ressortie uniquement avec la dépression. Le SS négatif est associé positivement avec les symptômes de TSPT, d’anxiété et de dépression. Finalement, des différences entre les hommes et les femmes n’ont été mesurées que pour le TSPT. Soit, les hommes présentent plus de symptômes que les femmes, mais ceux-ci bénéficient davantage du SS positif. Conclusion. La présente étude appuie l’importance de s’intéresser à la qualité du SS, car elle a une influence sur le développement et le maintien des conséquences psychologiques de la VAT. Aussi, le sexe semble également avoir un rôle modérateur de cette relation.Background. Workplace violence is part of the people working for Youth Protection's daily lives due to the vulnerable population served. The exposure of workplace violence is linked to psychological consequences such as post-traumatic stress disorder (PTSD), anxiety, and depression. Among the factors that influence the development of the different mental health symptoms, social support is known to be one of the strongest predictors of PTSD. Most recent studies also reveal the importance of measuring social support's quality (positive or negative) to understand how it can impact workers. Finally, some studies also show that workplace violence reactions might vary depending on the victim's gender. Objectives. The main objective of that study is to measure if the quality of social support impacts the development and evolution of the symptoms of PTSD, anxiety and depression. The secondary objective is to explore if the sex of the participants can moderate the association between social support and the previously measured symptoms. Methods. A sample of 150 Youth Protection workers answered self-reported surveys that examine their evolution four times over 12 months. Mixed linear models have been used to analyze the development of PTSD, anxiety's and depression's symptoms according to the quality of social support and then the sex of the participants. Results. First, positive social support wasnegatively linked to depression's symptoms. Workers who perceived their social support being positive had fewer symptoms. For negative social support, it was linked to PTSD, anxiety and depression. Finally, the difference between men and women was only measured for PTSD. Men had more symptoms than women, although they benefit more from positive social support than women. Conclusion. This study confirms the importance of measuring the quality of social support on workplace violence victims to understand its impact on psychological consequences better. Also, the sex seems to be a moderator only for PTSD's association with workplace violence

Key Features of the Intragraft Microenvironment that Determine Long-Term Survival Following Transplantation

In this review, we discuss how changes in the intragraft microenvironment serve to promote or sustain the development of chronic allograft rejection. We propose two key elements within the microenvironment that contribute to the rejection process. The first is endothelial cell proliferation and angiogenesis that serve to create abnormal microvascular blood flow patterns as well as local tissue hypoxia, and precedes endothelial-to-mesenchymal transition. The second is the overexpression of local cytokines and growth factors that serve to sustain inflammation and, in turn, function to promote a leukocyte-induced angiogenesis reaction. Central to both events is overexpression of vascular endothelial growth factor (VEGF), which is both pro-inflammatory and pro-angiogenic, and thus drives progression of the chronic rejection microenvironment. In our discussion, we focus on how inflammation results in angiogenesis and how leukocyte-induced angiogenesis is pathological. We also discuss how VEGF is a master control factor that fosters the development of the chronic rejection microenvironment. Overall, this review provides insight into the intragraft microenvironment as an important paradigm for future direction in the field

Neuregulin/ErbB regulate neuromuscular junction development by phosphorylation of α-dystrobrevin

Neuregulin/ErbB signaling maintains high efficacy of synaptic transmission by stabilizing the postsynaptic apparatus via phosphorylation of α-dystrobrevin1

Regulation of mTOR Signaling by Semaphorin 3F-Neuropilin 2 Interactions In Vitro and In Vivo

Semaphorin 3F (SEMA3F) provides neuronal guidance cues via its ability to bind neuropilin 2 (NRP2) and Plexin A family molecules. Recent studies indicate that SEMA3F has biological effects in other cell types, however its mechanism(s) of function is poorly understood. Here, we analyze SEMA3F-NRP2 signaling responses in human endothelial, T cell and tumor cells using phosphokinase arrays, immunoprecipitation and Western blot analyses. Consistently, SEMA3F inhibits PI-3K and Akt activity, and responses are associated with the disruption of mTOR/rictor assembly and mTOR-dependent activation of the RhoA GTPase. We also find that the expression of vascular endothelial growth factor, as well as mTOR-inducible cellular activation responses and cytoskeleton stability are inhibited by SEMA3F-NRP2 interactions in vitro. In vivo, local and systemic overproduction of SEMA3F reduces tumor growth in NRP2-expressing xenografts. Taken together, SEMA3F regulates mTOR signaling in diverse human cell types, suggesting that it has broad therapeutic implications

Mechanisms of congenital heart disease caused by NAA15 haploinsufficiency

Rationale: NAA15 is a component of the N-terminal (Nt) acetyltransferase complex, NatA. The mechanism by which NAA15 haploinsufficiency causes congenital heart disease (CHD) remains unknown. To better understand molecular processes by which NAA15 haploinsufficiency perturbs cardiac development, we introduced NAA15 variants into human induced pluripotent stem cells (iPSCs) and assessed the consequences of these mutations on RNA and protein expression. Objective: We aim to understand the role of NAA15 haploinsufficiency in cardiac development by investigating proteomic effects on NatA complex activity, and identifying proteins dependent upon a full amount of NAA15. Methods and Results: We introduced heterozygous LoF, compound heterozygous and missense residues (R276W) in iPS cells using CRISPR/Cas9. Haploinsufficient NAA15 iPS cells differentiate into cardiomyocytes, unlike NAA15-null iPS cells, presumably due to altered composition of NatA. Mass spectrometry (MS) analyses reveal ~80% of identified iPS cell NatA targeted proteins displayed partial or complete Nt-acetylation. Between null and haploinsufficient NAA15 cells Nt-acetylation levels of 32 and 9 NatA-specific targeted proteins were reduced, respectively. Similar acetylation loss in few proteins occurred in NAA15 R276W iPSCs. In addition, steady-state protein levels of 562 proteins were altered in both null and haploinsufficient NAA15 cells; eighteen were ribosomal-associated proteins. At least four proteins were encoded by genes known to cause autosomal dominant CHD. Conclusions: These studies define a set of human proteins that requires a full NAA15 complement for normal synthesis and development. A 50% reduction in the amount of NAA15 alters levels of at least 562 proteins and Nt-acetylation of only 9 proteins. One or more modulated proteins are likely responsible for NAA15-haploinsufficiency mediated CHD. Additionally, genetically engineered iPS cells provide a platform for evaluating the consequences of amino acid sequence variants of unknown significance on NAA15 function

Electrophysiological evidence for an early processing of human voices

<p>Abstract</p> <p>Background</p> <p>Previous electrophysiological studies have identified a "voice specific response" (VSR) peaking around 320 ms after stimulus onset, a latency markedly longer than the 70 ms needed to discriminate living from non-living sound sources and the 150 ms to 200 ms needed for the processing of voice paralinguistic qualities. In the present study, we investigated whether an early electrophysiological difference between voice and non-voice stimuli could be observed.</p> <p>Results</p> <p>ERPs were recorded from 32 healthy volunteers who listened to 200 ms long stimuli from three sound categories - voices, bird songs and environmental sounds - whilst performing a pure-tone detection task. ERP analyses revealed voice/non-voice amplitude differences emerging as early as 164 ms post stimulus onset and peaking around 200 ms on fronto-temporal (positivity) and occipital (negativity) electrodes.</p> <p>Conclusion</p> <p>Our electrophysiological results suggest a rapid brain discrimination of sounds of voice, termed the "fronto-temporal positivity to voices" (FTPV), at latencies comparable to the well-known face-preferential N170.</p

The Human Cell Atlas White Paper

The Human Cell Atlas (HCA) will be made up of comprehensive reference maps of all human cells - the fundamental units of life - as a basis for understanding fundamental human biological processes and diagnosing, monitoring, and treating disease. It will help scientists understand how genetic variants impact disease risk, define drug toxicities, discover better therapies, and advance regenerative medicine. A resource of such ambition and scale should be built in stages, increasing in size, breadth, and resolution as technologies develop and understanding deepens. We will therefore pursue Phase 1 as a suite of flagship projects in key tissues, systems, and organs. We will bring together experts in biology, medicine, genomics, technology development and computation (including data analysis, software engineering, and visualization). We will also need standardized experimental and computational methods that will allow us to compare diverse cell and tissue types - and samples across human communities - in consistent ways, ensuring that the resulting resource is truly global. This document, the first version of the HCA White Paper, was written by experts in the field with feedback and suggestions from the HCA community, gathered during recent international meetings. The White Paper, released at the close of this yearlong planning process, will be a living document that evolves as the HCA community provides additional feedback, as technological and computational advances are made, and as lessons are learned during the construction of the atlas

Extracorporeal Membrane Oxygenation for Severe Acute Respiratory Distress Syndrome associated with COVID-19: An Emulated Target Trial Analysis.

RATIONALE: Whether COVID patients may benefit from extracorporeal membrane oxygenation (ECMO) compared with conventional invasive mechanical ventilation (IMV) remains unknown. OBJECTIVES: To estimate the effect of ECMO on 90-Day mortality vs IMV only Methods: Among 4,244 critically ill adult patients with COVID-19 included in a multicenter cohort study, we emulated a target trial comparing the treatment strategies of initiating ECMO vs. no ECMO within 7 days of IMV in patients with severe acute respiratory distress syndrome (PaO2/FiO2 <80 or PaCO2 ≥60 mmHg). We controlled for confounding using a multivariable Cox model based on predefined variables. MAIN RESULTS: 1,235 patients met the full eligibility criteria for the emulated trial, among whom 164 patients initiated ECMO. The ECMO strategy had a higher survival probability at Day-7 from the onset of eligibility criteria (87% vs 83%, risk difference: 4%, 95% CI 0;9%) which decreased during follow-up (survival at Day-90: 63% vs 65%, risk difference: -2%, 95% CI -10;5%). However, ECMO was associated with higher survival when performed in high-volume ECMO centers or in regions where a specific ECMO network organization was set up to handle high demand, and when initiated within the first 4 days of MV and in profoundly hypoxemic patients. CONCLUSIONS: In an emulated trial based on a nationwide COVID-19 cohort, we found differential survival over time of an ECMO compared with a no-ECMO strategy. However, ECMO was consistently associated with better outcomes when performed in high-volume centers and in regions with ECMO capacities specifically organized to handle high demand. This article is open access and distributed under the terms of the Creative Commons Attribution Non-Commercial No Derivatives License 4.0 (http://creativecommons.org/licenses/by-nc-nd/4.0/)