Workers as objects: The nature of working objectification and the role of perceived alienation

The aim of the present study is to advance the research on working objectification by analyzing its nature and the mechanism underlying this process. In particular, we hypothesized that working objectification involved an automatic association of the worker with an object and a full denial of humanness related to both agency and experience. Further, we expected that perceived alienation could explain the relationship between critical working conditions and objectifying perceptions. Results showed that, compared to an artisan, a factory worker was automatically associated with the objectrelated words rather than with person-related words. Furthermore, the factory worker was perceived as having less agency and experience than the artisan. Finally, the perception of the factory work as fragmented, repetitive, and other-directed was related to a view of work as being more alienating, which, in turn, led to the increased objectification of the worker. Theoretical and practical implications are discussed

Intergroup biologization and outgroup prejudice in the time of COVID-19

Through two studies (N = 602) conducted in Italy between February and March 2020, we examined the impact of the COVID-19 emergency on biologization\u2014a form of dehumanization that involves the perception of others as contagious entities\u2014and outgroup prejudice. Overall, results showed that higher emergency perception was associated with greater biologization toward the groups most affected by the virus, namely the Chinese outgroup and the Italian ingroup. In turn, biologization toward the outgroup increased prejudice against that group. We also found that when the pandemic hit Italy, the greater emergency perception was associated with increased emotional closeness with Chinese people, resulting in reduced biologization and prejudice toward them. However, these results held true only for Italian respondents who reported higher levels of ingroup biologization. Taken together, our findings contribute to the knowledge gaps of biologization and prejudice by also providing relevant insights into the ongoing health emergency

Rectifiability and upper Minkowski bounds for singularities of harmonic Q-valued maps

In this article we prove that the singular set of Dirichlet-minimizing Q-valued functions is countably .m2/-rectifiable and we give upper bounds for the .m2/-dimensional Minkowski content of the set of singular points with multiplicity Q

Objectified conformity: Working self-objectification increases conforming behavior

The present work explores whether self-objectification triggered by doing peculiar work activities would increase people\u2019s conforming behavior. We conducted an experimental study in which participants (N = 140) were asked to perform a high objectifying activity (vs. low objectifying activity vs. baseline condition) simulating a real computer job. Afterwards, their levels of self-objectification and conforming behavior were assessed. Results revealed that participants who performed the high objectifying activity self-objectified (i.e., perceived themselves as lacking human mental states) more than the other conditions and, in turn, conformed more to the judgments of unknown similar others. Crucially, increased self-objectification mediated the effects of the high objectifying activity on enhancing conforming behavior. Theoretical and applied implications of these findings are discusse

The PRRT2 knockout mouse recapitulates the neurological diseases associated with PRRT2 mutations.

Heterozygous and rare homozygous mutations in PRoline-Rich Transmembrane protein 2 (PRRT2) underlie a group of paroxysmal disorders including epilepsy, kinesigenic dyskinesia episodic ataxia and migraine. Most of the mutations lead to impaired PRRT2 expression and/or function. Recently, an important role for PRTT2 in the neurotransmitter release machinery, brain development and synapse formation has been uncovered. In this work, we have characterized the phenotype of a mouse in which the PRRT2 gene has been constitutively inactivated (PRRT2 KO)beta-galactosidase staining allowed to map the regional expression of PRRT2 that was more intense in the cerebellum, hindbrain and spinal cord, while it was localized to restricted areas in the fore-brain. PRRT2 KO mice are normal at birth, but display paroxysmal movements at the onset of locomotion that persist in the adulthood. In addition, adult PRRT2 KO mice present abnormal motor behaviors characterized by wild running and jumping in response to audiogenic stimuli that are ineffective in wild type mice and an increased sensitivity to the convulsive effects of pentylentetrazol. Patch-clamp electrophysiology in hippocampal and cerebellar slices revealed specific effects in the cerebellum, where PRRT2 is highly expressed, consisting in a higher excitatory strength at parallel fiber-Purkinje cell synapses during high frequency stimulation. The results show that the PRRT2 KO mouse reproduces the motor paroxysms present in the human PRRT2-linked pathology and can be proposed as an experimental model for the study of the pathogenesis of the disease as well as for testing personalized therapeutic approaches

Validation of an Engineered Cell Model for In Vitro and In Vivo HIF-1 alpha Evaluation by Different Imaging Modalities

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APache Is an AP2-Interacting Protein Involved in Synaptic Vesicle Trafficking and Neuronal Development

Synaptic transmission is critically dependent on synaptic vesicle (SV) recycling. Although the precise mechanisms of SV retrieval are still debated, it is widely accepted that a fundamental role is played by clathrin-mediated endocytosis, a form of endocytosis that capitalizes on the clathrin/adaptor protein complex 2 (AP2) coat and several accessory factors. Here, we show that the previously uncharacterized protein KIAA1107, predicted by bioinformatics analysis to be involved in the SV cycle, is an AP2-interacting clathrin-endocytosis protein (APache). We found that APache is highly enriched in the CNS and is associated with clathrin-coated vesicles via interaction with AP2. APache-silenced neurons exhibit a severe impairment of maturation at early developmental stages, reduced SV density, enlarged endosome-like structures, and defects in synaptic transmission, consistent with an impaired clathrin/AP2-mediated SV recycling. Our data implicate APache as an actor in the complex regulation of SV trafficking, neuronal development, and synaptic plasticity

Sphingosine-1-phosphate (S1P) impacts presynaptic functions by regulating synapsin i localization in the presynaptic compartment

Growing evidence indicates that sphingosine-1-P (S1P) upregulates glutamate secretion in hippocampal neurons. However, the molecular mechanisms through which S1P enhances excitatory activity remain largely undefined. The aim of this study was to identify presynaptic targets of S1P action controlling exocytosis. Confocal analysis of rat hippocampal neurons showed that S1P applied at nanomolar concentration alters the distribution of Synapsin I (SynI), a presynaptic phosphoprotein that controls the availability of synaptic vesicles for exocytosis. S1P induced SynI relocation to extrasynaptic regions of mature neurons, as well as SynI dispersion from synaptic vesicle clusters present at axonal growth cones of developing neurons. S1P-induced SynI relocation occurred in a Ca2+- independent but ERK-dependent manner, likely through the activation of S1P3 receptors, as it was prevented by the S1P3 receptor selective antagonist CAY1044 and in neurons in which S1P3 receptor was silenced. Our recent evidence indicates that microvesicles (MVs) released by microglia enhance the metabolism of endogenous sphingolipids in neurons and stimulate excitatory transmission. We therefore investigated whether MVs affect SynI distribution and whether endogenous S1P could be involved in the process. Analysis of SynI immunoreactivity showed that exposure to microglial MVs induces SynI mobilization at presynaptic sites and growth cones, whereas the use of inhibitors of sphingolipid cascade identified S1P as the sphingolipid mediating SynI redistribution. Our data represent the first demonstration that S1P induces SynI mobilization from synapses, thereby indicating the phosphoprotein as a novel target through which S1P controls exocytosis. Significance Statement Growing evidence indicates that the bioactive lipid sphingosine and its metabolite sphingosine-1-P (S1P) stimulate excitatory transmission. While it has been recently clarified that sphingosine influences directly the exocytotic machinery by activating the synaptic vesicle protein VAMP2 to form SNARE fusion complexes, the molecular mechanism by which S1P promotes neurotransmission remained largely undefined. In this study, we identify Synapsin I, a presynaptic phosphoprotein involved in the control of availability of synaptic vesicles for exocytosis, as the key target of S1P action. In addition, we provide evidence that S1P can be produced at mature axon terminals as well as at immature growth cones in response to microglia-derived signals, which may be important to stabilize nascent synapses and to restore or potentiate transmission