Of precarity and conspiracy: introducing a socio-functional model of conspiracy beliefs

Conspiracy Beliefs (CB) are a key vector of violent extremism, radicalism and unconventional political events. So far, social-psychological research has extensively documented how cognitive, emotional and intergroup factors can promote CB. Evidence also suggests that adherence to CB moves along social class lines: low-income and low-education are among the most robust predictors of CB. Yet, the potential role of precarity—the subjective experience of permanent insecurity stemming from objective material strain—in shaping CB remains largely unexplored. In this paper, we propose for the first time a socio-functional model of CB. We test the hypothesis that precarity could foster increased CB because it undermines trust in government and the broader political ‘elites’. Data from the World Value Survey (n = 21,650; Study 1, electoral CB) and from representative samples from polls conducted in France (n = 1760, Study 2a, conspiracy mentality) and Italy (n = 2196, Study 2b, COVID-19 CB), corroborate a mediation model whereby precarity is directly and indirectly associated with lower trust in authorities and higher CB. In addition, these links are robust to adjustment on income, self-reported SES and education. Considering precarity allows for a truly social-psychological understanding of CB as the by-product of structural issues (e.g. growing inequalities). Results from our socio-functional model suggest that implementing solutions at the socio-economic level could prove efficient in fighting CB

Alteration of endosomal trafficking is associated with early-onset parkinsonism caused by SYNJ1 mutations

Recently, a new form of autosomal recessive early-onset parkinsonism (PARK20), due to mutations in the gene encoding the phosphoinositide phosphatase, Synaptojanin 1 (Synj1), has been reported. Several genes responsible for hereditary forms of Parkinson's disease are implicated in distinct steps of the endolysosomal pathway. However, the nature and the degree of endocytic membrane trafficking impairment in early-onset parkinsonism remains elusive. Here, we show that depletion of Synj1 causes drastic alterations of early endosomes, which become enlarged and more numerous, while it does not affect the morphology of late endosomes both in non-neuronal and neuronal cells. Moreover, Synj1 loss impairs the recycling of transferrin, while it does not alter the trafficking of the epidermal growth factor receptor. The ectopic expression of Synj1 restores the functions of early endosomes, and rescues these trafficking defects in depleted cells. Importantly, the same alterations of early endosomal compartments and trafficking defects occur in fibroblasts of PARK20 patients. Our data indicate that Synj1 plays a crucial role in regulating the homeostasis and functions of early endosomal compartments in different cell types, and highlight defective cellular pathways in PARK20. In addition, they strengthen the link between endosomal trafficking and Parkinson's disease

Search for bottom-type, vectorlike quark pair production in a fully hadronic final state in proton-proton collisions at s=13 TeV

A search is described for the production of a pair of bottom-type vectorlike quarks (VLQs), each decaying into a b or ¯ b quark and either a Higgs or a Z boson, with a mass greater than 1000 GeV. The analysis is based on data from proton-proton collisions at a 13 TeV center-of-mass energy recorded at the CERN LHC, corresponding to a total integrated luminosity of 137     fb − 1 . As the predominant decay modes of the Higgs and Z bosons are to a pair of quarks, the analysis focuses on final states consisting of jets resulting from the six quarks produced in the events. Since the two jets produced in the decay of a highly Lorentz-boosted Higgs or Z boson can merge to form a single jet, nine independent analyses are performed, categorized by the number of observed jets and the reconstructed event mode. No signal in excess of the expected background is observed. Lower limits are set on the VLQ mass at 95% confidence level equal to 1570 GeV in the case where the VLQ decays exclusively to a b quark and a Higgs boson, 1390 GeV for when it decays exclusively to a b quark and a Z boson, and 1450 GeV for when it decays equally in these two modes. These limits represent significant improvements over the previously published VLQ limits

The role of in-group identification in infra-humanization.

People tend to infra-humanize by attributing more human essence to their in-group than to out-groups. In the present article, we focus on the attribution of primary and secondary emotions to operationalize the human essence. We propose that, in order to infra-humanize, people need to be categorized in meaningful groups. In addition, we argue that what differentiates meaningful from nonmeaningful groups is that the people essentialize, perceiving members of the group as sharing an underlying, common essence. Also, we hypothesize that participants will identify more with their in-group in the case of meaningful groups. Three types of groups were created to manipulate the meaningfulness of the categorization. Participants were either randomly assigned to a group or they chose their group as a function of their preferences for a colour or the type of career they wished to pursue. As expected, infra-humanization occurred only where the categorization's criterion was meaningful. In addition, in-group identification, but not essentialism, mediated the impact of the categorization criteria on the tendency to infra-humanize. Data also showed that infra-humanization is different from classic in-group favouritism. This is because in-group favouritism, but not infra-humanization, was observed in the situation where group membership was based on random assignment. In other words, for infra-humanization to occur mere categorization is not enough; meaningfulness is also needed. For in-group favouritism to arise, the knowledge of being part of a group is a sufficient prerequisite. The discussion focuses on conditions for reducing infra-humanization and on the relationship between in-group favouritism and out-group derogation

Second language competence of the Italian-speaking population of Alto Adige/Sudtirol: Evidence for a linguistic stereotype threat

Stereotype threat theory suggests that a negative stereotype about a social group can undermine the performance of group members in a stereotype-relevant domain. The present research examines this in the domain of second language (L2) competence. Two studies were conducted to test the effects of stereotype threat on L2 performance in a group of Italian-speaking people living in Alto Adige/S\ufcdtirol (AA/ST), a bilingual region of Italy. Participants were members of the Italian-speaking community who are generally not very proficient in L2 (i.e., German). When reminded of the negative stereotype, participants who highly identified with the domain (i.e., German language; Study 1) and those who believed that their linguistic group was in a disadvantaged position in AA/ST (Study 2) underperformed in a German language test. These findings are discussed in relation with people\u2019s mastery of L2 in bilingual contexts and their consequences for the study of stereotype threat

Novel mutations in dystonin provide clues to the pathomechanisms of HSAN-VI

Objective: To describe a second hereditary sensory autonomic neuropathy type VI (HSAN-VI) family harboring 2 novel heterozygous mutations in the dystonin (DST) gene and to evaluate their effect on neurons derived from induced pluripotent stem cells (iPSC). Methods: The family consisted of 3 affected siblings from nonconsanguineous healthy parents. All members underwent clinical and electrophysiologic evaluation and genetic analysis. Two patients underwent quantitative sensory testing (QST), cardiovascular reflexes, dynamic sweat test, and skin biopsy to evaluate somatic and autonomic cutaneous innervation and to get fibroblast cultures for developing iPSC-derived neurons. Results: Onset occurred in the first decade, with painless and progressive mutilating distal ulcerations leading to amputation and joint deformity. Sensation to pain, touch, and vibration was reduced. Autonomic disturbances included hypohidrosis, pupillary abnormalities, and gastrointestinal and sexual dysfunction. Nerve conduction studies showed a severe axonal sensory neuropathy. QST and autonomic functional studies were abnormal. Skin biopsy revealed a lack of sensory and autonomic nerve fibers. Genetic analysis revealed 2 pathogenic mutations in the DST gene affecting exclusively the DST neuronal isoform-a2. Neurons derived from iPSC showed absence or very low levels of DST protein and short and dystrophic neuritis or no projections at all. Conclusions: Unlike the previous HSAN-VI family, our description indicates that DST mutations may be associated with a nonlethal and nonsyndromic phenotype. Neuronal loss affects large and small sensory nerve fibers as well as autonomic ones. Induced-PSC findings suggest that dystonin defect might alter proper development of the peripheral nerves. Dystonin-a2 plays a majorrole in the HSAN-VI phenotype

A y(+)LAT-1 mutant protein interferes with y(+)LAT-2 activity: implications for the molecular pathogenesis of lysinuric protein intolerance.

Lysinuric protein intolerance (LPI) is an inherited aminoaciduria caused by defective cationic amino acid (CAA) transport at the basolateral membrane of epithelial cells in the intestine and kidney. The SLC7A7 gene, mutated in LPI, encodes the y(+)LAT-1 protein, which is the light subunit of the heterodimeric CAA transporter in which 4F2hc is the heavy chain subunit. Co-expression of 4F2hc and y(+)LAT-1 induces the y(+)L activity. This activity is also exerted by another complex composed of 4F2hc and y(+)LAT-2, the latter encoded by the SLC7A6 gene and more ubiquitously expressed than SLC7A7. On the basis of both the pattern of expression and the transport activity, y(+)LAT-2 might compensate for CAA transport when y(+)LAT-1 is defective. By expression in Xenopus laevis oocytes and mammalian cells, we functionally analysed two SLC7A7 mutants, E36del and F152L, respectively, the former displaying a partial dominant-negative effect. The results of the present study provide further insight into the molecular pathogenesis of LPI: a putative multiheteromeric structure of both [4F2hc/y(+)LAT-1] and [4F2hc/y(+)LAT-2], and the interference between y(+)LAT-1 and y(+)LAT-2 proteins. This interference can explain why the compensatory mechanism, that is, an increased expression of SLC7A6 as seen in lymphoblasts from LPI patients, may not be sufficient to restore the y(+)L system activity