Phenomenon of Nightclub Shots: Mass Psychogenic Disease?

This article examines the possibility that the "nightclub shots" epidemic is a "mass psychogenic disease" phenomenon, by comparing the various cases of "mass sociogenic diseases" reported in the literature. We carried out a literature review on PubMed. The keywords used were "mass hysteria", "mass sociogenic disease", "mass psychogenic disease" and "epidemic of multiple unexplained symptoms". Our review of the literature revealed several elements common to the various "mass hysterias" we identified. These phenomena generally appear in a climate of anxiety specific to the era in which they occur, in this case the fear of bioterrorism in the 21st century. Symptoms are generally benign and transient, appearing and resolving easily without the identification of an organic cause. They usually occur in a small group of individuals, and more frequently in young people and women. The media can exacerbate the phenomenon. The phenomenon of epidemics of nightclub shots seems to fit into the common framework of "mass psychogenic diseases" identified in the literature. This diagnosis could therefore be evoked, in the absence of any other objective somatic explanation

Assessment of colocalization of arsenic, ferric oxide and organic matter within weland soil through NanoSIMS mapping

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Interactions between natural organic matter, sulfur, arsenic and iron oxides in re-oxidation compounds within riparian wetlands: NanoSIMS and X-ray adsorption spectroscopy evidences

International audienceArsenic (As) is a toxic and ubiquitous element which can be responsible for severe health problems. Recently,Nano-scale Secondary IonsMass Spectrometry (nanoSIMS) analysis has been used to map organomineral assemblages.Here,we present a method adapted fromBelzile et al. (1989) to collect freshly precipitated compounds ofthe re-oxidation period in a natural wetland environment using a polytetrafluoroethylene (PTFE) sheet scavenger.This method provides information on the bulk samples and on the specific interactions between metals (i.e.As) and the natural organic matter (NOM). Our method allows producing nanoSIMS imaging on natural colloidprecipitates, including 75As−, 56Fe16O−, sulfur (32S−) and organic matter (12C14N) and to measure X-ray adsorptionof sulfur (S) K-edge. A first statistical treatment on the nanoSIMSimages highlights two main colocalizations:(1) 12C14N−, 32S−, 56Fe16O− and 75As−, and (2) 12C14N−, 32S− and 75As−. Principal component analyses (PCAs)support the importance of sulfur in the two main colocalizations firstly evidenced. The first component explains70% of the variance in the distribution of the elements and is highly correlated with the presence of 32S−. The secondcomponent explains 20% of the variance and is highly correlated with the presence of 12C14N−. The X-ray adsorption near edge spectroscopy (XANES) on sulfur speciation provides a quantification of the organic (55%)and inorganic (45%) sulfur compositions. The co-existence of reduced and oxidized S forms might be attributedto a slow NOM kinetic oxidation process. Thus, a direct interaction between As and NOM through sulfur groupsmight be possible

Elevated expression of complement C4 in the mouse prefrontal cortex causes schizophrenia-associated phenotypes

International audienceAccumulating evidence supports immune involvement in the pathogenesis of schizophrenia, a severe psychiatric disorder. In particular, high expression variants of C4, a gene of the innate immune complement system, were shown to confer susceptibility to schizophrenia. However, how elevated C4 expression may impact brain circuits remains largely unknown. We used in utero electroporation to overexpress C4 in the mouse prefrontal cortex. We found reduced glutamatergic input to pyramidal cells of juvenile and adult, but not of newborn C4-overexpressing (C4-OE) mice, together with decreased spine density, which mirrors spine loss observed in the schizophrenic cortex. Using time-lapse two-photon imaging in vivo, we observed that these deficits were associated with decreased dendritic spine gain and elimination in juvenile C4-OE mice, which may reflect poor formation and/or stabilization of immature spines. In juvenile and adult C4-OE mice, we found evidence for NMDA receptor hypofunction, another schizophrenia-associated phenotype, and synaptic accumulation of calcium-permeable AMPA receptors. Alterations in cortical GABAergic networks have been repeatedly associated with schizophrenia. We found that functional GABAergic transmission was reduced in C4-OE mice, in line with diminished GABA release probability from parvalbumin interneurons, lower GAD67 expression, and decreased intrinsic excitability in parvalbumin interneurons. These cellular abnormalities were associated with working memory impairment. Our results substantiate the causal relationship between an immunogenetic risk factor and several distinct cortical endophenotypes of schizophrenia and shed light on the underlying cellular mechanisms