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1.
Anthropol Med ; 30(1): 31-47, 2023 Mar.
Artigo em Inglês | MEDLINE | ID: mdl-36861381

RESUMO

The global rise of populism and concomitant polarizations across disenfranchised and marginalized groups has been magnified by so-called echo chambers, and a major public health crisis like the COVID-19 pandemic has only served to fuel these intergroup tensions. Media institutions disseminating information on ways to prevent the propagation of the virus have reactivated a specific discursive phenomenon previously observed in many epidemics: the construction of a defiled 'Other'. With anthropological lenses, discourse on defilement is an interesting path to understand the continuous emergence of pseudo-scientific forms of racism. In this paper, the authors focus on 'borderline racism', that is the use of an institutionally 'impartial' discourse to reaffirm the inferiority of another race. The authors employed inductive thematic analysis of 1200 social media comments reacting to articles and videos published by six media in three different countries (France, United States and India). Results delineate four major themes structuring defilement discourses: food (and the relationship to animals), religion, nationalism and gender. Media articles and videos portrayed Western and Eastern countries through contrasting images and elicited a range of reaction in readers and viewers. The discussion reflects on how borderline racism can be an appropriate concept to understand the appearance of hygienic othering of specific subgroups on social media. Theoretical implications and recommendations on a more culturally sensitive approach of media coverage of epidemics and pandemics are discussed.


Assuntos
COVID-19 , Racismo , Mídias Sociais , Estados Unidos , Humanos , Pandemias , Antropologia Médica , França
2.
Clin Child Psychol Psychiatry ; 29(2): 687-699, 2024 Apr.
Artigo em Inglês | MEDLINE | ID: mdl-37542383

RESUMO

BACKGROUND: Data on children who grow up with parents adhering to violent extremism is scant. This makes it extremely delicate to inform policies and clinical services to protect such children from potential physical and psychological harm. OBJECTIVE: This paper explores the predicament of children whose caretakers were referred to a specialized clinical team in Montreal (Canada) because of concerns about risks or actual involvement in violent extremism processes. METHODS: This paper uses a mixed methods concurrent triangulation design. Quantitative data was obtained through a file review (2016-2020). Qualitative data was collected through semi-structured interviews and a focus group with the team practitioners. RESULTS: Clinicians reported the presence of stereotypes in the health and social services network frequently representing religious extremist parents as potentially dangerous or having inappropriate parenting skills while minimizing the perception of risk for parents adhering to political extremism. Children displayed high levels of psychological distress, mainly related to family separation, parental psychopathology, and conflicts of loyalty stemming from familial or social alienation. CONCLUSIONS: Training practitioners to be aware of their own personal and institutional bias may help them to understand the predicament of extremist parents' children and implement systemic, trauma and attachment informed interventions.


Assuntos
Pais , Serviço Social , Criança , Humanos , Pais/psicologia , Agressão , Pesquisa Qualitativa , Grupos Focais
3.
J Mol Neurosci ; 52(3): 378-83, 2014 Mar.
Artigo em Inglês | MEDLINE | ID: mdl-24203573

RESUMO

Chronic administration of antipsychotics (APs) has been associated with dopamine D2 receptor (D2R) upregulation and tardive dyskinesia. We previously showed that haloperidol, a first-generation AP, exerted a more robust increase in D2R expression than amisulpride, a second-generation AP and that (±)-α-lipoic acid pre-treatment reversed the AP-induced D2R upregulation. We also demonstrated that the Akt/GSK-3ß/ß-catenin pathway is involved in the control of D2R expression levels, but is unlikely implicated in the preventive effects of (±)-α-lipoic acid since co-treatment with haloperidol and (±)-α-lipoic acid exerts synergistic effects on Akt/GSK-3ß activation. These findings led us to examine whether the ERK/MAPK signaling pathway may be involved in D2R upregulation elicited by APs, and in its reversal by (±)-α-lipoic acid, in SH-SY5Y human neuroblastoma cells. Our results revealed that haloperidol, in parallel with an elevation in D2R mRNA levels, induced a larger increase of ERK (p42/p44) phosphorylation than amisulpride. Pre-treatment with the selective ERK inhibitor U0126 attenuated haloperidol-induced increase in D2R upregulation. Furthermore, (±)-α-lipoic acid prevented AP-induced ERK activation. These results show that (1) the ERK/MAPK pathway is involved in haloperidol-induced D2R upregulation; (2) the preventive effect of (±)-α-lipoic acid on haloperidol-induced D2R upregulation is in part mediated by an ERK/MAPK-dependent signaling cascade. Taken together, our data suggest that (±)-α-lipoic acid exerts synergistic effects with haloperidol on the Akt/GSK-3ß pathway, potentially involved in the therapeutic effects of APs, and antagonism of ERK activation and D2R upregulation, potentially involved in tardive dyskinesia and treatment resistance.


Assuntos
Antipsicóticos/farmacologia , Haloperidol/farmacologia , Neurônios/efeitos dos fármacos , Fármacos Neuroprotetores/farmacologia , Receptores de Dopamina D2/metabolismo , Ácido Tióctico/farmacologia , Regulação para Cima , Amissulprida , Linhagem Celular Tumoral , Sobrevivência Celular , Humanos , Proteína Quinase 1 Ativada por Mitógeno/metabolismo , Proteína Quinase 3 Ativada por Mitógeno/metabolismo , Neurônios/metabolismo , RNA Mensageiro/genética , RNA Mensageiro/metabolismo , Receptores de Dopamina D2/genética , Sulpirida/análogos & derivados , Sulpirida/farmacologia
4.
J Mol Neurosci ; 50(1): 134-45, 2013 May.
Artigo em Inglês | MEDLINE | ID: mdl-22975849

RESUMO

Chronic administration of antipsychotics has been associated with dopamine D2 receptor (D2R) upregulation and tardive dyskinesia. We have previously shown that haloperidol, a first-generation antipsychotic (FGA), exerted an increase in D2R expression and oxidative stress and that (±)-α-lipoic acid reversed its effect. Previous studies have implicated the Akt/glycogen synthase kinase-3ß (GSK-3ß) signaling pathway in antipsychotic action. These findings led us to examine whether the Akt/GSK-3ß pathway was involved in D2R upregulation and oxidative stress elicited by antipsychotics and, in (±)-α-lipoic acid-induced reversal of these phenomena, in SH-SY5Y cells. Antipsychotics increased phosphorylation of Akt and GSK-3ß, and additive effects were observed with (±)-α-lipoic acid. GSK-3ß inhibitors reversed haloperidol-induced overexpression of D2R mRNA levels but did not affect haloperidol-induced oxidative stress. Sustained antipsychotic treatment increased ß-arrestin-2 and D2R receptor interaction. Regarding Akt/GSK-3ß downstream targets, antipsychotics increased ß-catenin levels, whereas (±)-α-lipoic acid induced an elevation of mTOR activation. These results suggest (1) that the effect of antipsychotics on the Akt/GSK-3ß pathway in SH-SY5Y cells is reminiscent of their in vivo action, (2) that (±)-α-lipoic acid partially synergizes with antipsychotic drugs (APDs) on the same pathway, and (3) that the Akt/GSK-3ß signaling cascade is not involved in the preventive effect of (±)-α-lipoic acid on antipsychotics-induced D2R upregulation.


Assuntos
Antipsicóticos/farmacologia , Quinase 3 da Glicogênio Sintase/metabolismo , Proteínas Proto-Oncogênicas c-akt/metabolismo , Receptores de Dopamina D2/metabolismo , Transdução de Sinais/efeitos dos fármacos , Ácido Tióctico/farmacologia , Arrestinas/metabolismo , Linhagem Celular Tumoral , Glicogênio Sintase Quinase 3 beta , Haloperidol/farmacologia , Humanos , Estresse Oxidativo , Fosforilação , Receptores de Dopamina D2/genética , Serina-Treonina Quinases TOR/metabolismo , Transcrição Gênica , beta Catenina/genética , beta Catenina/metabolismo , beta-Arrestina 2 , beta-Arrestinas
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