Unbalanced Scales of Global Capitalism: Analyzing Temporary Foreign Worker Programs in Canada

This article analyzes several characteristics of two of Canada’s Temporary Foreign Worker Programs (TFWPs): The Seasonal Agricultural Worker Program (SAWP) and the Live-in Caregiver Program (LCP). First, I consider the social and economic contexts in which these programs have emerged. Second, I discuss how these programs maintain racial and gendered hierarchies. Third, I problematize the relationship TFWPs have with citizenship status, as well as critique TFWPs as a long-term solution to Canadian labour shortages. Last, I discuss the potential benefits of these TFWPs and suggest alternatives and potential improvements to the programs. Using a Marxist framework, this analysis situates Canada’s TFWPs within the broader political economy and argues that global capitalism and the state interact to serve the people and economies of the Global North at the expense of migrant workers from the Global South. Cet article examine deux programmes des travailleurs étrangers temporaires (PTET) du Canada: le Programme des travailleurs agricoles saisonniers (PTAS) et le Programme concernant les aides familiaux résidants (PAFR). Cet essai examine plusieurs aspects des PTET. Premièrement, je tiens compte du contexte social et économique dans lequel ces programmes sont apparus. Deuxièmement, j’explique comment ces programmes maintiennent une hiérarchie basée sur la race et le sexe. Troisièmement, je pose le problème des relations entre les PTET et le statut de citoyen, et je formule également une critique du PTET comme solution à long terme à la pénurie de main-d’œuvre canadienne. Enfin, je discute des avantages potentiels de ces PTET et propose des solutions de rechange et des façons d’améliorer les programmes. À l’aide d’un cadre d’analyse marxiste, les PTET du Canada sont évalués globalement dans le contexte de l’économie politique et il est proposé que le capitalisme mondial et l’État interagissent au service des citoyens et des économies de l’hémisphère nord, au détriment des travailleurs migrants en provenance de l’hémisphère sud

Translating environments

Far from being inert materials activated by human ingenuity, natural resources come to be made and unmade through ongoing processes of translation, through which they acquire new potentialities and meanings. In this introduction, we review the key concept of translation for anthropology and explore some of its multiple analytical possibilities in the context of human-environment relations. Based on insights offered by the articles in this collection, we propose a twofold definition of environments as both translating subjects and objects of translation. In grounding our analytical definition, we focus on the enactment of material transformations (as the result of both relations of mutual determination with humans and processes of objectification of the environment), the implications of incommensurability and erasure in processes of (attempted) translation, and the indeterminacy that accompanies (re)configurations of materials, relations and values

FLNA-filaminopathy skeletal phenotypes are not due to an osteoblast autonomous loss-of-function

Mutations in FLNA, which encodes the cytoskeletal protein FLNA, cause a spectrum of sclerosing skeletal dysplasias. Although many of these genetic variants are recurrent and cluster within the gene, the pathogenic mechanism that underpins the development of these skeletal phenotypes is unknown. To determine if the skeletal dysplasia in FLNA-related conditions is due to a cell-autonomous loss-of-function localising to osteoblasts and/or osteocytes, we utilised mouse models to conditionally remove Flna from this cellular lineage. Flna was conditionally knocked out from mature osteocytes using the Dmp1-promoter driven Cre-recombinase expressing mouse, as well as the committed osteoblast lineage using the Osx-Cre or Col1a1-Cre expressing lines. We measured skeletal parameters with μCT and histological methods, as well as gene expression in the mineralised skeleton. We found no measureable differences between the conditional Flna knockout mice, and their control littermate counterparts. Moreover, all of the conditional Flna knockout mice, developed and aged normally. From this we concluded that the skeletal dysplasia phenotype associated with pathogenic variants in FLNA is not caused by a cell-autonomous loss-of-function in the osteoblast-osteocyte lineage, adding more evidence to the hypothesis that these phenotypes are due to gain-of-function in FLNA

Brain exposure to SARS-CoV-2 virions perturbs synaptic homeostasis

International audienceSevere acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection is associated with short- and long-term neurological complications. The variety of symptoms makes it difficult to unravel molecular mechanisms underlying neurological sequalae after coronavirus disease 2019 (COVID-19). Here we show that SARS-CoV-2 triggers the up-regulation of synaptic components and perturbs local electrical field potential. Using cerebral organoids, organotypic culture of human brain explants from individuals without COVID-19 and post-mortem brain samples from individuals with COVID-19, we find that neural cells are permissive to SARS-CoV-2 to a low extent. SARS-CoV-2 induces aberrant presynaptic morphology and increases expression of the synaptic components Bassoon, latrophilin-3 (LPHN3) and fibronectin leucine-rich transmembrane protein-3 (FLRT3). Furthermore, we find that LPHN3-agonist treatment with Stachel partially restored organoid electrical activity and reverted SARS-CoV-2-induced aberrant presynaptic morphology. Finally, we observe accumulation of relatively static virions at LPHN3-FLRT3 synapses, suggesting that local hindrance can contribute to synaptic perturbations. Together, our study provides molecular insights into SARS-CoV-2-brain interactions, which may contribute to COVID-19-related neurological disorders