COVID-19's Impact Upon Labor and Value Chains in the Agrifood Industry: A case study

We explore the impact of automation and digitalization on labor in the US agrifood system during the COVID-19 pandemic. This study considers each of the primary nodes in the system stretching from consumer through grocery stores and restaurants to last-mile delivery, distribution, food processing, farming, and agri-inputs. Not only automation and digitalization, but also the role of platforms such as Amazon, and food delivery firms such as GrubHub, Instacart, and Uber Eats are discussed. For restaurants, we consider not only dine-in restaurants, but also “ghost kitchens”. Furthermore, the possibility that farmers or distributors could disintermediate other nodes and deal directly with consumers is discussed. We conclude that, as a generalization, the further upstream one goes from the consumer, the less immediate and disruptive automation is likely to be for labor. However, our overall conclusion is that, given the current trajectories, labor is becoming increasingly precarious. If the current labor shortages continue, then automation is likely to accelerate. Platformization, while rampant in the relationships with final consumers, is likely to be less rapidly adopted further upstream where relationships are B-to-B and thus composed of actors that are wary of sharing data

Along the energy justice continuum: An examination of energy disposal through the lens of feminist community based participatory action research

Energy justice research tends to focus on inequalities that result from energy systems, including from fossil fuel extraction to production, distribution, and consumption. However, little research has investigated local effects of the disposal of waste products from fossil fuel extraction. To better understand these impacts, we employed a case study approach with qualitative interviews of residents of Kettleman City, a rural community in California's Central Valley (USA) that hosts a hazardous waste landfill which accepts predominantly waste from fossil fuel production. Informed by a novel feminist community-based participatory action research approach (CBPAR), interview data were collected from residents in the Summer of 2019 and analyzed using deductive and inductive coding strategies. Resident interviews highlighted the disproportionate distribution of pollution and environmental degradation shouldered by the community along with their experiences of adverse health and social impacts. Our analysis revealed the importance of incorporating an intersectional perspective to frame resident experiences of energy injustice. Our research highlights the untapped potential of feminist-informed CBPAR to catalyze change and challenge the production of energy injustice from energy waste disposal

Loss of G0/G1 switch gene 2 (G0S2) promotes disease progression and drug resistance in chronic myeloid leukaemia (CML) by disrupting glycerophospholipid metabolism

Abstract Tyrosine kinase inhibitors (TKIs) targeting BCR::ABL1 have turned chronic myeloid leukaemia (CML) from a fatal disease into a manageable condition for most patients. Despite improved survival, targeting drug‐resistant leukaemia stem cells (LSCs) remains a challenge for curative CML therapy. Aberrant lipid metabolism can have a large impact on membrane dynamics, cell survival and therapeutic responses in cancer. While ceramide and sphingolipid levels were previously correlated with TKI response in CML, the role of lipid metabolism in TKI resistance is not well understood. We have identified downregulation of a critical regulator of lipid metabolism, G0/G1 switch gene 2 (G0S2), in multiple scenarios of TKI resistance, including (1) BCR::ABL1 kinase‐independent TKI resistance, (2) progression of CML from the chronic to the blast phase of the disease, and (3) in CML versus normal myeloid progenitors. Accordingly, CML patients with low G0S2 expression levels had a worse overall survival. G0S2 downregulation in CML was not a result of promoter hypermethylation or BCR::ABL1 kinase activity, but was rather due to transcriptional repression by MYC. Using CML cell lines, patient samples and G0s2 knockout (G0s2−/−) mice, we demonstrate a tumour suppressor role for G0S2 in CML and TKI resistance. Our data suggest that reduced G0S2 protein expression in CML disrupts glycerophospholipid metabolism, correlating with a block of differentiation that renders CML cells resistant to therapy. Altogether, our data unravel a new role for G0S2 in regulating myeloid differentiation and TKI response in CML, and suggest that restoring G0S2 may have clinical utility