剑桥大学伊曼纽尔学院

Some feminist theorists have proposed that one way to combat commonplace sexist or racist conduct is to develop new terminology that “calls out” these oppressive behaviors. Drawing from enactivist accounts of language and the theoretical notion of “affordance” from ecological psychology, I examine how neologisms such as “sexual harassment” have the potential to promote epistemic familiarity and deepen agents’ recognitional capacities. They do so, in large part, by arousing bodily-affective feelings and prompting a specific sort of evaluative orientation. At the same time, these terms promote practical familiarity, reposition agents in relation to their sociomaterial world, and help them to engage effectively with a field of relevant affordances. This discussion reveals the way in which the epistemic, affective, and practical dimensions of familiarization are intertwined, and how the introduction of new terms sometimes proves to be emancipatory.

Autoethnography is increasingly used in nursing education research to examine the relational, embodied, and often hidden dimensions of teaching, learning, and professional socialization. Yet uneven use of variant-sensitive approaches, quality frameworks, and ethics reporting suggests continuing methodological inconsistency. We conducted an integrative review of autoethnographic nursing education literature published between 2010 and 2025, examining five dimensions: (1) variant definitions and operationalization, (2) quality appraisal frameworks, (3) reflexivity and positionality practices, (4) credibility strategies, and (5) ethical procedures, including attention to implicated others. Systematic searches of CINAHL, MEDLINE, ERIC, Scopus, ScienceDirect, and Web of Science yielded 23 eligible studies. Collaborative autoethnography predominated (56%), and several studies, especially those examining the experiences of racially minoritized faculty, explicitly positioned autoethnography as a decolonizing approach and demonstrated stronger reported reflexive practices. Reflexivity, as represented in published manuscripts, ranged from integrated positionality analyses that informed analytic decisions to brief, largely token acknowledgment. Findings suggest that nursing education scholarship may benefit from a fit-for-variant approach to appraisal and clearer field expectations for relational ethics reporting, especially given power differentials when faculty write about students, colleagues, and institutions. More explicit linking of standpoint to analysis may advance methodological transparency and interpretive credibility.

Large-scale cooperation is characterized by complex interaction patterns with nonlinear outcomes. Deepening our understanding may be critical to addressing real-world collective challenges.

ABSTRACT Premature termination of transcription (PTT), also known as attenuation, is a conserved gene regulatory mechanism that operates across all domains of life and in viruses. Attenuation enables rapid cellular responses to environmental and metabolic changes and fine-tunes expression of biosynthetic genes. In Saccharomyces cerevisiae , attenuation of RNA Polymerase II (Pol II) transcription was first linked to the Nrd1-Nab3-Sen1 (NNS) termination pathway for non-coding RNAs, and the mRNA 3’-end processing factor Hrp1 has been implicated more recently. Substitutions in Hrp1 RNA Recognition Motifs (RRMs) cause attenuator readthrough and reduce RNA-binding affinity in vitro , but direct evidence for Hrp1 functioning at attenuators in vivo remains limited. Here, we characterized 5’-end RNA terminator elements from several genes, including RAD3 , SNG1 , MNR2 , and CPR8 . Readthrough mutations clustered in AU-rich regions resembling polyadenylation site (pA) efficiency elements, consistent with Hrp1 binding targets. Amino acid substitutions of Hrp1 RRM residue F162 revealed a general requirement for aromaticity in RNA recognition that varied to some degree by gene context. To test Hrp1-RNA interactions independent of other yeast factors, we adapted a bacterial 3-hybrid (B3H) assay. Hrp1 interacted with RNA derived from the GAL7 3’-end pA site and 5’-end terminator regions of RAD3 , MNR2 , and CPR8 . Mutations in AU-rich RNA regions that disrupted Pol II attenuation in yeast generally impaired B3H interactions. However, some Hrp1 mutants (M191T, I270T, D271G, M275V, T280I) retained binding to CPR8 terminator RNA, suggesting their defects require additional yeast components. These results demonstrate that Hrp1 is sufficient to bind multiple UA-rich attenuator RNAs in vivo , expanding Hrp1 function to include early transcription events.

Abstract Maintenance of lipid and redox homeostasis is essential for stress resistance and longevity, but the transcriptional networks coordinating these processes remain incompletely understood. In Caenorhabditis elegans, the transcription factors SKN-1A/Nrf1 and SKN-1C/Nrf2 mediate distinct stress responses that promote proteostasis, lipid homeostasis, and oxidative stress resistance. Here, we identify the Krüppel-like factor KLF-1 as a regulator of lipid accumulation that modulates SKN-1 activity. KLF-1 was required for SKN-1A and SKN-1C activation and for the oxidative stress resistance and longevity of germline-deficient animals, without changing skn-1 transcript abundance. KLF-1 selectively modulated the lipid homeostatic response of SKN-1A but was dispensable for its proteasome recovery response. Genetic and supplementation experiments further indicated that KLF-1 influences SKN-1A activation through lipid accumulation, while its regulation of SKN-1C involves both lipid-dependent and lipid-independent mechanisms. KLF-1 and the related KLF-2 exerted opposing effects on lipid accumulation while acting independently of the lipogenic regulator Sterol regulatory element-Binding Protein 1 (SBP-1/SREBP1). Consistent with these opposing effects, KLF-1 and KLF-2 regulated the expression of unc-51/ULK1, atg-9/ATG9A, and lipl-1/LIPJ/K in opposite directions, implicating lipophagy-associated pathways in their regulation of lipid homeostasis. Together, these findings establish KLF-dependent regulation of lipid homeostasis as an upstream physiological determinant of SKN-1 activity, linking lipid metabolism with oxidative stress resistance and longevity.