Editorial: The Intersectionality of Hate

Editorial for Atlantis 39.1 Special Section on the Intersectionality of Hat

Introduction: Intimacies/Affect

Introduction: Intimacies/Affec

Non-monogamies and the space of discourse theorizing the intersections of non/monogamy and intimate privilege in the public sphere

This dissertation uses genealogical discourse analysis to unpack recent Western conceptions of monogamy and non-monogamy in the public sphere. Beginning from the premise that discourses surrounding monogamy and non-monogamy (taken together as a system of non/monogamy) have come into particular prominence in recent years, this dissertation deploys a thread of queer theory focused on the study of broader conceptions of "intimacy" to explore the ramifications of such a prominence in the public sphere. More specifically, drawing on theorizations of spatiality (Temporary Autonomous Zones, Mapping/Reterritorialization, Heterotopia) and the concept of "privilege", I formulate the theoretical lens of "intimate privilege" to explore how non/monogamy is distributed throughout, takes up, and creates forms of intimate space. In exploding the overly-simple notion that monogamous sexuality is societally privileged, while non-monogamies are marginalized, I show how while there is a societal meta-narrative that centres monogamy, it is really the intersectionality of non/monogamy with other forms of privilege/oppression that truly locates a subject practicing (or connected to) non-monogamous intimacy as having intimate privilege, defined as the emergent state in which one's intimacies hold societal privilege. Engaging in theoretical and discursive analyses of the contemporary public sphere presences of three major forms of non-monogamy (adultery, polygamy and polyamory) through texts such as journalistic articles, policy documents, self-help literature, television programs and Internet sites, I continue the academic discussion surrounding non-monogamies that is just beginning to come into its own in the fields of social science and humanities, as well as to complicate less-nuanced discourses on non/monogamy that are circulating more broadly in the public sphere

Queer digital cultures

This chapter examines queer digital culture, a term that refers to the ways in which LGBTQ+ identities, practices, and theories have been mixed up in the emergence, design, and constitution of digital technology. It highlights significant shifts at the intersections of queer identity and politics and digital communication technologies from the 1980s to the early twenty-first century, including transitions from textual to audiovisual media; from subcultural to mainstream politics; from utopian political aspirations (Afrofuturism; cyberfeminism; cyberqueer) to commercialization; and from identity play and performance to consumer authentication. It concludes by drawing out the contradictory dimensions of queer digital culture which both exacerbate forms of oppression and offer liberatory trajectories. Alongside the rise of new forms of heteroactivism, commodified identities, and ubiquitous but unequal digital access, LGBTQ+ digital media continues to offer the promise of solidarity and intervention in relation to social justice

Intimacies/affect

Open access. Article licensed under a CC-BY-NO-ND 3.0 Unported LicenseAbstract not available.Ye

In vivo Partial Reprogramming by Bacteria Promotes Adult Liver Organ Growth without Fibrosis and Tumorigenesis

Ideal therapies for regenerative medicine or healthy aging require healthy organ growth and rejuvenation, but no organ-level approach is currently available. Using Mycobacterium leprae (ML) with natural partial cellular reprogramming capacity and its animal host nine-banded armadillos, we present an evolutionarily refined model of adult liver growth and regeneration. In infected armadillos, ML reprogram the entire liver and significantly increase total liver/body weight ratio by increasing healthy liver lobules, including hepatocyte proliferation and proportionate expansion of vasculature, and biliary systems. ML-infected livers are microarchitecturally and functionally normal without damage, fibrosis, or tumorigenesis. Bacteria-induced reprogramming reactivates liver progenitor/developmental/fetal genes and upregulates growth-, metabolism-, and anti-aging-associated markers with minimal change in senescence and tumorigenic genes, suggesting bacterial hijacking of homeostatic, regeneration pathways to promote de novo organogenesis. This may facilitate the unraveling of endogenous pathways that effectively and safely re-engage liver organ growth, with broad therapeutic implications including organ regeneration and rejuvenation

Reprogramming diminishes retention of Mycobacterium leprae in Schwann cells and elevates bacterial transfer to fibroblasts

Background: Bacterial pathogens can manipulate or subvert host tissue cells to their advantage at different stages during infection, from initial colonization in primary host niches to dissemination. Recently, we have shown that Mycobacterium leprae (ML), the causative agent of human leprosy, reprogrammed its preferred host niche de-differentiated adult Schwann cells to progenitor/stem cell-like cells (pSLC) which appear to facilitate bacterial spread. Here, we studied how this cell fate change influences bacterial retention and transfer properties of Schwann cells before and after reprogramming. Results: Using primary fibroblasts as bacterial recipient cells, we showed that non-reprogrammed Schwann cells, which preserve all Schwann cell lineage and differentiation markers, possess high bacterial retention capacity when co-cultured with skin fibroblasts; Schwann cells failed to transfer bacteria to fibroblasts at higher numbers even after co-culture for 5 days. In contrast, pSLCs, which are derived from the same Schwann cells but have lost Schwann cell lineage markers due to reprogramming, efficiently transferred bacteria to fibroblasts within 24 hours. Conclusions: ML-induced reprogramming converts lineage-committed Schwann cells with high bacterial retention capacity to a cell type with pSLC stage with effective bacterial transfer properties. We propose that such changes in cellular properties may be associated with the initial intracellular colonization, which requires long-term bacterial retention within Schwann cells, in order to spread the infection to other tissues, which entails efficient bacterial transfer capacity to cells like fibroblasts which are abundant in many tissues, thereby potentially maximizing bacterial dissemination. These data also suggest how pathogens could take advantage of multiple facets of host cell reprogramming according to their needs during infection

Despite the presence of UVB-induced DNA damage, HLA-DR+ cells from ex vivo UVB-exposed human skin are able to migrate and show no impaired allostimulatory capacity

In this study, we investigated the effect of ultraviolet B radiation on human Langerhans cell function. Normal human skin was irradiated ex vivo with single doses of ultraviolet B. For assessment of T-cell stimulatory function, cells that spontaneously migrated from epidermal sheets were used, whereas full-thickness skin biopsies were used to investigate alterations in migratory properties. The cells migrating from ultraviolet B-exposed epidermal sheets demonstrated a decrease in the percentage of HLA-DR positive Langerhans cells, as well as a reduced capacity to induce proliferation of allogeneic T cells, when compared with cells migrating from nonexposed sheets. When a correction was made for the decreased number of HLA-DR positive Langerhans cells migrating from ultraviolet B-exposed epidermis, however, it appeared that the capacity to induce T-cell proliferation was identical for Langerhans cells migrating from ultraviolet B-exposed and nonexposed epidermis. The presence of ultraviolet B-induced DNA damage could be demonstrated in the Langerhans cells from ultraviolet B-treated skin, indicating that the cells had received significant doses of ultraviolet B. As regards the effect of ultraviolet B on migratory properties of Langerhans cells, we found not only that reduced numbers of CD1a-positive Langerhans cells migrated from the ultraviolet B-exposed full-thickness skin, but also that there was a reduction in CD1a-positive Langerhans cells in the epidermis. This implies that ultraviolet B induces death of Langerhans cells as well as loss of cell surface molecules rather than altering Langerhans cells migration, whereas the Langerhans cells that were still able to migrate fully retained the capacity to activate allogeneic T cells