58 research outputs found

    A Multiplicity of Holes:MarilĂ­a Librandi

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    This talk focuses on the material, artistic, narrative, and shamanic images of nets, ’redes‘, in Portuguese. Besides referring to fishing nets (’redes de pescar‘) and to the digital social networks, ‘redes‘, has received an interesting extension: it also refers to hammocks (called ’redes de dormir‘) since Pero Vaz de Caminha, in his 1500’s Letter of Discovery, translated the surprising technnology of the Tupinambá’s Indigenous hammocks (in Tupi, ’ini‘; in Aruak, ’hamaca‘) he saw in the coast of Brazil through an analogy with the fishing nets. From this tangle of nets, Marilia Librandi weaves this talk. Hammocks are an Amerindian artifact par excellence, found from the Antilles to South America. Fishing nets are an artifact of riverside communities that are being more and more attacked through the building of dams and mining activities empoisoning waters and people’s lives. From these two materials, fishing nets and hammocks, the idea is to explore a chain of free associations: from hammocks to shamanic dreams, from fishing nets to aquatic beings and ’acoustic baits‘ (Albert). Examples from literature, ethnographies, and the visual arts will help to think the net as a territory of activist, ecological and artistic interactions in relation to Amerindian and riverside cosmogonies. Marilía Librandi is a writer and literary theorist; her work intersects Indigenous knowledge and Western literary theory. Holding a PhD in Literary Theory and Comparative Literature from the Universidade de São Paulo, she is currently affiliated with the Brazil Lab at Princeton University and collaborates with the Graduate Research Center “Diversitas. Humanities, Rights and Other Legitimacies” at the University of São Paulo. After teaching at the Southwest State University of Bahia, she taught Brazilian Literature at Stanford University from 2008 to 2018. Her publications include Writing by Ear. Clarice Lispector and the Aural Novel (University of Toronto Press, 2018), Maranhão-Manhattan. Ensaios de literatura brasileira (2009) and Transpoetic Exchange. Haroldo de Campos, Octavio Paz and Other Multiversal Dialogues (2020).‘A Multiplicity of Holes: Marilía Librandi’, lecture presented at the workshop Intra/ Sections: Post-Anthropocentric Concepts of Multiplicity, ICI Berlin, 24 March 2022, video recording, mp4, 55:29 <https://doi.org/10.25620/e220324-1

    Impact of Right Atrial Physiology on Heart Failure and Adverse Events after Myocardial Infarction

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    Background: Right ventricular (RV) function is a known predictor of adverse events in heart failure and following acute myocardial infarction (AMI). While right atrial (RA) involvement is well characterized in pulmonary arterial hypertension, its relative contributions to adverse events following AMI especially in patients with heart failure and congestion need further evaluation. Methods: In this cardiovascular magnetic resonance (CMR)-substudy of AIDA STEMI and TATORT NSTEMI, 1235 AMI patients underwent CMR after primary percutaneous coronary intervention (PCI) in 15 centers across Germany (n = 795 with ST-elevation myocardial infarction and 440 with non-ST-elevation MI). Right atrial (RA) performance was evaluated using CMR myocardial feature tracking (CMR-FT) for the assessment of RA reservoir (total strain Δs), conduit (passive strain Δe), booster pump function (active strain Δa), and associated strain rates (SR) in a blinded core-laboratory. The primary endpoint was the occurrence of major adverse cardiac events (MACE) 12 months post AMI. Results: RA reservoir (Δs p = 0.061, SRs p = 0.049) and conduit functions (Δe p = 0.006, SRe p = 0.030) were impaired in patients with MACE as opposed to RA booster pump (Δa p = 0.579, SRa p = 0.118) and RA volume index (p = 0.866). RA conduit function was associated with the clinical onset of heart failure and MACE independently of RV systolic function and atrial fibrillation (AF) (multivariable analysis hazard ratio 0.95, 95% confidence interval 0.92 to 0.99, p = 0.009), while RV systolic function and AF were not independent prognosticators. Furthermore, RA conduit strain identified low- and high-risk groups within patients with reduced RV systolic function (p = 0.019 on log rank testing). Conclusions: RA impairment is a distinct feature and independent risk factor in patients following AMI and can be easily assessed using CMR-FT-derived quantification of RA strain

    Intra/ Sections:Post-Anthropocentric Concepts of Multiplicity

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    The DFG-Network ‘Dispositiv der Menge’ (= crowd, mass, multitude) is based on the recognition that ‘the crowd’ has been constituted, classified, regulated, or dispersed throughout history in various, heterogenous, conflictual ways, which make it impossible to hold onto any understanding of the crowd as a clearly delimited and substantiated entity or to the forms in which it is represented as such. This workshop extends this approach by taking ‘the crowd’ itself as a multitude or multiplicity. It will address phenomena related to more fluctuating and in/determinate intra/sections of collectivities in order to transform the image of ‘the crowd’ from an in-divi-dual-ized One into a mani-fold multiplicity. Such a multiplicity in the singular plural is characterized by movement and motion, fragmentation and friction, ongoingness and inherent contestation. By focusing on this multiplicity, the workshop seeks to un-work a persistent conceptual anthropocentrism of the ways in which agentiality is conceptualized and imagined, instead searching for more dynamic relations with/in a variety of agencies (human, animal, plant, things, propositions) that can be seen as ‘intra-active’. Yet, while ‘the crowd’ will be approached from a critique of anthropomorphism, the turn towards ecological or relational co-existence cannot be a turn away from the violent asymmetrical relations of power and the continued flexibilization and hierarchical re- ordering of global social structures. The workshop sounds out conceptual and phenomenal resonances between what in Western academic discourses has of late become known as ‘New Materialism’ (in its different strands) and the long tradition of (but also always newly emerging) indigenous and decolonial epistemologies. The idea is to look for ways to concretize the potential for intra/sections in-between posthuman(ist) and indigenous/decolonial thought-practices, hoping for a dialogue between more Western-oriented approaches — e.g., actor-network theory (Bruno Latour), the figures of the cyborg and companion species (Donna Haraway), vital materialism (Jane Bennett), un/limited ecologies (Vicky Kirby), or agential realism (Karen Barad) — and alternative indigenous cosmologies and ethical praxes such as ‘buen vivir/sumac kawsay’ (Alberto Acosta/Eduardo Gudynas), Amerindian perspectivalism (Eduardo Viveiros de Castro) or shape-shifting border/lands (AnzaldĂșa). The workshop invites its participants to diffract heterogeneous ways of thinking and enacting multiplicity. Collecting insights from literary and cultural studies, natural sciences, sociology, non-western cosmologies, or religion, it hopes to produce a vision of how a post- anthropocentric perspective can enrich an understanding of ‘world’ as a plurivocal worlding process.Intra/ Sections: Post-Anthropocentric Concepts of Multiplicity, workshop, ICI Berlin, 24–25 March 2022 <https://doi.org/10.25620/e220324

    SAMHD1-Deficient CD14+ Cells from Individuals with Aicardi-GoutiĂšres Syndrome Are Highly Susceptible to HIV-1 Infection

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    Myeloid blood cells are largely resistant to infection with human immunodeficiency virus type 1 (HIV-1). Recently, it was reported that Vpx from HIV-2/SIVsm facilitates infection of these cells by counteracting the host restriction factor SAMHD1. Here, we independently confirmed that Vpx interacts with SAMHD1 and targets it for ubiquitin-mediated degradation. We found that Vpx-mediated SAMHD1 degradation rendered primary monocytes highly susceptible to HIV-1 infection; Vpx with a T17A mutation, defective for SAMHD1 binding and degradation, did not show this activity. Several single nucleotide polymorphisms in the SAMHD1 gene have been associated with Aicardi-GoutiĂšres syndrome (AGS), a very rare and severe autoimmune disease. Primary peripheral blood mononuclear cells (PBMC) from AGS patients homozygous for a nonsense mutation in SAMHD1 (R164X) lacked endogenous SAMHD1 expression and support HIV-1 replication in the absence of exogenous activation. Our results indicate that within PBMC from AGS patients, CD14+ cells were the subpopulation susceptible to HIV-1 infection, whereas cells from healthy donors did not support infection. The monocytic lineage of the infected SAMHD1 -/- cells, in conjunction with mostly undetectable levels of cytokines, chemokines and type I interferon measured prior to infection, indicate that aberrant cellular activation is not the cause for the observed phenotype. Taken together, we propose that SAMHD1 protects primary CD14+ monocytes from HIV-1 infection confirming SAMHD1 as a potent lentiviral restriction factor

    Generation and characterization of embryonic stem cell lines derived from the YAC128 mouse model of Huntington disease.

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    Huntington Disease (HD) is an autosomal dominant neurodegenerative disorder caused by a CAG trinucleotide repeat expansion in the Huntingtin gene. Patients typically present in mid-life with progressive motor dysfunction, cognitive deficits, and neuropsychiatric abnormalities. Recently, researchers have provided evidence that HD is associated with significant pathology in peripheral tissues as well. At the current time no effective treatment has been proven to alter or cure progression of HD which leads to complete loss of independence and eventual death an average of 20 years after disease onset. The ability to model Huntington disease in animals has enabled studies which have provided new insights into the mechanisms of HD pathogenesis. However, the development of simple cell culture-based systems will be useful to accelerate our research efforts into the basic underlying pathogenic pathways of HD and will allow dissection of cellular interactions and the identification of novel targets for intervention that offer the greatest hope of a cure. The YAC mouse model of HD expresses full-length human Huntingtin with either 18 polyglutamines (YAC18) or 128 polyglutamines (YAC128), and develops age-dependent cognitive deficits, motor dysfunction, and selective striatal neurodegeneration similar to that seen in human HD patients. I have generated novel embryonic stem (ES) cell lines from wild-type, YAC18 and YAC128 mice on two genetic backgrounds. These cell lines have been cultured under defined conditions over long periods of time, and express characteristic markers of pluripotency, such as alkaline phosphatase, Oct-4 and Nanog. Neurons and macrophages derived from these novel cell lines using established in vitro protocols have been characterized via immunocytochemistry and challenged in functional assays. To confirm results attained from functional assays in our ES-derived macrophages, I examined primary macrophages and microglia cultures derived from the YAC mice and determined the functional response of these cells to endotoxin stimulation. Primary cell cultures isolated from YAC128 mice produced significantly more IL-6 than wild-type cultures. In comparison, with the same endotoxin stimulation, YAC18 primary macrophages and microglia responded with similar levels of IL-6 release as cultures of wild-type cells, suggesting that the over-activity in the YAC128 cytokine response is caused by the mutant Huntingtin transgene.Medicine, Faculty ofMedical Genetics, Department ofGraduat
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