Affective technologies of welfare deterrence in Australia and the United Kingdom

Across the political spectrum of different historical periods, welfare deterrence has shaped social security and immigration policy in both Australia and the United Kingdom. Deterrence discourages access to state welfare through the production and mobilization of negative affect to deter specific groups from claiming state support, and by crafting public affect (of fear and disgust) about these target populations in order to garner consent for punitive policies. In this paper, we argue that deterrence works as a human technology where the crafting of negative affect operates as a technology of statecraft. Through critical juxtaposition and multiple genealogies of deterrence, this paper meshes time and space, and colony/colonizer and metropole, to show the historical and contemporary connectivity of the affective nature of deterrence. We identify five main operations that produce the ‘feel’ of deterrence: stigmatization by design, destitution by design, deterrent architecture, the control of movement, and the centrality of labour; as well as tracing the political economy of deterrence

ADAM28 deletion in mice impacts lung metastasis formation

ADAM28 expression is upregulated in non-small cell lung carcinoma and correlated with cell proliferation and metastatic dissemination. In addition, ADAM28 is thought to be an important regulator of inflammatory signaling pathways as this protease shed the pro-inflammatory cytokine, pro-TNF-alpha. ADAM28 also interacts with integrins and a P-selectin ligand (PSGL-1) involved in inflammatory cell migration. All these findings suggest that ADAM28 contributes to cancer development and progression. This project aims to characterize the effects of host-derived ADAM28 on lung metastasis formation using an ADAM28-/- mouse model. Lewis Lung Carcinoma cells and B16K1 melanoma cells were intravenously injected in ADAM28-/- and wild-type (WT) mice. An unexpected increased tumor development was found in lungs of ADAM28-/- mice. As ADAM28 is associated with lymphocyte transendothelial migration, lymphocyte subtypes implicated in tumor cytotoxicity or in regulation of immune response were studied by flow cytometry. Results showed that less CD8+ T and NK cells were infiltrated within lungs of ADAM28-/- tumor-bearing mice as compared to WT mice. Moreover, less CD8+ T cells were counted within the spleen of naïve ADAM28-/- mice. These data were confirmed in a mouse model where 4T1 breast carcinoma cells were intravenously injected in ADAM28-/- BALB/c mice. Intrinsic properties of CD8+ T cells from ADAM28-/- mice were not affected by ADAM28 depletion as they were able to proliferate, to be activated and to migrate. Further investigations are required to explain the CD8+ T cell phenotype in ADAM28-deficient mice. Our results suggest a protective effect of ADAM28 derived from the host microenvironment by indirectly regulate the immune response. This is an ERS International Congress abstract. No full-text version is available. Further material to accompany this abstract may be available at www.ers-education.org (ERS member access only)

Transfer function analysis of dynamic cerebral autoregulation: a CARNet white paper 2022 update

Cerebral autoregulation (CA) refers to the control of cerebral tissue blood flow (CBF) in response tochanges in perfusion pressure. Due to the challenges of measuring intracranial pressure, CA is oftendescribed as the relationship between mean arterial pressure (MAP) and CBF. Dynamic CA (dCA) canbe assessed using multiple techniques, with transfer function analysis (TFA) being the most common.A 2016 white paper by members of an international Cerebrovascular Research Network (CARNet)that is focused on CA strove to improve TFA standardization by way of introducing data acquisition,analysis, and reporting guidelines. Since then, additional evidence has allowed for the improvementand refinement of the original recommendations, as well as for the inclusion of new guidelines toreflect recent advances in the field. This second edition of the white paper contains more robust,evidence-based   recommendations,   which   have   been   expanded   to   address   current   streams   ofinquiry, including optimizing MAP variability, acquiring CBF estimates from alternative methods,estimating   alternative   dCA   metrics,   and   incorporating   dCA   quantification   into   clinical   trials.Implementation of these new and revised recommendations is important to improve the reliabilityand   reproducibility   of   dCA   studies,   and   to   facilitate   inter-institutional   collaboration   and   thecomparison of results between studies.</p