Text and Subject Position after Althusser

Althusser\u27s achievement is that he redefined Marxism. He reconceptualizes history and totality in terms of different times, construes knowledge as the outcome of a process of construction, and interprets subjectivity as an effect of ideology and unconscious processes. Unfortunately, Althusser\u27s functionalist view of ideology claims that the subject recognizes itself as a subject because it duplicates— reflects—an absolute subject. However, Lacan\u27s notion of the mirror stage remedies this fault. Lacan\u27s subject always misrecognizes itself in a process of contradiction that threatens the stability of any given social order. Moreover, unlike Foucault\u27s subject, which is limited in that subjectivity is folded back into a vaguely expanded notion of power, this revised Althusserian subject allows careful reading of texts. The critic does not simply read against the grain; he or she exposes the multiple points of identification offered the reader. For example, Wordsworth\u27s The Solitary Reaper installs the reader in multiple positions: a devotee of high culture and the national canon, a lover of the verbal signifier and its play, a consumer of confessional discourse, and a masculine I desiring a laboring, singing woman

Translation Studies versus Comparative Literature?

Comparative literature is one of the main disciplines out of which translation studies emerged, so it is hardly surprising if at times the relationship between the two subjects has been marked by antagonism. Comparative literary scholars, in particular – perennially anxious about the status of comparative literature itself – have argued that their discipline has been subsumed and superseded by translation studies. Yet in recent decades the two subject areas have also been growing further apart, to the extent that Susan Bassnett, one of the key exponents of the antagonistic view, has modified her stance and argued instead for a rapprochement between the two under the heading of intercultural studies

Genetic mechanisms of critical illness in COVID-19.

Host-mediated lung inflammation is present1, and drives mortality2, in the critical illness caused by coronavirus disease 2019 (COVID-19). Host genetic variants associated with critical illness may identify mechanistic targets for therapeutic development3. Here we report the results of the GenOMICC (Genetics Of Mortality In Critical Care) genome-wide association study in 2,244 critically ill patients with COVID-19 from 208 UK intensive care units. We have identified and replicated the following new genome-wide significant associations: on chromosome 12q24.13 (rs10735079, P = 1.65 × 10-8) in a gene cluster that encodes antiviral restriction enzyme activators (OAS1, OAS2 and OAS3); on chromosome 19p13.2 (rs74956615, P = 2.3 × 10-8) near the gene that encodes tyrosine kinase 2 (TYK2); on chromosome 19p13.3 (rs2109069, P = 3.98 ×  10-12) within the gene that encodes dipeptidyl peptidase 9 (DPP9); and on chromosome 21q22.1 (rs2236757, P = 4.99 × 10-8) in the interferon receptor gene IFNAR2. We identified potential targets for repurposing of licensed medications: using Mendelian randomization, we found evidence that low expression of IFNAR2, or high expression of TYK2, are associated with life-threatening disease; and transcriptome-wide association in lung tissue revealed that high expression of the monocyte-macrophage chemotactic receptor CCR2 is associated with severe COVID-19. Our results identify robust genetic signals relating to key host antiviral defence mechanisms and mediators of inflammatory organ damage in COVID-19. Both mechanisms may be amenable to targeted treatment with existing drugs. However, large-scale randomized clinical trials will be essential before any change to clinical practice

Literary into cultural studies

Antony Easthope.xii, 202 p. : ill. ; 23 cm

“He Was Struck Out. Deleted”: We Need to Talk about Wesley in Nicola Barker’s Behindlings

From Crossref journal articles via Jisc Publications RouterHistory: epub 2021-02-18, issued 2021-02-1