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- Berríos-Negrón, Luis, 1971-
(författare)
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Breathtaking Greenhouse Parastructures : a supplement to the Arcades Project from a Caribbean Perspective [and a call for a careful practice of epistemológica].
- 2020
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Konstnärligt arbete (övrigt vetenskapligt/konstnärligt)abstract
- Breathtaking Greenhouse Parastructures is a doctoral work that supplements the unfinished modern opus The Arcades Project [in German Das Passagen-Werk (Mit Bindestrich und Werk mit Capital W) ]. The supplement takes the form of a sculptural, historical, and technological deposition of ‘greenhouse’ that presently oscillates between a past-background and future-foreground to Walter Benjamin's ‘theatrical’ handling of the Parisian arcades. From my Caribbean perspective, that oscillating treatment of ‘greenhouse’ affords me a prop from which to activate the following question: is colonial memory the drive of Global Warming? That core question has led me to retrospectively hypothesise that the technology of ‘greenhouse’ is—beyond metaphor—the illusory (dis)embodiment of the toxic binaries of interior & exterior that are still shaping various influential frameworks such as the modern & Marxian ideas of superstructure, as well as the past & future of Western natural sciences (and their histories). Because of that illusory, spectral, if paranormal power, ‘greenhouse’ becomes at once the Western colonial enframing to both the messianic promise for conserving biological history, as well as the messianic remedy to suppress the traumæ that are destining Global Warming. Also, because of that potent (dis)embodied character, the robust analysis of the manifold instrumentalisation of ‘greenhouse’ is set to play a primary role in deposing the geological timeline of the Anthropocene. Now, while the book-supplement is itself the dissertation (as an unpacking of the aforementioned hypothetical findings), the PhD also relies on two other research devices that are worth mentioning: an installation (titled Anarquivo Negantrópico), and an online journal (titled Intransitive Journal). Altogether, the dissertation offers a field from which to asses my broader experimentation with infrastructures, epistemic things, and social pedestals. Moreover, the dissertation revises the so-called forgotten list of ‘Epistemologica’ (the categorical of Western display preparations and phenomenotechnologies) so to format my study and practice into an adaptable, careful, and differentiated kind of epistemológica…a careful study and practice that we may share as object-relations that proportionately (dis)play more-than-human perspectives for (re)mediating the forms and forces of the climate crises.
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2. |
- Feldhahn, Niklas, et al.
(författare)
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Activation-induced cytidine deaminase acts as a mutator in BCR-ABL1-transformed acute lymphoblastic leukemia cells
- 2007
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Ingår i: Journal of Experimental Medicine. - : Rockefeller University Press. - 0022-1007 .- 1540-9538. ; 204:5, s. 1157-1166
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Tidskriftsartikel (refereegranskat)abstract
- The Philadelphia chromosome (Ph) encoding the oncogenic BCR-ABL1 kinase defines a subset of acute lymphoblastic leukemia (ALL) with a particularly unfavorable prognosis. ALL cells are derived from B cell precursors in most cases and typically carry rearranged immunoglobulin heavy chain (IGH) variable (V) region genes devoid of somatic mutations. Somatic hypermutation is restricted to mature germinal center B cells and depends on activation-induced cytidine deaminase (AID). Studying AID expression in 108 cases of ALL, we detected AID mRNA in 24 of 28 Ph(+) ALLs as compared with 6 of 80 Ph(-) ALLs. Forced expression of BCR-ABL1 in Ph(-) ALL cells and inhibition of the BCR-ABL1 kinase showed that aberrant expression of AID depends on BCR-ABL1 kinase activity. Consistent with aberrant AID expression in Ph(+) ALL, IGH V region genes and BCL6 were mutated in many Ph(+) but unmutated in most Ph(-) cases. In addition, AID introduced DNA single-strand breaks within the tumor suppressor gene CDKN2B in Ph(+) ALL cells, which was sensitive to BCR-ABL1 kinase inhibition and silencing of AID expression by RNA interference. These findings identify AID as a BCR-ABL1-induced mutator in Ph(+) ALL cells, which may be relevant with respect to the particularly unfavorable prognosis of this leukemia subset.
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