Suffering, Justice, and the Politics of Becoming

Also CSST Working Paper #113.http://deepblue.lib.umich.edu/bitstream/2027.42/51304/1/540.pd

Freedom, Teleodynamism, Creativity

After presenting a critique of both negative and positive freedom this essay pursues the relation between creativity and freedom, drawing upon Foucault, Deleuze and Nietzsche to do so.  Once you have understood Nietzsche’s reading of a culturally infused nest of drives in a self, the task becomes easier.  A drive is not merely a force pushing forward; it is also a simple mode of perception and intention that pushes forward and enters into creative relations with other drives when activated by an event.  You can also understand more sharply how the Foucauldian tactics of the self work.  We can now carry this insight into the Deleuzian territory of micropolitics and collective action by reviewing his work on flashbacks and “the powers of the false.” If a flashback in film pulls us back to a bifurcation point where two paths were possible and one was taken, the powers of the false refer to the subliminal role the path not taken can play in the formation of creative action.  As you pursue these themes you see that neither old, organic notions of belonging to the world nor do negative notions of detachment as such do the work needed.  Deleuze’s notion of freedom carries us to the idea of cultivating “belief” in a world of periodic punctuations.  The latter are essential to creativity and incompatible with organic belonging.  They are also indispensable supports of a positive politics today

Recombination-Based In Vivo Expression Technology Identifies Helicobacter Pylori Genes Important For Host Colonization

Here we undertook to identify colonization and gastric disease-promoting factors of the human gastric pathogen Helicobacter pylori as genes that were induced in response to the stomach environment. Using recombination-based in vivo expression technology (RIVET), we identified six promoters induced in the host compared to laboratory conditions. Three of these promoters, designated Pivi10, Pivi66, and Pivi77, regulate genes that H. pylori may use to interact with other microbes or the host. Pivi10 likely regulates the mobA, mobB, and mobD genes, which have potential roles in horizontal gene transfer through plasmid mobilization. Pivi66 occurs in the cytotoxin-associated gene pathogenicity island, a genomic region known to be associated with more severe disease outcomes, and likely regulates cagZ, virB11, and virD4. Pivi77 likely regulates HP0289, an uncharacterized paralogue of the vacA cytotoxin gene. We assessed the roles of a subset of these genes in colonization by creating deletion mutants and analyzing them in single-strain and coinfection experiments. We found that a mobABD mutant was defective for murine host colonization and that a cagZ mutant outcompeted the wild-type strain in a coinfection analysis. Our work supports the conclusion that RIVET is a valuable tool for identifying H. pylori factors with roles in host colonization

Ghosts in the Smart Home

We are in the midst of a ‘post-anthropocentric’ turn in design, research and technology. The term refers to a renewed interest in a wide range of concepts, theoretical perspectives, and methodologies. Ghosts in the Smart Home is a post-anthropocentric experiment which manifests as a film whose cast of characters are all internet connected ‘smart’ devices. The motivation is to prototype and establish new ways to see, to be, and to know, which respond to the 21st century’s complex socio-technical system

Regulation and localization of endogenous human tristetraprolin

Tumor necrosis factor (TNF) has been implicated in the development and pathogenicity of infectious diseases and autoimmune disorders, such as septic shock and arthritis. The zinc-finger protein tristetraprolin (TTP) has been identified as a major regulator of TNF biosynthesis. To define its intracellular location and examine its regulation of TNF, a quantitive intracellular staining assay specific for TTP was developed. We establish for the first time that in peripheral blood leukocytes, expression of endogenous TTP is confined to the cytoplasm. Baseline expression of TTP was higher in monocytes than in lymphocytes or neutrophils. After in vitro incubation with lipopolysaccharide (LPS), leukocyte TTP levels increased rapidly, peaking after approximately 2 hours. Monocytes showed the greatest response to LPS stimulation and lymphocytes the least. TTP levels were also studied in leukocytes isolated from healthy volunteers infused with a bolus dose of LPS. TTP expression and initial upregulation in response to LPS infusion were consistent with the in vitro data. Neutrophil TTP levels responded first, reaching an initial peak within 1 hour, monocyte levels peaked next at 2 hours, followed by lymphocytes at 4 hours. This response paralleled plasma TNF levels, which peaked 2 hours after infusion and were no longer detectable after 12 hours. A second rise in intracellular TTP levels, which did not parallel plasma TNF levels, was observed in all leukocyte populations, starting 12 hours after infusion. These data establish the cytoplasmic location of TTP, supporting a major role for this protein in regulating TNF production, and suggest that TTP levels are not regulated solely by TNF

Temporal pattern of C1q deposition after transient focal cerebral ischemia

Recent studies have focused on elucidating the contribution of individual complement proteins to post-ischemic cellular injury. As the timing of complement activation and deposition after cerebral ischemia is not well understood, our study investigates the temporal pattern of C1q accumulation after experimental murine stroke. Brains were harvested from mice subjected to transient focal cerebral ischemia at 3, 6, 12, and 24 hr post reperfusion. Western blotting and light microscopy were employed to determine the temporal course of C1q protein accumulation and correlate this sequence with infarct evolution observed with TTC staining. Confocal microscopy was utilized to further characterize the cellular localization and characteristics of C1q deposition. Western Blot analysis showed that C1q protein begins to accumulate in the ischemic hemisphere between 3 and 6 hr post-ischemia. Light microscopy confirmed these findings, showing concurrent C1q protein staining of neurons. Confocal microscopy demonstrated co-localization of C1q protein with neuronal cell bodies as well as necrotic cellular debris. These experiments demonstrate the accumulation of C1q protein on neurons during the period of greatest infarct evolution. This data provides information regarding the optimal time window during which a potentially neuroprotective anti-C1q strategy is most likely to achieve therapeutic success. © 2006 Wiley-Liss, Inc.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/50651/1/20775_ftp.pd