Queer Affect Theory : Zum Verhältnis von Affekt und Trieb bei Sedgwick und Freud

Im Feld von Queer Theory, das entscheidende Impulse für die neuere Affekt-Diskussion lieferte, bleibt der Status des Affekts oft ungeklärt. Dieses lässt sich durch eine Kontrastierung der Affekt-Theorie Sedgwicks mit Freud nachholen. Wie die Lektüre zeigt, beerbt der Begriff des Affekts in mancher Hinsicht den des Triebes und liefert so Anhaltspunkte dafür, die Psychoanalyse affekttheoretisch auszulegen. Ausgehend von dieser Nähe der Diskurse zueinander, lässt sich aber auch herausstellen, wo Affekt-Theorie nicht mehr der Psychoanalyse folgt. Jenseits psychoanalytischer Mythologien beansprucht sie nicht länger, Endlichkeit und Gewalt als Bedingungen menschlicher Existenz zu verhandeln. // Within the field of queer theory, which has delivered important impulses for more recent discussions of affect, the status of affect nonetheless often remains vague. This shortcoming can be responded to by juxtaposing Sedgwick’s affect theory with Freud. As a close reading of their texts shows, the concept of affect in some ways inherits the concept of the drive. This allows for a reading of psychoanalysis as affect theory. Taking the proximity of these discourses as a point of departure, we then see, however, where affect theory departs from psychoanalysis. Moving beyond psychoanalytic mythologies, affect theory no longer claims to address finitude and violence as conditions of human existence

Ccl2 and Ccl3 Mediate Neutrophil Recruitment via Induction of Protein Synthesis and Generation of Lipid Mediators

Objective: Although the chemokines monocyte chemoattractant protein-1 (Ccl2/JE/MCP-1) and macrophage inflammatory protein-1α (Ccl3/MIP-1α) have recently been implicated in neutrophil migration, the underlying mechanisms remain largely unclear. Methods and Results: Stimulation of the mouse cremaster muscle with Ccl2/JE/MCP-1 or Ccl3/MIP-1α induced a significant increase in numbers of firmly adherent and transmigrated leukocytes (>70% neutrophils) as observed by in vivo microscopy. This increase was significantly attenuated in mice receiving an inhibitor of RNA transcription (actinomycin D) or antagonists of platelet activating factor (PAF; BN 52021) and leukotrienes (MK-886; AA-861). In contrast, leukocyte responses elicited by PAF and leukotriene-B4 (LTB4) themselves were not affected by actinomycin D, BN 52021, MK-886, or AA-861. Conversely, PAF and LTB4, but not Ccl2/JE/MCP-1 and Ccl3/MIP-1α, directly activated neutrophils as indicated by shedding of CD62L and marked upregulation of CD11b. Moreover, Ccl2/JE/ MCP-1- and Ccl3/MIP-1α-elicited leakage of fluorescein isothiocyanate dextran as well as collagen IV remodeling within the venular basement membrane were completely absent in neutrophil-depleted mice. Conclusions: Ccl2/JE/MCP-1 and Ccl3/MIP-1α mediate firm adherence and (subsequent) transmigration of neutrophils via protein synthesis and secondary generation of leukotrienes and PAF, which in turn directly activate neutrophils. Thereby, neutrophils facilitate basement membrane remodeling and promote microvascular leakage

Atrial Natriuretic Peptide Protects against Histamine-Induced Endothelial Barrier Dysfunction in Vivo

Endothelial barrier dysfunction is a hallmark of many severe pathologies, including sepsis or atherosclerosis. The cardiovascular hormone atrial natriuretic peptide (ANP) has increasingly been suggested to counteract endothelial leakage. Surprisingly, the precise in vivo relevance of these observations has never been evaluated. Thus, we aimed to clarify this issue and, moreover, to identify the permeability-controlling subcellular systems that are targeted by ANP. Histamine was used as important pro-inflammatory, permeability-increasing stimulus. Measurements of fluorescein isothiocyanate (FITC)-dextran extravasation from venules of the mouse cremaster muscle and rat hematocrit values were performed to judge changes of endothelial permeability in vivo. It is noteworthy that ANP strongly reduced the histamine-evoked endothelial barrier dysfunction in vivo. In vitro, ANP blocked the breakdown of transendothelial electrical resistance (TEER) induced by histamine. Moreover, as judged by immunocytochemistry and Western blot analysis, ANP inhibited changes of vascular endothelial (VE)-cadherin, β-catenin, and p120ctn morphology; VE-cadherin and myosin light chain 2 (MLC2) phosphorylation; and F-actin stress fiber formation. These changes seem to be predominantly mediated by the natriuretic peptide receptor (NPR)-A, but not by NPR-C. In summary, we revealed ANP as a potent endothelial barrier protecting agent in vivo and identified adherens junctions and the contractile apparatus as subcellular systems targeted by ANP. Thus, our study highlights ANP as an interesting pharmacological compound opening new therapeutic options for preventing endothelial leakage

Simulated-tempering approach to spin-glass simulations

After developing an appropriate iteration procedure for the determination of the parameters, the method of simulated tempering has been successfully applied to the 2D Ising spin glass. The reduction of the slowing down is comparable to that of the multicanonical algorithm. Simulated tempering has, however, the advantages to allow full vectorization of the programs and to provide the canonical ensemble directly.Comment: 12 pages (LaTeX), 4 postscript figures, uufiles encoded, submitted to Physical Review