Adapted continuous unitary transformation to treat systems with quasiparticles of finite lifetime

An improved generator for continuous unitary transformations is introduced to describe systems with unstable quasiparticles. Its general properties are derived and discussed. To illustrate this approach we investigate the asymmetric antiferromagnetic spin-1/2 Heisenberg ladder which allows for spontaneous triplon decay. We present results for the low energy spectrum and the momentum resolved spectral density of this system. In particular, we show the resonance behavior of the decaying triplon explicitly.Comment: 40 pages, 12 figure

The Atypical Inhibitor of NF-kappa B, I kappa B zeta, Controls Macrophage Interleukin-10 Expression

Macrophages constitute a first line of pathogen defense by triggering a number of inflammatory responses and the secretion of various pro-inflammatory cytokines. Recently, we and others found that IκBζ, an atypical IκB family member and transcriptional coactivator of selected NF-κB target genes, is essential for macrophage expression of a subset of pro-inflammatory cytokines, such as IL-6, IL-12, and CCL2. Despite defective pro-inflammatory cytokine expression, however, IκBζ-deficient mice develop symptoms of chronic inflammation. To elucidate this discrepancy, we analyzed a regulatory role of IκBζ for the expression of anti-inflammatory cytokines and identified IκBζ as an essential activator of IL-10 expression. LPS-challenged peritoneal and bone marrow-derived macrophages from IκBζ-deficient mice revealed strongly decreased transcription and secretion of IL-10 compared with wild-type mice. Moreover, ectopic expression of IκBζ was sufficient to stimulate Il10 transcription. On the molecular level, IκBζ directly activated the Il10 promoter at a proximal κB site and was required for the transcription-enhancing trimethylation of histone 3 at lysine 4. Together, our findings show for the first time the IκBζ-dependent expression of an anti-inflammatory cytokine that is crucial in controlling immune responses