CP-odd observables in neutralino production with transverse e+ and e- beam polarization

We consider neutralino production and decay e^+e^ --> chi^0_i chi^0_j, chi^0_j --> chi^0_1 f \bar{f} at a linear collider with transverse e^+ and e^- beam polarization. We propose CP asymmetries by means of the azimuthal distribution of the produced neutralinos and of that of the final leptons, while taking also into account the subsequent decays of the neutralinos. We include the complete spin correlations between production and decay. Our framework is the Minimal Supersymmetric Standard Model with complex parameters. In a numerical study we show that there are good prospects to observe these CP asymmetries at the International Linear Collider and estimate the accuracy expected for the determination of the phases in the neutralino sector.Comment: 30 pages, minor changes in the introduction, references adde

Searches for new physics

Review of prospects for discovery of new physics signals at LEP2. The areas covered include SUSY, exotic fermions, BESS models, leptoquarks, virtual effects and CP violating observables

STAT1 and STAT3 Exhibit a Crosstalk and Are Associated with Increased Inflammation in Hepatocellular Carcinoma

Liver cancers, which are mostly hepatocellular carcinoma (HCC) and cholangiocarcinoma (CCA), are very aggressive tumors with poor prognosis. Therapeutic options with curative intent are largely limited to surgery and available systemic therapies show limited benefit. Signal transducer and activator of transcription 1 (STAT1) and 3 (STAT3) are key transcription factors activated by pro-inflammatory cytokines such as interferon-γ (IFN-γ) and interleukin-6 (IL-6). In this study, we combined in vitro cell culture experiments and immunohistochemical analyses of human HCC (N = 124) and CCA (N = 138) specimens. We observed that in the absence of STAT3, IL-6 induced the activation of STAT1 and its target genes suggesting that IL-6 derived from the tumor microenvironment may activate both STAT1 and STAT3 target genes in HCC tumor cells. In addition, STAT1 and STAT3 were highly activated in a subset of HCC, which exhibited a high degree of infiltrating CD8- and FOXP3-positive immune cells and PD-L1 expression. Our results demonstrate that STAT1 and STAT3 are expressed and activated in HCC and tumor infiltrating immune cells. In addition, HCC cases with high STAT1 and STAT3 expression also exhibited a high degree of immune cell infiltration, suggesting increased immunological tolerance