The finiteness of the four dimensional antisymmetric tensor field model in a curved background

A renormalizable rigid supersymmetry for the four dimensional antisymmetric tensor field model in a curved space-time background is constructed. A closed algebra between the BRS and the supersymmetry operators is only realizable if the vector parameter of the supersymmetry is a covariantly constant vector field. This also guarantees that the corresponding transformations lead to a genuine symmetry of the model. The proof of the ultraviolet finiteness to all orders of perturbation theory is performed in a pure algebraic manner by using the rigid supersymmetry.Comment: 23 page

Algebraic structure of gravity in Ashtekar variables

The BRST transformations for gravity in Ashtekar variables are obtained by using the Maurer-Cartan horizontality conditions. The BRST cohomology in Ashtekar variables is calculated with the help of an operator $\delta$ introduced by S.P. Sorella, which allows to decompose the exterior derivative as a BRST commutator. This BRST cohomology leads to the differential invariants for four-dimensional manifolds.Comment: 19 pages, report REF. TUW 94-1

JAK-STAT inhibition impairs K-RAS-driven lung adenocarcinoma progression

Oncogenic KRAS has been difficult to target and currently there is no KRASbased targeted therapy available for patients suffering from KRASdriven lung adenocarcinoma (AC). Alternatively, targeting KRASdownstream effectors, KRAScooperating signaling pathways or cancer hallmarks, such as tumorpromoting inflammation, has been shown to be a promising therapeutic strategy. Since the JAKSTAT pathway is considered to be a central player in inflammationmediated tumorigenesis, we investigated here the implication of JAKSTAT signaling and the therapeutic potential of JAK1/2 inhibition in KRASdriven lung AC. Our data showed that JAK1 and JAK2 are activated in human lung AC and that increased activation of JAKSTAT signaling correlated with disease progression and KRAS activity in human lung AC. Accordingly, administration of the JAK1/2 selective tyrosine kinase inhibitor ruxolitinib reduced proliferation of tumor cells and effectively reduced tumor progression in immunodeficient and immunocompetent mouse models of KRASdriven lung AC. Notably, JAK1/2 inhibition led to the establishment of an antitumorigenic tumor microenvironment, characterized by decreased levels of tumorpromoting chemokines and cytokines and reduced numbers of infiltrating myeloid derived suppressor cells, thereby impairing tumor growth. Taken together, we identified JAK1/2 inhibition as promising therapy for KRASdriven lung AC.(VLID)510233