Ionizing radiation reduces the capacity of activated macrophages to induce T-cell proliferation, but does not trigger dendritic cell-mediated non-targeted effects.

Purpose: Previous investigations revealed influences of irradiation up to 2Gy on the cytokine secretion profile of inflammatory and peritoneal mouse macrophages (pMCYRILLIC CAPITAL LETTER EF). This raised the question if those alterations impact on dendritic cells and consecutive T-cell responses. Further, the impact of irradiation directly on pMCYRILLIC CAPITAL LETTER EF capacity to induce T-cell responses was analyzed. Materials and methods: pMCYRILLIC CAPITAL LETTER EF were LPS-activated, irradiated and the expression of activation markers was assessed. Treated pMCYRILLIC CAPITAL LETTER EF were co-incubated with T-cells to investigate proliferation. To verify modulating properties of pMCYRILLIC CAPITAL LETTER EF supernatants isolated 24 h after irradiation, bone marrow-derived dendritic cells (BMDC) were co-incubated with supernatants and activation markers as well as the BMDC-induced proliferation of T-cells were measured. Results: pMCYRILLIC CAPITAL LETTER EF showed a highly significantly decreased major histocompatibility complexII (MHCII) expression within a dose range from 0.7-2Gy. Further, the proliferation rate of cluster of differentiation 4(+) (CD4(+)) T-cells was decreased after co-incubation particularly with 2 Gy irradiated pMCYRILLIC CAPITAL LETTER EF. The co-incubation of BMDC with supernatants of activated, irradiated pMCYRILLIC CAPITAL LETTER EF significantly reduced the CD40 expression, but did not impact on the BMDC-derived induction of T-cell proliferation. Conclusions: Inflammatory macrophages being exposed to irradiation have the potential to modulate consecutive adaptive immune reactions. But supernatants of irradiated macrophages do not influence the dendritic cells (DC)-mediated induction of T cell proliferation

Interconnection between DNA damage, senescence, inflammation, and cancer.

In order to deal with endogenous and exogenous factors, including radiation or pathogens, cells evolved different strategies. This includes highly complex processes such as DNA damage response, senescence, cell death, and inflammatory reactions. Recent research indicates an interconnection between the mentioned cellular pathways whilst all of them seem to play a role in induction and progression, but also the prevention of cancerous diseases and therefore qualify for potential prevention and treatment strategies. On the basis of their pivotal functions in cancer biology in general, each of the cellular processes represents promising single therapeutic targets. Further, due to their strong interconnection, targeting all of them in a multimodal approach could be another promising strategy to treat cancer. We, therefore, review the mechanisms of DNA damage induction, detection and repair as well as the induction of cell death. Further, features of senescence and mechanism of inflammation induction and abrogation are outlined. A special focus is set on how senescence and inflammation are related to diseases and how targeting them could contribute to improvement of cancer therapies

Iterative fluid dynamics

An iterative scheme is presented to solve analytically the relativistic fluid dynamics equations. The scheme is applied to longitudinal expansion, transversal symmetric and transversal asymmetric (triaxial) expansion as well. Within this scheme it is possible to describe the dynamics of a strongly coupled (i.e. conformal) medium for parameters referring to heavy-ion collisions at LHC.Comment: 16 pages, 12 figures, accepted for publication in EPJA: Topical issue on "Relativistic Hydro- and Thermodynamics