Constraining decaying dark matter with FERMI-LAT gamma rays

High energy electrons and positrons from decaying dark matter can produce a significant flux of gamma rays by inverse Compton off low energy photons in the interstellar radiation field. This possibility is inevitably related with the dark matter interpretation of the observed PAMELA and FERMI excesses. We will describe a simple and universal method to constrain dark matter models which produce electrons and positrons in their decay by using the FERMI-LAT gammaray observations in the energy range between 0.5GeV and 300 GeV, by exploiting universal response functions that, once convolved with a specific dark matter model, produce the desired constraint. The response functions contain all the astrophysical inputs. We discuss the uncertainties in the determination of the response functions and apply them to place constraints on some specific dark matter decay models that can well fit the positron and electron fluxes observed by PAMELA and FERMI LAT, also taking into account prompt radiation from the dark matter decay. With the available data decaying dark matter cannot be excluded as source of the PAMELA positron excess

Not only time delay. Ultra-high-energy cosmic rays as probes of quantum gravity scenarios

The time delays between gamma-rays of different energies from extragalactic sources have often been used to probe quantum gravity models in which Lorentz symmetry is violated. It has been claimed that these time delays can be explained by or at least put the strongest available constraints on quantum gravity scenarios that cannot be cast within an effective field theory framework, such as the space-time foam, D-brane model. Here we show that this model would predict too many photons in the ultra-high-energy cosmic-ray flux to be consistent with observations. The resulting constraints on the space-time foam model are much stronger than limits from time delays and allow for Lorentz violation effects way too small for explaining the observed time delays

Gamma-ray polarization constraints on Planck scale violations of special relativity

Using recent polarimetric observations of the Crab Nebula in the hard X-ray band by INTEGRAL, we show that the absence of vacuum birefringence effects constrains O(E/M) Lorentz violation in QED to the level |\xi| < 9x10^{-10} at three sigma CL, tightening by more than three orders of magnitude previous constraints. We show that planned X-ray polarimeters have the potential the potential to probe |\xi|~ 10^{-16} by detecting polarization in active galaxies at red-shift ~1.Comment: 4 pages, 3 figure

On Modified Dispersion Relations and the Chandrasekhar Mass Limit

Modified dispersion relations from effective field theory are shown to alter the Chandrasekhar mass limit. At exceptionally high densities, the modifications affect the pressure of a degenerate electron gas and can increase or decrease the mass limit, depending on the sign of the modifications. These changes to the mass limit are unlikely to be relevant for the astrophysics of white dwarf or neutron stars due to well-known dynamical instabilities that occur at lower densities. Generalizations to frameworks other than effective field theory are discussed.Comment: 14 pages, 2 figures; v2: version accepted for publication, minor changes; v3: note added correcting comments on the applicability of the calculation to the DSR context, references added, results unchange

High-resolution bioelectrical imaging of A&#946;-induced network dysfunction on CMOS-MEAs for neurotoxicity and rescue studies

Neurotoxicity and the accumulation of extracellular amyloid-beta1-42 (A\u3b2) peptides are associated with the development of Alzheimer's disease (AD) and correlate with neuronal activity and network dysfunctions, ultimately leading to cellular death. However, research on neurodegenerative diseases is hampered by the paucity of reliable readouts and experimental models to study such functional decline from an early onset and to test rescue strategies within networks at cellular resolution. To overcome this important obstacle, we demonstrate a simple yet powerful in vitro AD model based on a rat hippocampal cell culture system that exploits large-scale neuronal recordings from 4096-electrodes on CMOS-chips for electrophysiological quantifications. This model allows us to monitor network activity changes at the cellular level and to uniquely uncover the early activity-dependent deterioration induced by A\u3b2-neurotoxicity. We also demonstrate the potential of this in vitro model to test a plausible hypothesis underlying the A\u3b2-neurotoxicity and to assay potential therapeutic approaches. Specifically, by quantifying N-methyl D-aspartate (NMDA) concentration-dependent effects in comparison with low-concentration allogenic-A\u3b2, we confirm the role of extrasynaptic-NMDA receptors activation that may contribute to A\u3b2-neurotoxicity. Finally, we assess the potential rescue of neural stem cells (NSCs) and of two pharmacotherapies, memantine and saffron, for reversing A\u3b2-neurotoxicity and rescuing network-wide firing