On the background in the γp→ω(π0γ)p\gamma p \to \omega(\pi^0\gamma) p reaction and mixed event simulation

In this paper we evaluate sources of background for the $\gamma p \to \omega p$, with the $\omega$ detected through its $\pi^0 \gamma$ decay channel, to compare with the experiment carried out at ELSA. We find background from $\gamma p \to \pi^0 \pi^0 p$ followed by decay of a $\pi^0$ into two $\gamma$, recombining one $\pi^0$ and one $\gamma$, and from the $\gamma p \to \pi^0 \eta p$ reaction with subsequent decay of the $\eta$ into two photons. This background accounts for the data at $\pi^0 \gamma$ invariant masses beyond 700 MeV, but strength is missing at lower invariant masses which was attributed to photon misidentification events, which we simulate to get a good reproduction of the experimental background. Once this is done, we perform an event mixing simulation to reproduce the calculated background and we find that the method provides a good description of the background at low $\pi^0 \gamma$ invariant masses but fakes the background at high invariant masses, making background events at low invariant masses, which are due to $\gamma$ misidentification events, responsible for the background at high invariant masses which is due to the $\gamma p \to \pi^0 \pi^0 p$ and $\gamma p \to \pi^0 \eta p$ reactions.Comment: 10 pages, 5 figure

Effects of diadenosine tetraphosphate on FGF9-induced chloride flux changes in achondroplastic chondrocytes

Achondroplasia, the most common type of dwarfism, is characterized by a mutation in the fibroblast growth factor receptor 3 (FGFR3). Achondroplasia is an orphan pathology with no pharmacological treatment so far. However, the possibility of using the dinucleotide diadenosine tetraphosphate (Ap4A) with therapeutic purposes in achondroplasia has been previously suggested. The pathogenesis involves the constitutive activation of FGFR3, resulting in altered biochemical and physiological processes in chondrocytes. Some of these altered processes can be influenced by changes in cell volume and ionic currents. In this study, the action of mutant FGFR3 on chondrocyte size and chloride flux in achondroplastic chondrocytes was investigated as well as the effect of the Ap4A on these processes triggered by mutant FGFR3. Stimulation with the fibroblast growth factor 9 (FGF9), the preferred ligand for FGFR3, induced an enlarged achondroplastic chondrocyte size and an increase in the intracellular chloride concentration, suggesting the blockade of chloride efflux. Treatment with the Ap4A reversed the morphological changes triggered by FGF9 and restored the chloride efflux. These data provide further evidence for the therapeutic potential of this dinucleotide in achondroplasia treatment