Lifting of the Landau level degeneracy in graphene devices in a tilted magnetic field

We report on transport and capacitance measurements of graphene devices in magnetic fields up to 30 T. In both techniques, we observe the full splitting of Landau levels and we employ tilted field experiments to address the origin of the observed broken symmetry states. In the lowest energy level, the spin degeneracy is removed at filling factors $\nu=\pm1$ and we observe an enhanced energy gap. In the higher levels, the valley degeneracy is removed at odd filling factors while spin polarized states are formed at even $\nu$. Although the observation of odd filling factors in the higher levels points towards the spontaneous origin of the splitting, we find that the main contribution to the gap at $\nu= -4,-8$, and $-12$ is due to the Zeeman energy.Comment: 5 pages, 4 figure

Shedding New Light on Kaon-Nucleon/Nuclei Interaction and Its Astrophysical Implications with the AMADEUS Experiment at DAFNE

The AMADEUS experiment deals with the investigation of the low-energy kaon-nuclei hadronic interaction at the DA{\Phi}NE collider at LNF-INFN, which is fundamental to respond longstanding questions in the non-perturbative QCD strangeness sector. The antikaon-nucleon potential is investigated searching for signals from possible bound kaonic clusters, which would open the possibility for the formation of cold dense baryonic matter. The confirmation of this scenario may imply a fundamental role of strangeness in astrophysics. AMADEUS step 0 consisted in the reanalysis of 2004/2005 KLOE dataset, exploiting K- absorptions in H, 4He, 9Be and 12C in the setup materials. In this paper, together with a review on the multi-nucleon K- absorption and the particle identification procedure, the first results on the {\Sigma}0-p channel will be presented including a statistical analysis on the possible accomodation of a deeply bound stateComment: 6 pages, 2 figure, 1 table, HADRON 2015 conferenc

Inverse remodelling of K2P3.1 K+ channel expression and action potential duration in left ventricular dysfunction and atrial fibrillation: implications for patient-specific antiarrhythmic drug therapy

AIMS: Atrial fibrillation (AF) prevalence increases with advanced stages of left ventricular (LV) dysfunction. Remote proarrhythmic effects of ventricular dysfunction on atrial electrophysiology remain incompletely understood. We hypothesized that repolarizing K2P3.1 K+ channels, previously implicated in AF pathophysiology, may contribute to shaping the atrial action potential (AP), forming a specific electrical substrate with LV dysfunction that might represent a target for personalized antiarrhythmic therapy. METHODS AND RESULTS: A total of 175 patients exhibiting different stages of LV dysfunction were included. Ion channel expression was quantified by real-time polymerase chain reaction and Western blot. Membrane currents and APs were recorded from atrial cardiomyocytes using the patch-clamp technique. Severely reduced LV function was associated with decreased atrial K2P3.1 expression in sinus rhythm patients. In contrast, chronic (c)AF resulted in increased K2P3.1 levels, but paroxysmal (p)AF was not linked to significant K2P3.1 remodelling. LV dysfunction-related suppression of K2P3.1 currents prolonged atrial AP duration (APD) compared with patients with preserved LV function. In individuals with concomitant LV dysfunction and cAF, APD was determined by LV dysfunction-associated prolongation and by cAF-dependent shortening, respectively, consistent with changes in K2P3.1 abundance. K2P3.1 inhibition attenuated APD shortening in cAF patients irrespective of LV function, whereas in pAF subjects with severely reduced LV function, K2P3.1 blockade resulted in disproportionately high APD prolongation. CONCLUSION: LV dysfunction is associated with reduction of atrial K2P3.1 channel expression, while cAF leads to increased K2P3.1 abundance. Differential remodelling of K2P3.1 and APD provides a basis for patient-tailored antiarrhythmic strategies