The SuperB-Factory accelerator project

An international collaboration on the design of a Super B-Factory aiming at a 1036 cm-2 s-1 luminosity is in progress. The design relies on a new collision scheme with large Piwinski’s angle and very small IP beam sizes, where possible harmful resonances will be cancelled by the newly proposed “crab waist” method. A Conceptual Design Report has been published in April this year. A review of the design principles and of the project status will be given

Lacosamide: a new approach to target voltage-gated sodium currents in epileptic disorders

The mechanism of action of several antiepileptic drugs (AEDs) rests on their ability tomodulate the activity of voltage-gated sodium currents that are responsible for fast action potentialgeneration. Recent data indicate that lacosamide - a compound with analgesic and anticonvulsanteffects in animal models - shares a similar mechanism. When compared with other AEDs, lacosamidehas the unique ability to interact with sodium channel slow inactivation without affecting fastinactivation. This article reviews these findings and discusses their relevance within the context ofneuronal activity seen during epileptiform discharges generated by limbic neuronal networks in thepresence of chemical convulsants. These seizure-like events are characterized by sustained dischargesof sodium-dependent action potentials supported by robust depolarizations thus providingsynchronization within neuronal networks. Generally, AEDs such as phenytoin, carbamazepine andlamotrigine block sodium channels when activated. By contrasts, lacosamide facilitates slowinactivation of sodium channels both in term of kinetics and voltage-dependency. This effect may berelatively selective for repeatedly depolarized neurons such as those participating in seizure activity inwhich the persistence of sodium currents is more pronounced and promotes neuronal excitation. Theclinical effectiveness of lacosamide has been demonstrated in randomized placebo-controlled doubleblindparallel-group, adjunctive-therapy trials in patients with refractory partial seizures. Furtherstudies should determine whether lacosamide effects in animal models and in clinical settings are fullyexplained by its selective action on sodium current slow inactivation or whether other effects (e.g.,interactions with the collapsin-response mediator protein 2) play a contributory role

Impaired Activation of CA3 Pyramidal Neurons in the Epileptic Hippocampus.

We employed in vitro and ex vivo imaging tools to characterize the function of limbic neuron networks in pilocarpine-treated and age-matched, nonepileptic control (NEC) rats. Pilocarpine-treated animals represent an established model of mesial temporal lobe epilepsy. Intrinsic optical signal (IOS) analysis of hippocampal-entorhinal cortex (EC) slices obtained from epileptic rats 3 wk after pilocarpine-induced status epilepticus (SE) revealed hyperexcitability in many limbic areas, but not in CA3 and medial EC layer III. By visualizing immunopositivity for FosB/DeltaFosB-related proteins which accumulate in the nuclei of neurons activated by seizures we found that: (1) 24 h after SE, FosB/DeltaFosB immunoreactivity was absent in medial EC layer III, but abundant in dentate gyrus, hippocampus proper (including CA3) and subiculum; (2) FosB/DeltaFosB levels progressively diminished 3 and 7 d after SE, whereas remaining elevated (p < 0.01) in subiculum; (3) FosB/DeltaFosB levels sharply increased 2 wk after SE (and remained elevated up to 3 wk) in dentate gyrus and in most of the other areas but not in CA3. A conspicuous neuronal damage was noticed in medial EC layer III, whereas hippocampus was more preserved. IOS analysis of the stimulus-induced responses in slices 3 wk after SE demonstrated that IOSs in CA3 were lower (p < 0.05) than in NEC slices following dentate gyrus stimulation, but not when stimuli were delivered in CA3. These findings indicate that CA3 networks are hypoactive in comparison with other epileptic limbic areas. We propose that this feature may affect the ability of hippocampal outputs to control epileptiform synchronization in EC

Magnetic-field-induced Luttinger liquid

It is shown that a strong magnetic field applied to a bulk metal induces a Luttinger-liquid phase. This phase is characterized by the zero-bias anomaly in tunneling: the tunneling conductance scales as a power-law of voltage or temperature. The tunneling exponent increases with the magnetic field as BlnB. The zero-bias anomaly is most pronounced for tunneling with the field applied perpendicular to the plane of the tunneling junction.Comment: a reference added, minor typos correcte

Nucleation of superconducting pairing states at mesoscopic scales at zero temperature

We find the spin polarized disordered Fermi liquids are unstable to the nucleation of superconducting pairing states at mesoscopic scales even when magnetic fields which polarize the spins are substantially higher than the critical one. We study the probability of finding superconducting pairing states at mesoscopic scales in this limit. We find that the distribution function depends only on the film conductance. The typical length scale at which pairing takes place is universal, and decreases when the magnetic field is increased. The number density of these states determines the strength of the random exchange interactions between mesoscopic pairing states.Comment: 11 pages, no figure