Analyzing Fragmentation of Simple Fluids with Percolation Theory

We show that the size distributions of fragments created by high energy nuclear collisions are remarkably well reproduced within the framework of a parameter free percolation model. We discuss two possible scenarios to explain this agreement and suggest that percolation could be an universal mechanism to explain the fragmentation of simple fluids.Comment: 12 pages, 11 figure

Partial energies fluctuations and negative heat capacities

We proceed to a critical examination of the method used in nuclear fragmentation to exhibit signals of negative heat capacity. We show that this method leads to unsatisfactory results when applied to a simple and well controlled model. Discrepancies are due to incomplete evaluation of potential energies.Comment: Modified figures 3 and

LISACode : A scientific simulator of LISA

A new LISA simulator (LISACode) is presented. Its ambition is to achieve a new degree of sophistication allowing to map, as closely as possible, the impact of the different sub-systems on the measurements. LISACode is not a detailed simulator at the engineering level but rather a tool whose purpose is to bridge the gap between the basic principles of LISA and a future, sophisticated end-to-end simulator. This is achieved by introducing, in a realistic manner, most of the ingredients that will influence LISA's sensitivity as well as the application of TDI combinations. Many user-defined parameters allow the code to study different configurations of LISA thus helping to finalize the definition of the detector. Another important use of LISACode is in generating time series for data analysis developments

A Little Big Bang scenario of fragmentation

We suggest a multifragmentation scenario in which fragments are produced at an early, high temperature and high density, stage of the reaction. In this scenario, self-bound clusters of particles in the hot and dense fluid are the precursors of the observed fragments. This solves a number of recurrent problems concerning the kinetic energies and the temperature of the fragments, encountered with the standard low density fragmentation picture. The possibility to recover the initial thermodynamic parameters from the inspection of the asymptotic fragment size and kinetic energy distributions is discussed

A "Little Big Bang" Scenario of Multifragmentation

We suggest a multifragmentation scenario in which fragments are produced at an early, high temperature and high density, stage of the reaction. In this scenario, self-bound clusters of particles in the hot and dense fluid are the precursors of the observed fragments. This solves a number of recurrent problems concerning the kinetic energies and the temperature of the fragments, encountered with the standard low density fragmentation picture. The possibility to recover the initial thermodynamic parameters from the inspection of the asymptotic fragment size and kinetic energy distributions is discussed.Comment: 15 pages, 12 figure

The eLISA/NGO Data Processing Centre

International audienceData analysis for the eLISA/NGO mission is going to be performed in several steps. The telemetry is unpacked and checked at ESA's Science Operations Centre (SOC). The instrument teams are providing the necessary calibration files for the SOC to process the Level 1 data. The next steps, the source identification, parameter extraction and construction of a catalogue of sources is performed at the Data Processing Centre (DPC). This includes determining the physical and astrophysical parameters of the sources and their strain time series. At the end of the processing, the produced Level 2 and Level 3 data are then transferred back to the SOC, which provides the data archive and the interface for the scientific community. The DPC is organised by the member states of the consortium. In this paper we describe a possible outline of the data processing centre, including the tasks to be performed, and the organisational structure

How does the elastic scattering of 12C + 20Ne compare with that of 16O + 16O ?

Excitation functions for 5 exit channels of the 12C + 20Ne system are given in the range 22-28 MeV centre of mass incident energy. An important structure is observed in the elastic scattering excitation functions taken at 90° and 130° (C.M.). This structure, which reminds one of the 16O + 16O case, is studied in terms of angular momentum matching. An angular distribution taken at 24.7 MeV (C.M.) is also presented. The direct channel absorption is shown to be intermediate between the 16O + 16O and 18O + 18O cases

Signal transducer and activator of transcription 2 deficiency is a novel disorder of mitochondrial fission

Defects of mitochondrial dynamics are emerging causes of neurological disease. In two children presenting with severe neurological deterioration following viral infection we identified a novel homozygous STAT2 mutation, c.1836C4A (p.Cys612Ter), using whole exome sequencing. In muscle and fibroblasts from these patients, and a third unrelated STAT2-deficient patient, we observed extremely elongated mitochondria. Western blot analysis revealed absence of the STAT2 protein and that the mitochondrial fission protein DRP1 (encoded by DNM1L) is inactive, as shown by its phosphorylation state. All three patients harboured 15 decreased levels of DRP1 phosphorylated at serine residue 616 (P-DRP1S616), a post-translational modification known to activate DRP1, and increased levels of DRP1 phosphorylated at serine 637 (P-DRP1S637), associated with the inactive state of the DRP1 GTPase. Knockdown of STAT2 in SHSY5Y cells recapitulated the fission defect, with elongated mitochondria and decreased PDRP1 S616 levels. Furthermore the mitochondrial fission defect in patient fibroblasts was rescued following lentiviral transduction with wild-type STAT2 in all three patients, with normalization of mitochondrial length and increased P-DRP1S616 levels. Taken 20 together, these findings implicate STAT2 as a novel regulator of DRP1 phosphorylation at serine 616, and thus of mitochondrial fission, and suggest that there are interactions between immunity and mitochondria. This is the first study to link the innate immune system to mitochondrial dynamics and morphology. We hypothesize that variability in JAK-STAT signalling may contribute to the phenotypic heterogeneity of mitochondrial disease, and may explain why some patients with underlying mitochondrial disease decompensate after seemingly trivial viral infections. Modulating JAK-STAT activity may represent a novel 25 therapeutic avenue for mitochondrial diseases, which remain largely untreatable. This may also be relevant for more common neurodegenerative diseases, including Alzheimer’s, Huntington’s and Parkinson’s diseases, in which abnormalities of mitochondrial morphology have been implicated in disease pathogenesis