PPPC 4 DM ID: A Poor Particle Physicist Cookbook for Dark Matter Indirect Detection

We provide ingredients and recipes for computing signals of TeV-scale Dark Matter annihilations and decays in the Galaxy and beyond. For each DM channel, we present the energy spectra of electrons and positrons, antiprotons, antideuterons, gamma rays, neutrinos and antineutrinos e, mu, tau at production, computed by high-statistics simulations. We estimate the Monte Carlo uncertainty by comparing the results yielded by the Pythia and Herwig event generators. We then provide the propagation functions for charged particles in the Galaxy, for several DM distribution profiles and sets of propagation parameters. Propagation of electrons and positrons is performed with an improved semi-analytic method that takes into account position-dependent energy losses in the Milky Way. Using such propagation functions, we compute the energy spectra of electrons and positrons, antiprotons and antideuterons at the location of the Earth. We then present the gamma ray fluxes, both from prompt emission and from Inverse Compton scattering in the galactic halo. Finally, we provide the spectra of extragalactic gamma rays. All results are available in numerical form and ready to be consumed.Comment: 57 pages with many figures and tables. v4: updated to include a 125 higgs boson, computation and discussion of extragalactic spectra corrected, some other typos fixed; all these corrections and updates are reflected on the numerical ingredients available at http://www.marcocirelli.net/PPPC4DMID.html they correspond to Release 2.

A family with autosomal dominant leukodystrophy linked to 5q23.2-q23.3 without lamin B1 mutations.

Background and purpose: Duplications of lamin B1 (LMNB1) at 5q23 are implicated in adult-onset autosomal dominant leukodystrophy (ADLD) having been described in six families with diverse ethnic background but with a homogeneous phenotype. In a large Italian family, we recently identified a variant form of ADLD characterized clinically by absence of the autonomic dysfunction at onset described in ADLD and, on MRI, by milder cerebellar involvement with sparing of hemispheric white matter. Aim of this study was to investigate the genetic basis of this variant form of ADLD. Methods: We carried out a genome-wide linkage analysis using microsatellite markers, and the genes in the candidate region were screened for point mutations. LMNB1 was also screened for deletions/duplications by real-time PCR, multiplex ligation-dependent probe amplification and Southern blot. Results: We mapped the variant ADLD locus to 5q23.2-q23.3, a genomic region containing 11 genes including LMNB1. Neither gene copy-number defects nor point mutations in the LMNB1 gene were found. We also excluded point mutations in the coding exons of the other ten genes in the candidate region. However, expression of lamin B1 evaluated in lymphoblastoid cells was higher in patients than in healthy controls, and was similar to the lamin B1 expression levels found in a patient with LMNB1 duplication. Conclusions: This observation suggests that a mutation in an LMNB1 regulatory sequence underlies the variant ADLD phenotype. Thus, adult forms of ADLD linked to 5q23 appear to be more heterogeneous clinically and genetically than previously thought

Numerical simulation of the combustion of a single aluminium droplet in propellant gas environment

Communication to : 2nd European conference on launcher technology, space solid propulsion, Rome (Italie), November 21-24, 2000Available from INIST (FR), Document Supply Service, under shelf-number : 22419, issue : a.2001 / INIST-CNRS - Institut de l'Information Scientifique et TechniqueSIGLEFRFranc