The State of the Circumstellar Medium Surrounding Gamma-Ray Burst Sources and its Effect on the Afterglow Appearance

We present a numerical investigation of the contribution of the presupernova ejecta of Wolf-Rayet stars to the environment surrounding gamma-ray bursts (GRBs), and describe how this external matter can affect the observable afterglow characteristics. An implicit hydrodynamic calculation for massive stellar evolution is used here to provide the inner boundary conditions for an explicit hydrodynamical code to model the circumstellar gas dynamics. The resulting properties of the circumstellar medium are then used to calculate the deceleration of a relativistic, gas-dynamic jet and the corresponding afterglow light curve produced as the shock wave propagates through the shocked-wind medium. We find that variations in the stellar wind drive instabilities that may produce radial filaments in the shocked-wind region. These comet-like tails of clumps could give rise to strong temporal variations in the early afterglow lightcurve. Afterglows may be expected to differ widely among themselves, depending on the angular anisotropy of the jet and the properties of the stellar progenitor; a wide diversity of behaviors may be the rule, rather than the exception.Comment: 17 pages, 7 figures, ApJ in pres

Investigation of acceptor levels and hole scattering mechanisms in p-gallium selenide by means of transport measurements under pressure

The effect of pressure on acceptor levels and hole scattering mechanisms in p-GaSe is investigated through Hall effect and resistivity measurements under quasi-hydrostatic conditions up to 4 GPa. The pressure dependence of the hole concentration is interpreted through a carrier statistics equation with a single (nitrogen) or double (tin) acceptor whose ionization energies decrease under pressure due to the dielectric constant increase. The pressure effect on the hole mobility is also accounted for by considering the pressure dependencies of both the phonon frequencies and the hole-phonon coupling constants involved in the scattering rates.Comment: 13 pages, Latex, 4 ps figures. to appear in High Pressure Research 69 (1997

Relevance of death receptors in nervous system: role in the pathogenesis of neurodegenerative diseases and targets for therapy

L'apoptosi és un procés fisiològic que controla el nombre de cèl·lules en organismes superiors. L'apoptosi està estrictament regulada i s'ha vist que està implicada en la patogènesi d'algunes malalties del sistema nerviós. En aquest sentit, un excés de mort cel·lular contribueix a les malalties neurodegeneratives, mentre que, el seu dèficit és una de les raons del desenvolupament de tumors. El punt principal de regulació del procés apoptòtic és l'activació de les caspases, cisteïna-proteases que tenen especificitat pels residus aspàrtic. Les caspases es poden activar per dos mecanismes principals: (1) alliberament de citocrom C dels mitocondris alterats al citoplasma i (2) l'activació dels receptors de la membrana anomenats receptors de mort (DR, de l'anglès death receptor). Aquests receptors s'han caracteritzat extensament en el sistema immunitari, mentre que en el sistema nerviós les seves funcions són encara desconegudes. El present article se centra en el paper dels DR en la patogènesi de malalties neurodegeneratives i suggereix el seu potencial des del punt de vista terapèutic. També es descriuen diverses molècules intracel·lulars caracteritzades per la seva habilitat en la modulació dels DR. Entre elles, presentem dues noves proteïnes – lifeguard i FAIM – que s'expressen específicament al sistema nerviós.Apoptosis is a strictly controlled, physiological process by which the number of cells in metazoan organisms is regulated. Recently, it has been shown that apoptosis is involved in the pathogenesis of certain nervous system diseases. Excess cell death is thought to contribute to neurodegenerative disorders while defects in apoptosis lead to the development of neoplasias. Regulation of apoptosis primarily occurs through the activation of caspases, cysteine proteases that specifically cleave aspartic acid residues. Caspases are activated by two mechanisms: (1) release of cytochrome C from mitochondria to the cytoplasm and (2) activation of plasma membrane death receptors (DRs). These latter proteins have been widely characterized in the immune system, whereas in the nervous system their function remains elusive. In this article we focus on the role of DRs in the pathogenesis of neurodegenerative diseases and on the potential of these proteins as therapeutic targets. We also discuss several intracellular molecules that modulate DR activation. Among these, we introduce two novel proteins, Lifeguard and FAIM, which are specifically expressed in the nervous system