RADIATIVE SIGNATURES OF RELATIVISTIC SHOCKS

Particle-in-cell simulations of relativistic, weakly magnetized collisionless shocks show that particles can gain energy by repeatedly crossing the shock front. This requires scattering off self-generated small length-scale magnetic fluctuations. The radiative signature of this first-order Fermi acceleration mechanism is important for models of both the prompt and afterglow emission in gamma-ray bursts and depends on the strength parameter a = lambda e/delta B/mc(2) of the fluctuations (lambda is the length scale and vertical bar delta B vertical bar is the magnitude of the fluctuations). For electrons (and positrons), acceleration saturates when the radiative losses produced by the scattering cannot be compensated by the energy gained on crossing the shock. We show that this sets an upper limit on both the electron Lorentz factor gamma <10(6) (n/1 cm(-3))(-1/6)(-1/6) and on the energy of the photons radiated during the scattering process h omega(max) <40Max(a, 1)(n/1 cm(-3))(1/6)(-1/6) eV, where n is the number density of the plasma and (gamma) over bar is the thermal Lorentz factor of the downstream plasma, provided a <a(crit) similar to 10(6). This rules out "jitter" radiation on self-excited fluctuations with a <I as a source of gamma rays, although high-energy photons might still be produced when the jitter photons are upscattered in an analog of the synchrotron self-Compton process. In fluctuations with a > 1, radiation is generated by the standard synchrotron mechanism, and the maximum photon energy rises linearly with a, until saturating at 70 MeV, when a = a(crit).

Stochastic particle acceleration in the lobes of giant radio galaxies

We investigate the acceleration of particles by Alfven waves via the second-order Fermi process in the lobes of giant radio galaxies. Such sites are candidates for the accelerators of ultra-high-energy cosmic rays (UHECR). We focus on the nearby Fanaroff-Riley type I radio galaxy Centaurus A. This is motivated by the coincidence of its position with the arrival direction of several of the highest energy Auger events. The conditions necessary for consistency with the acceleration time-scales predicted by quasi-linear theory are reviewed. Test particle calculations are performed in fields which guarantee electric fields with no component parallel to the local magnetic field. The results of quasi-linear theory are, to an order of magnitude, found to be accurate at low turbulence levels for non-relativistic Alfven waves and at both low and high turbulence levels in the mildly relativistic case. We conclude that for pure stochastic acceleration via Alfven waves to be plausible as the generator of UHECR in Cen A, the baryon number density would need to be several orders of magnitude below currently held upper limits.

STEADY-STATE SOLUTIONS IN NONLINEAR DIFFUSIVE SHOCK ACCELERATION

Stationary solutions to the equations of nonlinear diffusive shock acceleration play a fundamental role in the theory of cosmic-ray acceleration. Their existence usually requires that a fraction of the accelerated particles be allowed to escape from the system. Because the scattering mean free path is thought to be an increasing function of energy, this condition is conventionally implemented as an upper cutoff in energy space-particles are then permitted to escape from any part of the system, once their energy exceeds this limit. However, because accelerated particles are responsible for the substantial amplification of the ambient magnetic field in a region upstream of the shock front, we examine an alternative approach in which particles escape over a spatial boundary. We use a simple iterative scheme that constructs stationary numerical solutions to the coupled kinetic and hydrodynamic equations. For parameters appropriate for supernova remnants, we find stationary solutions with efficient acceleration when the escape boundary is placed at the point where growth and advection of strongly driven nonresonant waves are in balance. We also present the energy dependence of the distribution function close to the energy where it cuts off-a diagnostic that is in principle accessible to observation.

Ion acceleration by superintense laser-plasma interaction

Ion acceleration driven by superintense laser pulses is attracting an impressive and steadily increasing effort. Motivations can be found in the applicative potential and in the perspective to investigate novel regimes as available laser intensities will be increasing. Experiments have demonstrated, over a wide range of laser and target parameters, the generation of multi-MeV proton and ion beams with unique properties such as ultrashort duration, high brilliance, and low emittance. An overview is given of the state of the art of ion acceleration by laser pulses as well as an outlook on its future development and perspectives. The main features observed in the experiments, the observed scaling with laser and plasma parameters, and the main models used both to interpret experimental data and to suggest new research directions are described.

Mechanisms of modified LDL-induced pericyte loss and retinal injury in diabetic retinopathy

Aims/hypothesis: In previous studies we have shown that extravasated, modified LDL is associated with pericyte loss, an early feature of diabetic retinopathy (DR). Here we sought to determine detailed mechanisms of this LDLinduced pericyte loss.

Methods: Human retinal capillary pericytes (HRCP) were exposed to ‘highly-oxidised glycated’ LDL (HOG-LDL) (a model of extravasated and modified LDL) and to 4-hydroxynonenal or 7-ketocholesterol (components of oxidised LDL), or to native LDL for 1 to 24 h with or without 1 h of pretreatment with inhibitors of the following: (1) the scavenger receptor (polyinosinic acid); (2) oxidative stress (N-acetyl cysteine); (3) endoplasmic reticulum (ER) stress (4-phenyl butyric acid); and (4) mitochondrial dysfunction (cyclosporin A). Oxidative stress, ER stress, mitochondrial dysfunction, apoptosis and autophagy were assessed using techniques including western blotting, immunofluorescence, RT-PCR, flow cytometry and TUNEL assay. To assess the relevance of the results in vivo, immunohistochemistry was used to detect the ER stress chaperon, 78 kDa glucose-regulated protein, and the ER sensor, activating transcription factor 6, in retinas from a mouse model of DR that mimics exposure of the retina to elevated glucose and elevated LDL levels, and in retinas from human participants with and without diabetes and DR.

Results: Compared with native LDL, HOG-LDL activated oxidative and ER stress in HRCP, resulting in mitochondrial dysfunction, apoptosis and autophagy. In a mouse model of diabetes and hyperlipidaemia (vs mouse models of either condition alone), retinal ER stress was enhanced. ER stress was also enhanced in diabetic human retina and correlated with the severity of DR.

Conclusions/interpretation: Cell culture, animal, and human data suggest that oxidative stress and ER stress are induced by modified LDL, and are implicated in pericyte loss in DR.

Glycation, glycoxidation, and cross-linking of collagen by glucose. Kinetics, mechanisms, and inhibition of late stages of the Maillard reaction

The Maillard or browning reaction between sugar and protein contributes to the increased chemical modification and cross-linking of long-lived tissue proteins in diabetes. To evaluate the role of glycation and oxidation in these reactions, we have studied the effects of oxidative and antioxidative conditions and various types of inhibitors on the reaction of glucose with rat tail tendon collagen in phosphate buffer at physiological pH and temperature. The chemical modifications of collagen that were measured included fructoselysine, the glycoxidation products N epsilon-(carboxymethyl)lysine and pentosidine and fluorescence. Collagen cross-linking was evaluated by analysis of cyanogen bromide peptides using sodium dodecyl sulfate-polyacrylamide gel electrophoresis and by changes in collagen solubilization on treatment with pepsin or sodium dodecylsulfate. Although glycation was unaffected, formation of glycoxidation products and cross-linking of collagen were inhibited by antioxidative conditions. The kinetics of formation of glycoxidation products proceeded with a short lag phase and were independent of the amount of Amadori adduct on the protein, suggesting that autoxidative degradation of glucose was a major contributor to glycoxidation and cross-linking reactions. Chelators, sulfhydryl compounds, antioxidants, and aminoguanidine also inhibited formation of glycoxidation products, generation of fluorescence, and cross-linking of collagen without significant effect on the extent of glycation of the protein. We conclude that autoxidation of glucose or Amadori compounds on protein plays a major role in the formation of glycoxidation products and cross-liking of collagen by glucose in vitro and that chelators, sulfhydryl compounds, antioxidants, and aminoguanidine act as uncouplers of glycation from subsequent glycoxidation and cross-linking reactions.