Transport of Cosmic Rays in Chaotic Magnetic Fields

The transport of charged particles in disorganised magnetic fields is an important issue which concerns the propagation of cosmic rays of all energies in a variety of astrophysical environments, such as the interplanetary, interstellar and even extra-galactic media, as well as the efficiency of Fermi acceleration processes. We have performed detailed numerical experiments using Monte-Carlo simulations of particle propagation in stochastic magnetic fields in order to measure the parallel and transverse spatial diffusion coefficients and the pitch angle scattering time as a function of rigidity and strength of the turbulent magnetic component. We confirm the extrapolation to high turbulence levels of the scaling predicted by the quasi-linear approximation for the scattering frequency and parallel diffusion coefficient at low rigidity. We show that the widely used Bohm diffusion coefficient does not provide a satisfactory approximation to diffusion even in the extreme case where the mean field vanishes. We find that diffusion also takes place for particles with Larmor radii larger than the coherence length of the turbulence. We argue that transverse diffusion is much more effective than predicted by the quasi-linear approximation, and appears compatible with chaotic magnetic diffusion of the field lines. We provide numerical estimates of the Kolmogorov length and magnetic line diffusion coefficient as a function of the level of turbulence. Finally we comment on applications of our results to astrophysical turbulence and the acceleration of high energy cosmic rays in supernovae remnants, in super-bubbles, and in jets and hot spots of powerful radio-galaxies.Comment: To be published in Physical Review D, 20 pages 9 figure

Can altered production of interleukin-1β, interleukin-6, transforming growth factor-β and prostaglandin E2 by isolated human subchondral osteoblasts identify two subgroups of osteoarthritic patients

AbstractObjective To determine the capacity of human subchondral osteoarthritic osteoblasts (Ob) to produce interleukin (IL)-1β, IL-6, transforming growth factor-β (TGF-β) and prostaglandin E2 (PGE2), and determine if a relationship exists between IL-1β, TGF-β, PGE2 and IL-6 production.Methods We measured the abundance of IL-1β, IL-6, TGF-β and PGE2 using very sensitive ELISA in conditioned-media of human primary subchondral Ob from normal individuals and osteoarthritic patients. Selective inhibition of IL-6 or IL-6 receptor signaling was performed to determine its effect on PGE2 production whereas the inhibiton of PGE2 production was performed to determine its effect on IL-6 production. The expression of bone cell markers and urokinase plasminogen activator (uPA) activity was also determined.Results Osteoarthritic Ob produced all these factors with greater variability than normal cells. Interestingly, the production of IL-6 and PGE2 by osteoarthritic Ob separated patients into two subgroups, those whose Ob produced levels comparable to normal (low producers) and those whose Ob produced higher levels (high producers). In those cells classified as high osteoarthritic Ob, PGE2 and IL-6 levels were increased two- to three-fold and five- to six-fold, respectively, compared with normal. In contrast, while using their IL-6 and PGE2 production to separate osteoarthritic Ob into low and high producers, we found that IL-1β levels were similar in normal and all osteoarthritic Ob. Using the same criteria, TGF-β levels were increased in all osteoarthritic Ob compared with normal. Reducing PGE2 synthesis by Indomethacin [a cyclo-oxygenase (COX) -1 and -2 inhibitor] reduced IL-6 levels in all osteoarthritic Ob, whereas Naproxen (a more selective COX-2 inhbitor) reduced PGE2 and IL-6 levels only in the high osteoarthritic group. Conversely, PGE2 addition to osteoarthritic Ob enhanced IL-6 production in both groups. Moreover, the addition of parathyroid hormone also stimulated IL-6 production to similar normal levels in both osteoarthritic groups. In contrast, using an antibody against IL-6 or IL-6 receptors did not reduce PGE2 levels in either group. The evaluation of alkaline phosphatase activity, osteocalcin release, collagen type I and uPA activity in osteoarthritic Ob failed to show any differences between these cells regardless to which subgroup they were assigned.Conclusions These results indicate that IL-6 and PGE2 production by subchondral Ob can discriminate two subgroups of osteoarthritic patients that cannot otherwise be separated by their expression of cell markers, and that endogenous PGE2 levels influence IL-6 synthesis in osteoarthritic Ob. Copyright 2002 OsteoArthritis Research Society International. Published by Elsevier Science Ltd. All rights reserved

Learning safely from error: Reconsidering the ethics of simulation-based medical education through ethnography

‘Human factors’ is an influential rationale in the UK national health service to understand mistakes, risk and safety. Although there have been studies examining its implications in workplaces, there has been little investigation of how it is taught, as a form of professional morality. This article draws on an observational study of human factors teaching in four hospital simulation centres in London, UK. Its main argument is that the teaching of human factors is realised through an identification and positive evaluation of ‘non-technical skills’ and the espousal of ‘non-judgemental’ pedagogy, both of which mean that mistakes cannot be made. Professional solidarity is then maintained on the absence of mistakes. We raise questions about the ethics of this teaching. The study is situated within a history of ethnographic accounts of medical mistakes, to explore the relationship between claims to professional knowledge and claims about failure