Comparison of ground based and TOMS measurements of SO2 from volcanic emissions

The Brewer Ozone Spectrometer is being used in the World Ozone Network to monitor ozone and SO sub 2. SO sub 2 from natural as well as anthropogenic sources are measured. It has been demonstrated that SO sub 2 interferes with total ozone values as measured by the Dobson Spectrophotometer and the Total Ozone Mapping Spectrometer (TOMS). A small amount of manmade SO sub 2 is difficult to detect and quantify by TOMS because it is located near the surface. However, larger amounts of SO sub 2 injected into the stratosphere from volcanic emissions are detected by TOMS

Metastable dark matter mechanisms for INTEGRAL 511 keV γ\gamma rays and DAMA/CoGeNT events

We explore dark matter mechanisms that can simultaneously explain the galactic 511 keV gamma rays observed by INTEGRAL/SPI, the DAMA/LIBRA annual modulation, and the excess of low-recoil dark matter candidates observed by CoGeNT. It requires three nearly degenerate states of dark matter in the 4-7 GeV mass range, with splittings respectively of order an MeV and a few keV. The top two states have the small mass gap and transitions between them, either exothermic or endothermic, can account for direct detections. Decays from one of the top states to the ground state produce low-energy positrons in the galaxy whose associated 511 keV gamma rays are seen by INTEGRAL. This decay can happen spontaneously, if the excited state is metastable (longer-lived than the age of the universe), or it can be triggered by inelastic scattering of the metastable states into the shorter-lived ones. We focus on a simple model where the DM is a triplet of an SU(2) hidden sector gauge symmetry, broken at the scale of a few GeV, giving masses of order \lsim 1 GeV to the dark gauge bosons, which mix kinetically with the standard model hypercharge. The purely decaying scenario can give the observed angular dependence of the 511 keV signal with no positron diffusion, while the inelastic scattering mechanism requires transport of the positrons over distances \sim 1 kpc before annihilating. We note that an x-ray line of several keV in energy, due to single-photon decays involving the top DM states, could provide an additional component to the diffuse x-ray background. The model is testable by proposed low-energy fixed target experiments.Comment: 27 pp, 19 figures; v2. minor clarification, added refs; v3. corrected observed rate of positron production, added new section responding to criticisms of arXiv:0904.1025; v4. corrected typos in eqs. (6) and (40

Book Reviews

THE PHILANTHROPOIDS: FOUNDATIONS AND SOCIETY. By Ben Whitaker. New York: William Morrow & Company, 1974. Pp. 256. $7.95. CONGLOMERATES UNLIMITED: THE FAILURE OF REGULATION. By John F. Winslow. Bloomington: Indiana University Press, 1973. Pp. xx, 296.$10.00. BEFORE THE LAW: AN INTRODUCTION TO THE LEGAL PROCESS. Edited by John J. Bonsignore, Ethan Katsh, Peter d\u27Errico, Ronald M. Pipkin and Stephen Arons. Boston: Houghton Mifflin Company, 1974. Pp. xii, 388.,$6.95

MicroRNA29a regulates IL-33-mediated tissue remodelling in tendon disease

MicroRNA (miRNA) has the potential for cross-regulation and functional integration of discrete biological processes during complex physiological events. Utilizing the common human condition tendinopathy as a model system to explore the cross-regulation of immediate inflammation and matrix synthesis by miRNA we observed that elevated IL-33 expression is a characteristic of early tendinopathy. Using in vitro tenocyte cultures and in vivo models of tendon damage, we demonstrate that such IL-33 expression plays a pivotal role in the transition from type 1 to type 3 collagen (Col3) synthesis and thus early tendon remodelling. Both IL-33 effector function, via its decoy receptor sST2, and Col3 synthesis are regulated by miRNA29a. Downregulation of miRNA29a in human tenocytes is sufficient to induce an increase in Col3 expression. These data provide a molecular mechanism of miRNA-mediated integration of the early pathophysiologic events that facilitate tissue remodelling in human tendon after injury

Targeting danger molecules in tendinopathy: the HMGB1/TLR4 axis

Objectives: To seek evidence of the danger molecule, high-mobility group protein B1 (HMGB1) expression in human tendinopathy and thereafter, to explore mechanisms where HMGB1 may regulate inflammatory mediators and matrix regulation in human tendinopathy. Methods: Torn supraspinatus tendon (established pathology) and matched intact subscapularis tendon (representing ‘early pathology’) biopsies were collected from patients undergoing arthroscopic shoulder surgery. Control samples of subscapularis tendon were collected from patients undergoing arthroscopic stabilisation surgery. Markers of inflammation and HMGB1 were quantified by reverse transcriptase PCR (RT-PCR) and immunohistochemistry. Human tendon-derived primary cells were derived from hamstring tendon tissue obtained during hamstring tendon anterior cruciate ligament reconstruction and used through passage 3. In vitro effects of recombinant HMGB1 on tenocyte matrix and inflammatory potential were measured using quantitative RT-PCR, ELISA and immunohistochemistry staining. Results: Tendinopathic tissues demonstrated significantly increased levels of the danger molecule HMGB1 compared with control tissues with early tendinopathy tissue showing the greatest expression. The addition of recombinant human HMGB1 to tenocytes led to significant increase in expression of a number of inflammatory mediators, including interleukin 1 beta (IL-1β), IL-6, IL-33, CCL2 and CXCL12, in vitro. Further analysis demonstrated rhHMGB1 treatment resulted in increased expression of genes involved in matrix remodelling. Significant increases were observed in Col3, Tenascin-C and Decorin. Moreover, blocking HMGB1 signalling via toll-like receptor 4 (TLR4) silencing reversed these key inflammatory and matrix changes. Conclusion: HMGB1 is present in human tendinopathy and can regulate inflammatory cytokines and matrix changes. We propose HMGB1 as a mediator driving the inflammatory/matrix crosstalk and manipulation of the HMGB1/TLR4 axis may offer novel therapeutic approaches targeting inflammatory mechanisms in the management of human tendon disorders

Coupled Replicator Equations for the Dynamics of Learning in Multiagent Systems

Starting with a group of reinforcement-learning agents we derive coupled replicator equations that describe the dynamics of collective learning in multiagent systems. We show that, although agents model their environment in a self-interested way without sharing knowledge, a game dynamics emerges naturally through environment-mediated interactions. An application to rock-scissors-paper game interactions shows that the collective learning dynamics exhibits a diversity of competitive and cooperative behaviors. These include quasiperiodicity, stable limit cycles, intermittency, and deterministic chaos--behaviors that should be expected in heterogeneous multiagent systems described by the general replicator equations we derive.Comment: 4 pages, 3 figures, http://www.santafe.edu/projects/CompMech/papers/credlmas.html; updated references, corrected typos, changed conten

The Union-Nonunion Wage Differential: A Replication and Extension

This is the author's accepted manuscript, made available with the permission of the publisher.The research here was supported by the Office of Construction Industry Services, U.S. Department of Labor. Hugh Conway and Tom Mobley of that Office were especially helpful. Conclusions drawn and opinions expressed are those of the authors and do not represent the position of the U.S. Department of Labor or any of its officials. The authors would like to thank an anonymous referee for comments on an earlier draft. Fred Cleaver, formerly of the Center for Public Affairs, University of Kansas, assisted in data processing

The Galactic Inner Halo: Searching for White Dwarfs and Measuring the Fundamental Galactic Constant, Vo/Ro

We establish an extragalactic, zero-motion frame of reference within the deepest optical image of a globular star cluster, an HST 123-orbit exposure of M4 (GO 8679, cycle 9). The line of sight beyond M4 (l,b (deg) = 351,16) intersects the inner halo (spheroid) of our Galaxy at a tangent-point distance of 7.6 kpc (for Ro = 8 kpc). We isolate these spheroid stars from the cluster based on their proper motions over the 6-year baseline between these and previous epoch HST data (GO 5461, cycle 4). Distant background galaxies are also found on the same sight line using image-morphology techniques. This fixed reference frame allows us to independently determine the fundamental Galactic constant, Vo/Ro = 25.3 +/- 2.6 km/s/kpc, thus providing a velocity of the Local Standard of Rest, v = 202.7 +/- 24.7 km/s for Ro = 8.0 +/- 0.5 kpc. Secondly, the galaxies allow a direct measurement of M4's absolute proper motion, mu_total = 22.57 +/- 0.76 mas/yr, in excellent agreement with recent studies. The clear separation of galaxies from stars in these deep data also allow us to search for inner-halo white dwarfs. We model the conventional Galactic contributions of white dwarfs along our line of sight and predict 7.9 (thin disk), 6.3 (thick disk) and 2.2 (spheroid) objects to the limiting magnitude at which we can clearly delineate stars from galaxies (V = 29). An additional 2.5 objects are expected from a 20% white dwarf dark halo consisting of 0.5 Mo objects, 70% of which are of the DA type. After considering the kinematics and morphology of the objects in our data set, we find the number of white dwarfs to be consistent with the predictions for each of the conventional populations. However, we do not find any evidence for dark halo white dwarfs.Comment: 31 pages, including 6 diagrams and 2 tables. Accepted for publication in Ap

Fragmentation of decorin, biglycan, lumican and keratocan is elevated in degenerate human meniscus, knee and hip articular cartilages compared with age-matched macroscopically normal and control tissues

Introduction: The small leucine-rich proteoglycans (SLRPs) modulate tissue organization, cellular proliferation, matrix adhesion, growth factor and cytokine responses, and sterically protect the surface of collagen type I and II fibrils from proteolysis. Catabolism of SLRPs has important consequences for the integrity of articular cartilage and meniscus by interfering with their tissue homeostatic functions. Methods: SLRPs were dissociatively extracted from articular cartilage from total knee and hip replacements, menisci from total knee replacements, macroscopically normal and fibrillated knee articular cartilage from mature age-matched donors, and normal young articular cartilage. The tissue extracts were digested with chondroitinase ABC and keratanase-I before identification of SLRP core protein species by Western blotting using antibodies to the carboxyl-termini of the SLRPs. Results: Multiple core-protein species were detected for all of the SLRPs (except fibromodulin) in the degenerate osteoarthritic articular cartilage and menisci. Fibromodulin had markedly less fragments detected with the carboxyl-terminal antibody compared with other SLRPs. There were fewer SLRP catabolites in osteoarthritic hip than in knee articular cartilage. Fragmentation of all SLRPs in normal age-matched, nonfibrillated knee articular cartilage was less than in fibrillated articular cartilage from the same knee joint or total knee replacement articular cartilage specimens of similar age. There was little fragmentation of SLRPs in normal control knee articular cartilage. Only decorin exhibited a consistent increase in fragmentation in menisci in association with osteoarthritis. There were no fragments of decorin, biglycan, lumican, or keratocan that were unique to any tissue. A single fibromodulin fragment was detected in osteoarthritic articular cartilage but not meniscus. All SLRPs showed a modest age-related increase in fragmentation in knee articular and meniscal cartilage but not in other tissues. Conclusion: Enhanced fragmentation of SLRPs is evident in degenerate articular cartilage and meniscus. Specific decorin and fibromodulin core protein fragments in degenerate meniscus and/or human articular cartilage may be of value as biomarkers of disease. Once the enzymes responsible for their generation have been identified, further research may identify them as therapeutic targets