1,049 research outputs found
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 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. 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
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