151 research outputs found
Medium effects in high energy heavy-ion collisions
The change of hadron properties in dense matter based on various theoretical
approaches are reviewed. Incorporating these medium effects in the relativistic
transport model, which treats consistently the change of hadron masses and
energies in dense matter via the scalar and vector fields, heavy-ion collisions
at energies available from SIS/GSI, AGS/BNL, and SPS/CERN are studied. This
model is seen to provide satisfactory explanations for the observed enhancement
of kaon, antikaon, and antiproton yields as well as soft pions in the
transverse direction from the SIS experiments. In the AGS heavy-ion
experiments, it can account for the enhanced ratio, the difference
in the slope parameters of the and transverse kinetic energy
spectra, and the lower apparent temperature of antiprotons than that of
protons. This model also provides possible explanations for the observed
enhancement of low-mass dileptons, phi mesons, and antilambdas in heavy-ion
collisions at SPS energies. Furthermore, the change of hadron properties in hot
dense matter leads to new signatures of the quark-gluon plasma to hadronic
matter transition in future ultrarelativistic heavy-ion collisions at RHIC/BNL.Comment: RevTeX, 65 pages, including 25 postscript figures, invited topical
review for Journal of Physics G: Nuclear and Particle Physic
Fluctuations In ``BR-Scaled'' Chiral Lagrangians
We develop arguments for "mapping" the effective chiral Lagrangian whose
parameters are given by "BR scaling" to a Landau Fermi-liquid fixed-point
theory for nuclear matter in describing fluctuations in various flavor (e.g.,
strangeness) directions. We use for this purpose the effective Lagrangian used
by Furnstahl, Tang and Serot that incorporates the trace anomaly of QCD in
terms of a light-quark (quarkonium) degree of freedom with the heavy (gluonium)
degree of freedom integrated out. The large anomalous dimension for the scalar field found by Furnstahl et al to be needed for a correct
description of nuclear matter is interpreted as an indication for a
strong-coupling regime and the ground state given by the BR-scaled parameters
is suggested as the background around which fluctuations can be rendered weak
so that mean-field approximation is reliable. We construct a simple model with
BR scaled parameters that provides a satisfactory description of the properties
of matter at normal nuclear matter density. Given this, fluctuations around the
BR scaled background are dominated by tree diagrams. Our reasoning relies
heavily on recent developments in the study of nucleon and kaon properties in
normal and dense nuclear matter, e.g., nucleon and kaon flows in heavy-ion
processes, kaonic atoms, and kaon condensation in dense compact-star matter.Comment: 33 pages, Latex, 5 Postscript figure
Tumor Necrosis Factor α Inhibits Expression of the Iron Regulating Hormone Hepcidin in Murine Models of Innate Colitis
Background: Abnormal expression of the liver peptide hormone hepcidin, a key regulator of iron homeostasis, contributes to the pathogenesis of anemia in conditions such as inflammatory bowel disease (IBD). Since little is known about the mechanisms that control hepcidin expression during states of intestinal inflammation, we sought to shed light on this issue using mouse models. Methodology/Principal Findings: Hepcidin expression was evaluated in two types of intestinal inflammation caused by innate immune activation—dextran sulfate sodium (DSS)-induced colitis in wild-type mice and the spontaneous colitis occurring in T-bet/Rag2-deficient (TRUC) mice. The role of tumor necrosis factor (TNF) was investigated by in vivo neutralization, and by treatment of a hepatocyte cell line, as well as mice, with the recombinant cytokine. Expression and activation of Smad1, a positive regulator of hepcidin transcription, were assessed during colitis and following administration or neutralization of TNF. Hepcidin expression progressively decreased with time during DSS colitis, correlating with changes in systemic iron distribution. TNF inhibited hepcidin expression in cultured hepatocytes and non-colitic mice, while TNF neutralization during DSS colitis increased it. Similar results were obtained in TRUC mice. These effects involved a TNF-dependent decrease in Smad1 protein but not mRNA. Conclusions/Significance: TNF inhibits hepcidin expression in two distinct types of innate colitis, with down-regulation of Smad1 protein playing an important role in this process. This inhibitory effect of TNF may be superseded by other factors in the context of T cell-mediated colitis given that in the latter form of intestinal inflammation hepcidin is usually up-regulated
Mass Spectrometry Analysis of Hepcidin Peptides in Experimental Mouse Models
The mouse is a valuable model for unravelling the role of hepcidin in iron homeostasis, however, such studies still report hepcidin mRNA levels as a surrogate marker for bioactive hepcidin in its pivotal function to block ferroportin-mediated iron transport. Here, we aimed to assess bioactive mouse Hepcidin-1 (Hep-1) and its paralogue Hepcidin-2 (Hep-2) at the peptide level. To this purpose, fourier transform ion cyclotron resonance (FTICR) and tandem-MS was used for hepcidin identification, after which a time-of-flight (TOF) MS-based methodology was exploited to routinely determine Hep-1 and -2 levels in mouse serum and urine. This method was biologically validated by hepcidin assessment in: i) 3 mouse strains (C57Bl/6; DBA/2 and BABL/c) upon stimulation with intravenous iron and LPS, ii) homozygous Hfe knock out, homozygous transferrin receptor 2 (Y245X) mutated mice and double affected mice, and iii) mice treated with a sublethal hepatotoxic dose of paracetamol. The results showed that detection of Hep-1 was restricted to serum, whereas Hep-2 and its presumed isoforms were predominantly present in urine. Elevations in serum Hep-1 and urine Hep-2 upon intravenous iron or LPS were only moderate and varied considerably between mouse strains. Serum Hep-1 was decreased in all three hemochromatosis models, being lowest in the double affected mice. Serum Hep-1 levels correlated with liver hepcidin-1 gene expression, while acute liver damage by paracetamol depleted Hep-1 from serum. Furthermore, serum Hep-1 appeared to be an excellent indicator of splenic iron accumulation. In conclusion, Hep-1 and Hep-2 peptide responses in experimental mouse agree with the known biology of hepcidin mRNA regulators, and their measurement can now be implemented in experimental mouse models to provide novel insights in post-transcriptional regulation, hepcidin function, and kinetics
- …