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 $K^+/\pi^+$ ratio, the difference in the slope parameters of the $K^+$ and $K^-$ 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

Track D Social Science, Human Rights and Political Science

Peer Reviewedhttps://deepblue.lib.umich.edu/bitstream/2027.42/138414/1/jia218442.pd

The effect of high-altitude on human skeletal muscle energetics: 31P-MRS results from the caudwell xtreme everest expedition

Many disease states are associated with regional or systemic hypoxia. The study of healthy individuals exposed to high-altitude hypoxia offers a way to explore hypoxic adaptation without the confounding effects of disease and therapeutic interventions. Using 31P magnetic resonance spectroscopy and imaging, we investigated skeletal muscle energetics and morphology after exposure to hypobaric hypoxia in seven altitude-naïve subjects (trekkers) and seven experienced climbers. The trekkers ascended to 5300 m while the climbers ascended above 7950 m. Before the study, climbers had better mitochondrial function (evidenced by shorter phosphocreatine recovery halftime) than trekkers: 16±1 vs. 22±2 s (mean ± SE, p<0.01). Climbers had higher resting [Pi] than trekkers before the expedition and resting [Pi] was raised across both groups on their return (PRE: 2.6±0.2 vs. POST: 3.0±0.2 mM, p<0.05). There was significant muscle atrophy post-CXE (PRE: 4.7±0.2 vs. POST: 4.5±0.2 cm2, p<0.05), yet exercising metabolites were unchanged. These results suggest that, in response to high altitude hypoxia, skeletal muscle function is maintained in humans, despite significant atrophy

Effects of a direct injection of liposoluble iron into rat striatum. Importance of the rate of iron delivery to cells.

International audienceFor a better understanding of the role of iron imbalance in neuropathology, a liposoluble iron complex (ferric hydroxyquinoline, FHQ) was injected into striatum of rats. The effects of two modalities of iron injections on brain damage, hydroxyl radical (*OH) production (assessed by the salicylate method coupled to microdialysis) and tissue reactive iron level (evaluated ex vivo by the propensity of the injected structure for lipid peroxidation) were examined. Rapid injection of FHQ (10 nmoles of 5 mM FHQ pH 3 solution over 1-min period) but not that of corresponding vehicle led to extensive damage associated with increased tissue free iron level in the injected region. Conversely, neither lesion nor free iron accumulation was observed after slow FHQ injection (10 nmoles of a 100 microM FHQ pH 7 solution over 1-h period) as compared to corresponding vehicle injection. Production of *OH was induced by slow FHQ injection but not by rapid FHQ injection, probably as a result of in vivo abolition of iron-induced *OH formation by acid pH. Indeed, rapid injection of FAC pH 7 (ferric ammonium citrate, 5 mM in saline) was associated with *OH formation whereas rapid injection of FAC pH 3 did not. Our results identify the rate of iron delivery to cells as an important determinant of iron toxicity and do not support a major role for extracellular *OH in damage associated with intracerebral iron injection