In the framework of relativistic quantum molecular dynamics we find that the pion system produced in central heavy-ion collisions at E,,,/A-1 GeVInucl is out of chemical equilibrium. Pion chemical potential is large and decreases during the expansion stage. Data of pion production in heavy-ion collisions show the enhancement of n-spectra at low transverse momenta. This widely debated phenomenon looks quite universal: low-p, excess of pions is seen in CERN experiments at the bombarding energy El,,/A = 200GeV/nucl [I], in AGS at E,.,/A = 15 GeV/nucl [2] and in Bevalac at Ela,/A = 0.5 t 1.8 GeV/nucl [3]. Resonance decays and collective (transverse) flow were suggested to fit experimental data. One can find in the literature different combinations of these two mechanisms and also different conclusions (see reference [4] and references therein). An interesting idea to explain n-spectra in CERN experiments by positive pion chemical potential pn has been proposed in [5-71. Fitting n-spectra in 0 + Au at 200 GeV/nucl, the freeze-out temperature T and pion chemical potential pn are found to be: T = 167 MeV, px = 126 MeV [6] (without transverse collective flow), or T = 100 MeV, pn = 120 MeV [7] (with transverse collective flow). In [8] the possibility of pn > 0 was discussed for small bombarding energies-1 GeV/nucl. It was stressed that for the collisions of heavy nuclei the chemical potential of n+ is always smaller than that of n-and this difference can lead to some observable consequences. A positive value of pz means that at some stage of the particle production process the number of pions, generated by hadron dynamics, is larger than that corresponding to chemical equilibrium. Then the pion system can be thermally equilibrated due to elastic collisions, but it will be out of chemical equilibrium if the rate of inelastic reactions is not high enough. Bose-statistic effects then become very 5 Alexander van Humboldt Fellow.

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There are two misprints on the predicted α-decay half-lives in table 2 of the original article. The revision descriptions are listed as follows.(1) In line 3, column 7, the correct value is 1.70 × 10 −8 and not 1.70 × 10 −7 .(2) In line 10, column 7, the correct value is 9.49 × 10 −5 and not 9.49 × 10 −4 .The conflicting half-lives by different models are not found after revision.

Background: Henoch-Schonlein purpura (HSP) is a common hemorrhagic disease, which manifests the inflammation in the body's most microvasculars. Angiotensin II (Ang II) can induce the damage and apoptosis of vascular endothelial cells while angiotensin converting enzyme 2 (ACE2) can antagonist the action of Ang II. However, the effect of ACE2 on Ang II-induced endothelial damage remains unknown. Objective: To evaluate the effect of recombinant human angiotensin converting enzyme 2 (rhACE2) on the Ang II-induced damage of human umbilical vein endothelial cells (HUVECs) and the release of inflammatory mediator in vitro. Methods: Cultured HUVECs were randomly divided into 6 groups: the control group, rhACE2 group, Ang II group, and Ang II+ rhACE2 groups (3 subgroups). The cell vitality, cell cycle, apoptosis rate of the HUVECs and the levels of reactive oxygen species (ROS), interleukin 8 (IL-8), tumor necrosis factor-α (TNF-α), transforming growth factor-β1 (TGF-β1) and lactate dehydrogenase (LDH) were measured, respectively. Results: Compared with the control group, the cell viability and the rate of S phase cells in Ang II group significantly decreased ( P < .05) while the apoptosis percentage and the levels of ROS, IL-8, TNF-α, TGF-β1, and LDH in Ang II group significantly increased ( P < .05). There were no significant differences between the control group and rhACE2 group. Compared with the Ang II group, the cell viability and the rate of S phase cells in Ang II+rhACE2 groups were higher ( P < .05) and the apoptosis percentage, the level of ROS, IL-8, TNF-α, TGF-β1, LDH in Ang II+rhACE2 groups were lower ( P < .05). Conclusions: Ang II can induce the apoptosis of HUVECs and the release of inflammatory mediator, while rhACE2 can inhibit the detrimental effects of Ang II. The results of this study suggest that rhACE2 has a protective effect on HSP, which is probably a new way for the prevention and treatment of HSP.