We study the possible signals of a pion string associated with the QCD chiral phase transition in LHC Pb - Pb collision at energy $ \sqrt{s}=5.5$ TeV. In terms of the Kibble-Zurek mechanism we discuss the production and evolution of the pion string. The pion string is not topologically stable, it decays into neutral pions and sigma mesons which in turn decay into pions. Our results show that all the neutral pions from the pion string are distributed at the low momentum and the ratio of neutral to charged pions from the pion string violates the isospin symmetry. For the momentum spectra of the total pions, the signal from the sigma particle decay which is from the pion string will be affected by the large decay width of the sigma significantly.Comment: 8 pages, 3 figures, one reference added, title changed, version accepted for publication in Phys. Rev.

with an error in the author list. The second author's name should read as "Yan-Bing Cai." The author name has been corrected as of 2 June 2017. The author name is incorrect in the printed version of the journal.

ZFAS1 is one of cardiac-specific or cardiac-related lncRNAs. This study was to explore the functional involvement of ZFAS1 and its regulatory role in AMI. In this study, the models of AMI rat and myocardial cell cultured under hypoxia were made. The expression of ZFAS1 and miR-150 of myocardial infarction tissue or cardiac myocytes was determined by quantitative real time PCR. The regulatory role of ZFAS1 on miR-150 was examined by RNA pull down assay. The effect of miR-150 or ZFAS1 expression on cell viability was analyzed by MTT assay. The relative expression of ZFAS1 in the myocardium infracted zone and border zone was significantly upregulated at 1-48 h of AMI rats, but it downregulated at 1 week and 2 weeks; miR-150 was significantly downregulated at AMI-1-48 h and upregulated at 1 and 2 weeks after model establishment. The result of RNA pull down assay indicated that ZFAS1 could interact directly with miR-150. C-reactive protein (CRP) was regulated by ZFAS1/miR-150 axis and negatively targeted by miR-150. Hypoxia caused the decrease of cell viability and the upregulation of CRP at mRNA and protein levels; whereas this upregulation could be attenuated by miR-150 mimic or si-ZFAS1 in H9C2 cells and cardiomyocytes. Knockdown of ZFAS1 or miR-150 overexpression effectively relieved AMI-induced myocardial infarction in AMI-1 week rats. The ZFAS1/miR-150 axis was involved in the molecular mechanism of AMI induced cardiomyocytes apoptosis via regulating CRP. J. Cell. Biochem. 118: 3281-3289, 2017. © 2017 Wiley Periodicals, Inc.