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The modification of the width of the rho meson due to in-medium decays and collisions is evaluated. In high temperature and/or high density hadronic matter, the collision width is much larger than the one-loop decay width. The large width of the meson in matter seems to be consistent with some current interpretations of the e+e mass spectra measured at the CERN/SPS.
The modification of the width of rho mesons due to in-medium decays and collisions is evaluated. The decay width is calculated from the imaginary part of the one-loop selfenergy at finite temperature. The collision width is related to the cross sections of the rho + pion and the rho + nucleon reactions. A calculation based on an e ective Lagrangian shows the importance of including the direct pho pi - > pho pi scattering which is dominated by the a1 exchange. A large broadening of the spectral function is found, accompanied by a strength suppression at the pole. http://www.arxiv.org/abs/nucl-th/9812059
We investigate in stable strange hadronic matter (SHM) the modifica- tion of the masses of the scalar (sigma,sigma') and the vector (omega,phi) mesons. The baryon ground state is treated in the relativistic Hartree approximation in the nonlinear sigma-omega and linear sigma'- phi model. In stable SHM, the masses of all the mesons reveal considerable reduction due to large vacuum polarization contribution from the hyperons and small density dependent effects caused by larger binding. PACS: 21.65+f, 24.10Jv
Pancreatic cancer is a common malignant tumor with a high incidence and mortality rate. The prognosis of patients with pancreatic cancer is considerably poor due to the lack of effective treatment in clinically. Despite numerous studies have revealed that baicalein, a natural product, is responsible for suppressing multiple cancer cells proliferation, motility and invasion. The mechanism by which baicalein restraining pancreatic cancer progression remains unclear. In this study, we firstly verified that baicalein plays a critical role in inhibiting pancreatic tumorigenesis in vitro and in vivo. Then we analyzed the alteration of microRNAs (miRNAs) expression levels in Panc-1 cells incubated with DMSO, 50 and 100 μM baicalein by High-Throughput sequencing. Intriguingly, we observed that 20 and 39 miRNAs were accordingly up- and down-regulated through comparing Panc-1 cells exposed to 100 μM baicalein with the control group. Quantitative PCR analysis confirmed that miR-139-3p was the most up-regulated miRNA after baicalein treatment, while miR-196b-5p was the most down-regulated miRNA. Further studies showed that miR-139-3p induced, miR-196b-5p inhibited the apoptosis of Panc-1 cells via targeting NOB1 and ING5 respectively. In conclusion, we demonstrated that baicalein is a potent inhibitor against pancreatic cancer by modulating the expression of miR-139-3p or miR-196b-5p.