Dynamical properties of a trapped dipolar Fermi gas at finite temperature

We investigate the dynamical properties of a trapped finite-temperature normal Fermi gas with dipole-dipole interaction. For the free expansion dynamics, we show that the expanded gas always becomes stretched along the direction of the dipole moment. In addition, we present the temperature and interaction dependences of the asymptotical aspect ratio. We further study the collapse dynamics of the system by suddenly increasing the dipolar interaction strength. We show that, in contrast to the anisotropic collapse of a dipolar Bose-Einstein condensate, a dipolar Fermi gas always collapses isotropically when the system becomes globally unstable. We also explore the interaction and temperature dependences for the frequencies of the low-lying collective excitations.Comment: 11 pages, 7 figure

Density oscillations in trapped dipolar condensates

We investigated the ground state wave function and free expansion of a trapped dipolar condensate. We find that dipolar interaction may induce both biconcave and dumbbell density profiles in, respectively, the pancake- and cigar-shaped traps. On the parameter plane of the interaction strengths, the density oscillation occurs only when the interaction parameters fall into certain isolated areas. The relation between the positions of these areas and the trap geometry is explored. By studying the free expansion of the condensate with density oscillation, we show that the density oscillation is detectable from the time-of-flight image.Comment: 7 pages, 9 figure

SIRT3 Protects Rotenone-induced Injury in SH-SY5Y Cells by Promoting Autophagy through the LKB1-AMPK-mTOR Pathway.

SIRT3 is a class III histone deacetylase that modulates energy metabolism, genomic stability and stress resistance. It has been implicated as a potential therapeutic target in a variety of neurodegenerative diseases, including Parkinson's disease (PD). Our previous study demonstrates that SIRT3 had a neuroprotective effect on a rotenone-induced PD cell model, however, the exact mechanism is unknown. In this study, we investigated the underlying mechanism. We established a SIRT3 stable overexpression cell line using lentivirus infection in SH-SY5Y cells. Then, a PD cell model was established using rotenone. Our data demonstrate that overexpression of SIRT3 increased the level of the autophagy markers LC3 II and Beclin 1. After addition of the autophagy inhibitor 3-MA, the protective effect of SIRT3 diminished: the cell viability decreased, while the apoptosis rate increased; α-synuclein accumulation enhanced; ROS production increased; antioxidants levels, including SOD and GSH, decreased; and MMP collapsed. These results reveal that SIRT3 has neuroprotective effects on a PD cell model by up-regulating autophagy. Furthermore, SIRT3 overexpression also promoted LKB1 phosphorylation, followed by activation of AMPK and decreased phosphorylation of mTOR. These results suggest that the LKB1-AMPK-mTOR pathway has a role in induction of autophagy. Together, our findings indicate a novel mechanism by which SIRT3 protects a rotenone-induced PD cell model through the regulation of autophagy, which, in part, is mediated by activation of the LKB1-AMPK-mTOR pathway