Jing Qian

Publications (2)5.52 Total impact

• Article: Elimination of collisional effects in an R-type atom–molecule adiabatic passage

  Jing Qian, Keye Zhang, Lu Zhou, Weiping Zhang
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  ABSTRACT: We propose an efficient scheme to avoid collision-induced dynamical instabilities in the generation of heteronuclear molecular Bose–Einstein condensates based on an R-type photoassociative adiabatic passage. This scheme allows us to completely compensate the intraspecies collisions by tunable interspecies collisions, and thereby achieve a robust atom–molecule conversion which is equivalent to that in a collision-free case. By taking the formation of stable 41K87Rb molecules as an example, we study the feasibility of the scheme.
  Journal of Physics B Atomic Molecular and Optical Physics 07/2010; 43(15):155206. · 1.88 Impact Factor
• Article: Small peptide inhibitor of JNKs protects against MPTP-induced nigral dopaminergic injury via inhibiting the JNK-signaling pathway.

  Jing Pan, Jing Qian, Yu Zhang, Jianfang Ma, Gang Wang, Qin Xiao, Shengdi Chen, Jianqing Ding
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  ABSTRACT: Increasing evidence suggests that apoptosis may be the mechanism underlying cell death in selective loss of nigral dopaminergic neurons in Parkinson's disease (PD). Previous studies strongly suggested that c-Jun N-terminal kinase (JNK) signaling pathway has a critical role in the animal model with 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced PD. In this study, we report the inhibitory effect of a peptide designated as Tat-JBD on JNKs activation. The sequence of Tat is corresponding to the cell-membrane transduction domain of human immunodeficiency virus-type 1 (HIV-1) and the sequence of an 11-amino acid peptide is corresponding to the residues of JNK-binding domain (JBD) on JNK-interacting protein-1 (JIP-1). Tat-JBD is confirmed to perturb the assembly of JIP-1-JNKs complex, inhibit the activation of JNKs induced by MPTP and consequently diminish the phosphorylation of c-Jun. It also inhibits the phosphorylation of Bcl-2 and the releasing of Bax from Bcl-2/Bax dimmers, sequentially attenuates the translocation of Bax to mitochondria, the release of cytochrome c, the activation of caspase3 and the hydrolyzation of poly-ADP-ribose-polymerase. The death of dopaminergic neurons and the loss of dopaminergic axon in the striatum were significantly suppressed by infusion of the peptide Tat-JBD in MPTP-treated mice. Our findings imply that Tat-JBD offers neuroprotection against MPTP injury via inhibiting the JNK-signaling pathway, and may provide a promising therapeutic approach for PD.
  Laboratory Investigation 12/2009; 90(2):156-67. · 3.64 Impact Factor