Objective To explore the event-related potentials (ERPs) P300 is changeable or not before and after treatment. Methods 99 cases of patients with first onset of depression diagnosed by DSM-Ⅳ as case group,and 100 cases matched with patients as control group were collected. P300 of two groups were obtained before and after treatment for 6 weeks,12 weeks,24 weeks. T test was used to analysis the difference of indicators of P300 among groups; repeated measure analysis of variance was used to analysis the longitudinal changes. Results shorter latency of N2-P3 ( (P ＜ 0.01 ); and lower amplitude of N2, P3, N2-P3 (P ＜ 0. 05 ), higher amplitude of P2-tency and a upward one in N2-P3 latency in the four periods; a upward trend could also be found in P3, N2-P3 amplitude, but there were no statistical differences(P ＞ 0. 05 ). The results of paired-samples t test: P3, N2-P3 amplitude in case group were higher after treatment for 6 weeks than before, the difference was significant (P ＜ 0.01 ); no significant results were found in P300 latency or amplitude between the 62 cases of depression after treatment for 24 weeks and the 65 normal controls selected (P ＞ 0. 05 ). Conclusion P300 latencies and amplitudes tend to be partly recovered after the acute treatment in patients with depression, but after the long-term therapy not clear.

Objective To investigate the mechanism of hypoxia regulate osteopontin (OPN) secreting by mature dendritic cells (mDCs). Methods CD14 + cells were enriched using anti-CD14 immunomagnetic beads, for inducing to mDCs, CD14 + cells were cultured with GM-CSF and IL-4 in hypoxia or normoxiain vitro. Concentration of OPN and TGF-β1 in supernatant were detected by sandwich ELISA, OPN mRNA detected by RT-PCR. Approach regulating function of A2 R in expressing of OPN by mDCs by using NECA (surrogate of adenosine), A2R agonist (CGS21680), A2R antagonist (SCH58261) and investigate role of TGF-β1 in this process by using rhTGF-β1 and anti-TGF-β1 Ab. Results Hypoxia inreased the level of OPN and OPN mRNA in mDCs, and this effect could be reversed by A2 R antagonist. Under normoxia,both NECA and A2R agonist (CGS21680) could upregulate the level of OPN and OPN mRNA in mDCs significantly, but this positive effect could be reversed by A2 R antagonist. A2 R played a role in regulating TGF-β1, and confirmed TGF-β1 involved in regulation of OPN by using rhTGF-β1 and anti-TGF-β1 Ab. Conclusion High adenosine induce the generation of TGF-β1 through the A2R on mDCs, and then TGF-β1 raise the OPN secreting by mDCs.