OBJECTIVE To investigate the nosocomial infection knowledge nurses in graduating class. METHODS 286 nurses of graduating class were investigated by questionnaires. RESULTS The students were lacked of knowledge about nosocomial infection and 61.70% nurses of graduating class had never participated in the training of nosocomial infection knowledge (the average score only 58.67). They were interested in the disinfection and sterilization of infection diseases. And they wanted to get it through clinical infection control group (81.56% students selected this educational methods). CONCLUSIONS It is necessary to strengthen the training and education of nosocomial infection. And adjust the training mode and content according object.

BACKGROUND:Pathogenesis of Parkinson’s disease is not completely understood, and there is yet no effective therapy that can prevent the neurodegenerative process of the disease fundamentaly. OBJECTIVE:To explore the effects of pituitary adenylate cyclase-activating polypeptide (PACAP) on lactacystin-induced Parkinson’s disease dopaminergic PC12 cel apoptosis and its molecular mechanism. METHODS: Under induction by nerve growth factors, PC12 cels differentiated into dopaminergic neurons, and then were treated with different concentrations of lactacystin for different time. When the cel survival rate was about 50%,the concentration and action time oflactacystin were selected to establish cel models of Parkinson’s disease. In the study, there were control group, lactacystin group, PACAP1-27 group (intervention group 1) and PACAP1-27+PACAP6-27 co-intervention group (intervention group 2). Changes of cel morphology were observed under inverted microscope; cel viability was detected with MTT method; the expression of endoplasmic reticulum stress specific protein caspase-12 was detected by western blot. Then the action of PACAP1-27 and PACAP6-27 to the cytoxicity of lactacystin was observed. RESULTS AND CONCLUSION: With different concentrations and action time of lactacystin, the viability of PC12 cels presented a concentration- and time-dependent decline. When the lactacystin at 20μmol/L acted for 24 hours, the cel viability was declined by about 50%. Under same conditions of lactacystin concentration and action time (20 μmol/L, 24 hours), the cels in the lactacystin group appeared to have damaged changes, declined cel viability, and increased caspase-12 activity in comparison with the control group (P< 0.01). Compared with the lactacystin group, the cel damage was relieved and cel viability was increased significantly in the intervention group 1 as wel as the expression of caspase-12 was decreased (P < 0.01). Experimental findings in the intervention group 2 were similar to those in the lactacystin group. These results suggest that lactacystin, an ubiquitin proteasome inhibitor, can lead to cel damage; PACAP1-27 plays a protective role by regulating the above-mentioned signal pathway. As one PACAP1-27 receptor antagonist, PACAP6-27 can attenuate this effect of PACAP1-27.