一家三甲医院吸烟与控烟工作状况调查

Objective: To master the hospital smoking status and distribution, for providing a scientific basis for tobacco control measures in hospitals. Methods: A questionnaire was designed. Given a uniform standards, the synchronization investigation was carried out after the implementation of staff training. Results:  The overall smoking rate was 9.66% in the hospital, and smoking rate among males was 25.78%. The smoking rate among administrative and support staffs is higher than the medical staff. Conclusion: Hospital overall smoking rate is lower than average, but smoking rate among males is still high. The hospitals should vigorously strengthen tobacco control training system, and create a smoke-free hospital environment to drive the smoking rates decline.目的  了解医院吸烟现状情况分布，为医院控烟措施提供科学依据。方法  自行设计调查表，对实施调查人员集中培训，统一标准，然后分组同步调查。结果  总吸烟率为9.66%，男性吸烟率为25.78%，行政后勤人员吸烟率高于医务人员。结论  总吸烟率低于平均水平，但男性吸烟率较高。应大力加强系统的控烟培训，创建无烟医院环境，带动居民吸烟率下降

Depression of fast excitatory synaptic transmission in large aspiny neurons of the neostriatum after transient forebrain ischemia

Spiny neurons in the neostriatum die within 24 hr after transient global ischemia, whereas large aspiny (LA) neurons remain intact. To reveal the mechanisms of such selective cell death after ischemia, excitatory neurotransmission was studied in LA neurons before and after ischemia. The intrastriatally evoked fast EPSCs in LA neurons were depressed < or =24 hr after ischemia. The concentration-response curves generated by application of exogenous glutamate in these neurons were approximately the same before and after ischemia. A train of five stimuli (100 Hz) induced progressively smaller EPSCs, but the proportion of decrease in EPSC amplitude at 4 hr after ischemia was significantly smaller compared with control and at 24 hr after ischemia. Parallel depression of NMDA receptor and AMPA receptor-mediated EPSCs was also observed after ischemia, supporting the involvement of presynaptic mechanisms. The adenosine A1 receptor antagonist 8-cyclopentyl-1,3-dipropylxanthine blocked the inhibition of evoked EPSCs at 4 hr after ischemia but not at 24 hr after ischemia. Electron microscopic studies demonstrated that the most presynaptic terminals in the striatum had a normal appearance at 4 hr after ischemia but showed degenerating signs at 24 hr after ischemia. These results indicated that the excitatory neurotransmission in LA neurons was depressed after ischemia via presynaptic mechanisms. The depression of EPSCs shortly after ischemia might be attributable to the enhanced adenosine A1 receptor function on synaptic transmission, and the depression at late time points might result from the degeneration of presynaptic terminals