1.Guidance Effect of Monitoring Drug Sensitivity on Treatment of Non-gonoccocal Urethritis due to Ureaplasma urealyticum
Wencheng XUE ; Liangmin WANG ; Dongya MENG ; Xiuju FANG ; Yuning CHEN
Chinese Journal of Nosocomiology 2005;0(11):-
0.05).CONCLUSIONS The rising rates of the drug-resistant Uu strains may be resulted of no-standard treatments.The treatment time will be shortened and the curative effects will be better if the treatments are based on the results of the susceptibility test.
2.Dynamic changes in power of rat's brain electrocorticogram and electrohippocampogram after cerebral ischemia and the effects of 9602
Rui WANG ; Qinfei YANG ; Yipeng TANG ; Liangmin FANG
Chinese Journal of Pathophysiology 1986;0(01):-
AIM and METHODS: To observe the dynamic changes in relative power of rats brain electrocorticogram(ECoG) and electrohippocampogram(EHG) after ischemia, we studied the changes of rat's ECoG and EHG after ischemia using the method of chronic implanting electrodes in cortex and hippocampus and the effects of Chinese herbs 9602 on them. RESULTS: The frontal ECoG relative power of all bands and total power decreased in 8 hours after ischemia, restored in 24 hours and decreased again after 72 hours. It decreased significantly as compared with that of sham-control 7 day postischemia. The occipital ? band at 72 hour, all bands and total power decreased 7 day after ischemia. As compared with sham-operated control, the ??? and total power of EHG decreased notably at 8, 24 and 72 h after ischemia. The changes were more markedly in 7 day after ischemia. Treated with 9602 and hydergine, the ischemic animals showed significant elevation of ECoG and EHG relative power in comparison with ischemic rats. CONCLUSION: The power of ECoG and EHG decreased after ischemia, it may be correlated with delayed neuronal death induced by ischemia. 9602 prevented the decreases in ECoG and EHG power obviously after ischemia,which probably related to the neuroprotective effects.
3.Effect of Chinese herbs 9602 on the alterations of evoking population spike and morphology in hippocampal CA1 region after ischemia/reperfusion in rats
Rui WANG ; Liangmin FANG ; Qinfei YANG ; Yipeng TANG ; Qingta HONG
Chinese Journal of Pathophysiology 2000;0(07):-
AIM: To explore the relationship between dynamic changes of population spike (PS) and morphologic alterations in hippocampal CA1 region and morphology after transient ischemia/reperfusion and the improving effects of Chinese herbs 9602. METHODS: Changes of evoking population spike ware investigated by electrical stimulating Schaffer collateral in CA1 region of hippocampal slice after ischemia/reperfusion in vivo . Apoptosis and morphologic alterations at different time points after cerebral ischemia/reperfusion were detected by using TUNEL and Nissl staining. RESULTS: The threshold voltage of CA1 region in evoking population spike increased markedly as compared with sham control. The enhancement of wave amplitude was reduced significantly after tetanic stimulation. The duration of enhancement in amplitude decreased with the passage of reperfusion. Above all were observed from 8 h after ischemia/reperfusion. They became remarkable and got to its top at 7 day after ischemia/reperfusion treatment. TUNEL positive cells were observed in hippocampal CA1 region at 8 h, got to the top at 24 h and then gradually reduced after ischemia/reperfusion. A lot of abnormal cells in CA1 region was found, and the number of pyramidal cell reduced progressively by Nissl staining after ischemia/reperfusion. Chinese herbs 9602 reduced the threshold voltage of CA1 region in evoking population spike remarkably, enhanced the wave amplitude and prolonged the duration of PS enhancement; decreased the number of TUNEL positive cell, prevented the reduction of pyramidal cell in CA1 region. CONCLUSIONS: The excitability and reactivity were decreased and there was a gradual functional disturbance of synaptic transmission in CA1 pyramidal cell and most notable changes happened at 7 d ischemia/reperfusion, suggesting that was partly due to delayed neuronal death induced by ischemia/reperfusion. Apoptosis plays an important role in the functional deficiency of CA1 region of hippocampus induced by cerebral ischemia/reperfusion. The effects of 9602 on ameliorating the excitability and reactivity of CA1 pyramidal cells relate to inhibiting apoptosis, attanuating delayed neuron death induced by ischemia/reperfusion.