1.Effect and neuropathological mechanism of cholecystokinin on development of electrogastric arrhythmia in rats
Dailu CHEN ; Zhenhua WANG ; Zhengwu XIA
Chinese Journal of Digestion 2001;0(07):-
Objective To study effects of cholecystokinin (CCK) on occuring of electrogastric arrhythmias. Methods The contens of cholecystokinin (CCK) nerves, cholinergic (Ach) nerves and nitregic nervous (NOS) nerves in antral myenteric plexus were studied using histochemistry and immunocytochemistry. Results (1) The electrogastric dysrhythmias occurred in the model and CCK groups rats, the abnormal rhythm index and coefficent of variation (cv) of slow wave frequency were singnificantly increased compared with the control ( P
2.Bacterial culture of vaginal discharge and their resistance to antibiotics
Yun LI ; Zhongtao LI ; Zhengwu XIA ; Liang QU
Chinese Journal of Postgraduates of Medicine 2006;0(15):-
Objective To investigate the distribution of pathogenic bacteria of vaginal discharge in bacterial vaginosis.Methods The results of bacterial culture and drug sensitive tests of vaginal discharge from patients with bacterial vaginosis were analyzed.Results The positive rate of bacteria culture of vaginal discharge was 79.3%(115/145).The dominant bacteria were staphylococcus epidermidis 27.0%(31/115),staphylococcus intermedius and staphylococcus aureus 13.0%(15/115),which were obviously higher than other germs.The drug sensitive tests showed that staphylococcus were relatively sensitive to vancomycin,fosfomycin,amikacin and rifampin.But the drug resistance to penicillin,tetracycline,erythromycin and oxacillin was the highest.Conclusion The kinds of pathogenic bacteria in vaginal discharge are various.The main bacterium is staphylococcus,and drug resistance is very severe.The isolation and drug sensitive test of pathogenic bacteria play an important role in diagnosis and treatment of gynecological disease.
3.Effects of quetiapine on the memory and the expression of doublecortin in the hippocampus of schizophrenia model mice induced by cuprizone
Rui LI ; Shanshan HE ; Xia WANG ; Gaohua LIU ; Zhengwu PENG ; Huaning WANG ; Qingrong TAN
Chinese Journal of Behavioral Medicine and Brain Science 2015;24(11):970-973
Objective To investigate the effect of quetiapine (QUE) on the memory and doublecortin (DCX) expression in the hippocampus of C57BL/6 mice with cuprizone (CPZ)-induced schizophrenia in C57BL/ 6 mice.Methods 1% dimethyl sulfoxide (DMSO) was used as a vehicle to dissolve QUE.Three group of mice,16 in each of three groups,were treated with vehicle (control group),0.2% CPZ alone (CPZ group) or 0.2% CPZ combined with 10 mg· kg-1 · d-1 QUE (QUE+CPZ group) for six weeks,respectively.Spatial working memory was evaluated by Y-type maze test 24 hours after the completion of the treatment period.The number of DCX positivenew neurons was calculated by immunofluorescence staining assay.The expression of Notch1 and Hes1 mRNA were detected by reverse transcription-polymerase chain reaction (RT-PCR) assay.Results (1) Y-maze test:CPZ group achieved a much lower percentage of correct alternation than control group ((22.70±6.70) % vs (57.69 ±6.70)%) in Y-maze test (P<0.05).The percentage of correct alternation in CPZ + QUE group ((54.69± 10.06) %) was significantly increased compared with CPZ group (P<0.01).CPZ mice exhibited significant spatial working memory impairment.(2) Immunofluorescence staining:the number of DCX-positive cells in the hippocampus of the CPZ group (6342.85± 1801.72) was significantly decreased compared with that in control group (19428.57±2507.13) (P<0.01),and it was reversed by QUE intervention (15928.57±2049.97).(3) RT-PCR:the Notch1 and Hes1 mRNA expression in CPZ group were significant lower than that in sham and CPZ + QUE group,(Notch1 (0.97±0.29) vs (0.23±0.20),P<0.01);Hes1 (1.00±0.41) vs (0.38±0.30),P<0.01),and there was no significant difference between sham group and CPZ + QUE group.Conclusion QUE is helpful to relieve CPZ-induced cognitive impairment and decreases expression of DCX in hippocampal,which may be related with activation of Notch1 pathway.