Adult ; Delirium ; chemically induced ; Female ; Humans ; Thiocarbamates ; poisoning

OBJECTIVETo study the protective effect of Ligustrazine Injection (LI) against cisplatin-induced ototoxicity and to explore its mechanism.

METHODSThirty healthy adult guinea pigs were randomly divided into three groups, 10 in each group, i.e., the normal control group, the cisplatin group, and the LI group. Guinea pigs in the normal control group were intraperitoneally injected with normal saline at 3 mL/kg for 7 consecutive days. Those in the cisplatin group were intraperitoneally injected with cisplatin at 3 mg/kg for 7 consecutive days. Those in the LI group were intraperitoneally injected with LI at 140 mg/kg for 7 days, but cisplatin (3 mg/kg) was intraperitoneally injected from the opposite side starting from the 4th day. Brainstem auditory evoked potential (BAEP) was performed in all animals before and after injection. All animals were sacrificed after the final testing under anesthesia and their cochleas collected. Half the cochleas of each group were collected for silver nitrate staining of cochlear basilar membrane stretched. The other half the cochleas of each group made into paraffin sections to observe the apoptosis of cochlea cells by TUNEL method and the expression levels of c-Jun detected by immunohistochemistry.

RESULTSThere was no statistical difference in the difference of BAEP threshold among the 3 groups before injection (P > 0.05), but the BAEP threshold increased in the cisplatin group and the LI group (P < 0.05). Besides, it was higher in the cisplatin group (P < 0.05). In the cisplatin group, most hair cells were missing, spiral ganglion cells obviously decreased, more TUNEL positive cells occurred, and the expression of c-Jun was stronger. But the aforesaid impairment in the LI group was obviously lessened (P < 0.05).

CONCLUSIONSLI showed certain antagonist effect on cisplatin-induced ototoxicity. Its mechanism might be associated with scavenging oxygen radicals of the cochlea tissue, improving the microcirculation, and fighting against apoptosis.

Animals ; Apoptosis ; drug effects ; Cisplatin ; toxicity ; Cochlea ; drug effects ; metabolism ; pathology ; Evoked Potentials, Auditory, Brain Stem ; Guinea Pigs ; Pyrazines ; pharmacology ; Reactive Oxygen Species ; metabolism

Objective To evaluate the training quality of junior college graduates of clinical medicine based on the feedback from the graduates and their employers.Methods Totally 112 junior college graduates tailored to rural areas among all the three years' graduates were selected.These graduates and their employers were asked to do the questionnaire and discussion.Results The overall evaluation from the graduates on the school curriculum and teachers was good,with satisfactory rate being above 95％.The employers had nice impression on the graduates and spoke highly of them,with satisfactory rate reaching 97.4％.Of all the three years' graduates,one-time passing rate in the qualification examination for assistant practitioners came to 41.0％,much higher than the average passing rate of 20.12％ in the same area and at the same time.Conclusion The teaching effect for junior college graduates of clinical medicine tailored to rural areas is satisfactory and the reform on teaching is worka ble and effective,however,it needs further practice.

Based on the theoretical connotation of internal stirring of collateral wind in atherosclerosis (AS) and combined with the concepts related to collateral disease and diseased collaterals,this article suggests that angiogenesis in AS plague belong to collateral disease,of which many are deficiency,stasis and full of changes.Since its pathological changes resemble a lot to wind syndrome,this article suggests that the internal stirring of collateral wind is the core pathogenesis of angiogenesis in AS plague.According to the model building of internal stirring of collateral wind,the high correlation between angiogenesis in AS plague and the internal stirring of collateral wind is proved,which provides a new thought in prevent and treat AS with integrative medicine.

Objective To construct the serine protease gene(sprE)mutant and to study the pathogenicity of sprE gene of Enterococcus faecalis.Methods Recombinant suicide vector pCQ001 of Enterococcus faecalis with pTX4577,was constructed.Then,created isogenic sprE-deficient mu- tant(*sprE)by allelic replacement was constructed.Moreover,the growth ability and the virulence of the mutant were compared with those of the wide type in vitro and in vivo respectively.A mouse peritonitis model and a rabbit endocarditis model were utilized in the study.Results The *sprE was selected by kanamycin and identified by polymerase chain reaction(PCR),pulsed field gel electropho- resis(PFGE)and Southern blot.The evidences showed that the sprE gene had a major role in helping bacteria to resist the elevated temperature and oxidative stress.The virulence of mutant decreased af- ter sprE gene was knocked out.Conclusions The *sprE of Enterococcus faecalis is constructed suc- cessfully,sprE gene is important in the pathogenesis of Enterococcus faecalis,which probably is a major virulence factor of Enterococcus faecali.

BackgroundBiological behavior of choroidal melanoma is closely related with angiogenesis.The microcirculation pattern in which tumor cells may be involved is different from neovascularization.ObjectiveThis study was to observe the microcirculation pattern of the choroidal melanoma tissue and analyze its relationship with the clinical pathology factor and the degree of cellular proliferation.Methods Forty-eight specimen of choroidal melanoma tissue were collected at Beijing Tongren Eye Centre from November 1997 through March 2006.Periodate acid Schiff staining was used to determine the microcirculation pattern of choroidal melanoma.The morphology of the tumor cells and the distribution of microcirculation pattern in the tumor were observed under a fluorescence microscopy with 544 nm wavelength,and the Ki-67 expression in the tumor was detected by immunochemistry.The relationships between the choroidal melanoma clinical pathology factor with Ki-67 expression and microcirculation pattern were evaluated by multiple stepwise regression model.ResultsA total of 9 kinds of microcirculation patterns were found by periodate acid Schiff staining.The occurring rate of loop- or network-like vascular pattern showed a significant elevation in the tumor tissue with epithelial cells in comparison with the tumor with spindle-like cells (66.7％ vs.30.6％ ) ( P=0.027 ).The expression rates of Ki-67 were 18.961 ± 10.995 and 19.481 ± 12.167 in the tumor tissue with loop- or network-like microvascular pattern,and those in the tumor tissue without loop- or network-like microvascular pattern were 10.261 ±5.669 and 12.021 ± 6.802,presenting significant differences between them ( P =0.000,P =0.010).Loop-like microvascular pattern was determined as the risk factor of the proliferation and metastasis of choroidal melanoma by multiple stepwise regression analysis (P=0.002).ConclusionsAmong the nine microcirculation patterns in choroidal melanoma,networks pattern is the most fashion,and Ki-67 expression is more strong in the tumor with epitheliod cells,suggesting that this microcirculation pattern is associated to the malignant degree and extent of proliferation in choroidal melanoma.

Adult ; Atypical Hemolytic Uremic Syndrome ; etiology ; Female ; Glomerulonephritis, IGA ; complications ; Humans ; Puerperal Disorders ; etiology

AIM To observe whether limb ischemic preconditioning (LIP) could attenuate pyramidal neuronal apoptosis of the CA1 hippocampus and brain edema evoked by brain ischemia in rats. METHODSSeventy-two rats whose bilateral vertebral arteries occluded permanently were randomly assigned into 6 groups: sham, LIP(bilateral femoral arteries were clamped for 10 min, 3 times, in a 10-min interval), brain ischemic insult, LIP+brain ischemic insult, DMSO+LIP+brain ischemic insult and SB 203580+LIP+brain ischemic insult groups. Assays for neuronal apoptosis were performed using TUNEL staining. The percentage of wet over dry tissue weight of the brain was measured by weighing method. RESULTS There were almost no TUNEL-positive cells in the CA1 hippocampus in either sham or LIP group. Clear TUNEL-positive pyramidal neurons of the CA1 hippocampus and increase in brain water content were detected in rats subjected to brain ischemic insult. But the number of TUNEL-positive cells and the increase in brain water content were significantly decreased in LIP+brain ischemic insult group compared with that in brain ischemic insult group, indicated that LIP prevented the occurrence of apoptosis of pyramidal neurons of the CA1 hippocampus and brain edema induced by brain ischemic insult. Pretreatment with SB 203580, an inhibitor of mitogen activated protein kinase p38(p38 MAPK), significantly increased the number of TUNEL-positive cells and brain water in SB 203580+LIP+brain ischemic insult group compared with that in DMSO+LIP+brain ischemic insult group, indicated that SB 203580 blocked the protection of LIP against neuronal apoptosis in the CA1 hippocampus and brain edema. CONCLUSION LIP could attenuate pyramidal neurons apoptosis of the CA1 hippocampus and brain edema evoked by brain ischemia, which maybe related to the activation of p38 MAPK.

AIM To explore the role of superoxide dismutase (SOD) in the p38 mitogen-activated protein kinase (MAPK) mediated brain ischemic tolerance induced by limb ischemic preconditioning (LIP). METHODS The Wistar rats with permanent occlusion of the bilateral vertebral arteries were subjected to occlude the bilateral femoral arteries for 10 min, 3 times, at an interval of 10 min to get the LIP, then global brain ischemia was induced immediately by occluding the bilateral common carotid arteries for 8 min. SB 203580 (100 μmol·L-1, in a volume of 25 μL), an inhibitor of p38 MAPK, was intraventricularly injected 30 min before LIP in SB 203580+LIP+brain ischemia group. Xanthinoxidase and thiomalonylurea methods were used to determine SOD activity and malondialdehyde (MDA) content of the hippocampus, respectively. Thionin staining was used for observing histological changes of the hippocampus. RESULTS LIP significantly prevented the decrease of SOD activity, the increase of MDA content and the delayed neuronal death in the CA1 hippocampus induced by the brain ischemia. SB 203580 pretreatment evidently blocked the protective effect of LIP against the delayed neuronal death and the modulation on SOD activity and MDA content. CONCLUSIONSOD may play an important role served as a downstream molecule of p38 MAPK in the induction of brain ischemic tolerance by LIP.