0.01). There was a significant difference in TIMP-1,-2 expressions between saccule injury group and control group (P

Objective To identify the role of the IKK / NF-kappa B signaling pathways in the acquisition and consolidation of extinction memory in conditioning fear.Methods Aduh SD rats were treated with nuclei buried surgery.After a week recovery from nuclei buried surgery,adult SD rats accepted auditory fear conditioning training.Before the extinction training,bilateral intra-BLA infusion of sulfasalazine(SSZ),an inhibitor of IKK/NFκ B,and Vehicle were done.The freezing time were tested on the 24h and 1w after the extinction.Results After training,all the rats showed higher percentage of freezing time than the baseline(Vehicle:pre-CS 21.16％,post-CS 71.23％,P＜0.01 ; SSZ:pre-CS 22.23％,post-CS 72.14％,P＜0.01).The percentage of freezing time had no significant difference(SSZ 47.52％,Vehicle 46.20％,P＞0.05)between Vehicle and SSZ at the end of extinction training.However,SSZ groups showed significantly higher percentage of freezing time than the control group on the 24h(Vehicle 41.03％,SSZ 60.51％,P＜0.01) and the same was found on 1 weck test(Vehicle 34.17％,SSZ 57.21％,P＜ 0.01).The rats injection with SSZ showed significant fear response for the auditory fear condition.Conclusion All above results suggest that interference of IKK/NF-κ B signaling pathway impaire the consolida tion but have no effect on the acquisition of fear extinction memory in conditioning fear.The available date could provide us some clinical guidance in the treatment of post-traumatic stress disorder and panic disorder.

Objective To eukaryotically exp ress B7.1 extracellular domian and investigate its biological activities. Methods Recombinant expression vector pDisplay/B7.1(V+C) wa s transfected into Hela cells by electroporation method. The expression of B7.1( V+C) was identified by immunohistochemistry and in situ hybridization, respectiv ely. In vitro T lymphocyte activation activity was detected by 3H-TdR incoporation method and the aroused cytotoxicity after mixed culture of pDispla y/B7.1(V+C) transfected Hela cell-T cell was observed by MTT method. R esults B7.1(V+C) was expressed successfully on the surface of Hela c ells. The expressed B7.1(V+C) was able to activate T lymphocytes in the pres ence of anti-CD3 monoclonal antibody. Cytotoxicity could be observed when pDisp lay/B7.1(V+C) transfected Hela cells were mixed and co-cultured with T lymphocy tes. Conclusion Eukaryotically expressed B7.1(V+C) main tains its T lymphocyte costimulatory activity, and B7.1(V+C) can be adopted to construct bifunctional molecules for tumor immunotherapy.

Purpose To explore the role of histone H2B monoubiquitination in primary colonic carcinoma and clinicopathological pa-rameters of colonic carcinoma. Methods To detecte the expression of histone H2B monoubiquitination in 116 cases of primary colonic carcinoma and 15 cases of normal colonic mucosal tissue by avidin-biotin-peroxidase complex ( ABC)-immunohistochemistry. Results The level of histone H2B monoubiquitination was significantly reduced in poorly differentiated colonic carcinoma 19. 4% (6/31) compared with that of well-differentiated colonic carcinoma 49. 4%(42/85), moderately differentiated colonic carcinoma 49. 4% (42/85) and normal colonic mucosal tissue 86. 7% (13/15) (P<0. 05). The expression of histone H2B monoubiquitination was closely correlated with tumor differentiation, Dukes stage, TNM stage and lymph node metastasis (P<0. 05), but not depended on sex or age (P>0. 05). Conclusion Histone H2B monoubiquitination is obviously associated with the progression of primary colonic carcinoma. Although its specific mechanism still remains unclear, histone H2B monoubiquitination could be a novel potential molecular marker for early diagnosis, clinic treatment and prognosis evaluation.

Aim To explore the ethanol-induced apoptosis effect on hepatocellular carcinoma(HCC) cells and its relationship to the expression of apoptosis associated genes, bax and bcl-2. Methods The cytotoxic effect of 20～ 100 mL/ L ethanol on HCC cell line HCC-9204 was tested by thiazolyl-blue (MTT) assay. Then apoptosis of HCC-9204 cells was induced with 60 mL/ L of ethanol for 6 h. The morphological change, DNA breakage and the change of DNA content of different cell cycles of the apoptotic cells were detected by May-Grunwald Giemsa(MGG) staining, and terminal deoxynucleotidyl transferase mediated dUTP nick end labeling (TUNEL) assay and flow cytometer respectively. The changes of expression level of Bax and Bcl-2 proteins were detected by immunocytochemical staining and image analysis. Results The higher the concentration of ethanol was, the stronger the cytotoxic effect on HCC-9204 cells was. 60 mL/ L of ethanol could lead to obviously morphological apoptotic changes of HCC-9204 cells, and majority of the cells were TUNEL positive by TUNEL labeling assay. Typical apoptotic sub G1 peak was observed by flow cytometer. The level of Bax protein expression increased significantly after induced with 60 mL/ L of ethanol for 6 h, no expression of Bcl 2 were found before and after induced with ethanol. Conclusion Low dose of ethanol can induce apoptosis of HCC-9204 cells obviously, and occurance of the apoptosis is related to the increase of the level of Bax protein expression.

Objective:To investigate the application of photoplethysmogram in analyzing the fingertip pulse amplitude volume (PAV)to evaluate the endothelial function in diagnosing coronary heart disease,and to clarify its relationship with the risk factors of cardiovascular diseases.Methods:Total 409 patients with chest pain accepted coronary angiography (CAG)were selected and diveded into positive group (CAG+)(n=288)and negative group (CAG-) (n = 121)according to angiographic results.Fingertip photoplethysmogram was used to analyze the fingertip PAV by the way of applying endothelial function diagnostic after reactive ischemia,and the relationship between the PAV value and the risk factors of coronary heart diseases was analyzed,and the critical reference value of prediction index of coronary heart disease was determined.The risk factors such as age,gender,serum total cholesterol (TC ), low density lipoprotein (LDL ), high density lipoprotein (HDL ), non-HDL, serum triglyceride (TG),hypertension,diabetes,smoking,family history of coronary heart disease,body mass index (BMI)of the subjects in various groups were analyzed,and the relationship between the risk factors of coronary heart disease and PAV was analyzed by Logistic regression analysis.Results:The PAV of patients in CAG+group was significantly lower than that in CAG-group (P <0.01).The peak point of PAV was<1.37,if PAV<1.37 was used to predict the coronary heart disease,the predictive sensitivity,the specificity,the positive prediction and the negative prediction were 74.65%,44.63%, 76.24%, and 42.52%.The Logistic regression analysis showed that PAV was negatively associated with hypertension,smoking history,TG (OR= 1.476,OR=2.002, OR = 1.844;P < 0.01 ). Conclusion: PAV is associated with coronary heart disease and its risk factors (hypertension,smoking history,TG),and PAV=1.37 can be used as the peak point to predict the coronary heart disease.

ObjectiveTo identify the effects of venlafaxiue on the acquisition and consolidation of fear extinction memory in conditioning fear memory extinction model.MethodsMale Sprague-Dawley rats were treated with fear conditioning training in the A environment.Before the extinction training,all the experimental rats were given different doses of venlafaxine intraperitoneal injection.After 24 hours,all the rats test in the B environment.ResultsRepeated-measures ANOVA were conducted on the percent of freezing time for between-session extinction,test condition (F2,44 =458.958,P＜0.001 ) and VEN dose(F2,22 =43.026,P＜0.001 ) and a Test condition * Treatment interaction (F4,44 =31.363,P ＜ 0.001 ).For the within-session,post hoc comparisons indicated that the three groups that received different dose of VEN (0,20 and 40 mg/kg) did not differ from each other (P ＞ 0.05 ),indicating similar extinction following the post-conditioning.The rats injected with high-dose venlafaxine (40 mg/kg) intraperitoneally before extinction training showed pro,motion of between-subjects extinction of fear memory,but does not affect the within-subjects extinction.There was no significant catabolism in the rats injected with middle-dose (20 mg/kg).ConclusionThe available date indicate that venlafaxine could promote the extinction of fear memory and there is a dose-dependent relationship of venlafaxine in the facilitation of fear memory.Our results could provide some clinical guidance for the treatment of post-traumatic stress disorder and panic disorder.

Objective To investigate effects of N-acetylcysteine (NAC) on changes of the behavior and the monoamine neurotransmitters in prefrontal cortex (PFC), striatum (ST), amygdala (AM) and hippocampus (HIP) in rat model of chronic unpredictable stress (CUS), and to explore the possible mechanisms related to the NAC. Methods Thirty-two male Sprague-Dawle (SD) rats were divided into CUS group, fluoxetine group (FLX), NAC group and control group (n=8 for each group). Rats in CUS group, NAC group and FLX group were all fed alone and received CUS for 6 weeks to establish CUS model. Rats in NAC group and FLX group were given NAC and FLX by daily intragastric administration respectively during the last 3 weeks, while rats in CUS group and control group were given the same volume of solvent. Behavioral assessment including weight measurement, sucrose water consumption test, and opened field test were used for evaluation before and after CUS, and before and after intervention. The concentrations of the monoamine neurotransmitters (NE, DA, 5-HT) in PFC, ST, AM and HIP were measured with Coul array HPLC. Results (1) There were more increases in weight gain, sucrose consumption, and distance of horizontal moving and number of up-right, while the number of feces was less, after intervention in control group, NAC group and FLX group than those of CUS group (P<0.05). (2) Neurotransmitters including NE, DA and 5-HT were significantly decreased in PFC, ST, AM and HIP in CUS group compared with that of control group (P<0.05). The monoamine neurotransmitter (NE, DA and 5-HT) were significantly increased in the brain region (PFC, ST, AM and HIP) in NAC group and FLX group than those of CUS group (P < 0.05). Conclusion NAC and fluoxetine can effectively improve the depressive behavior of the CUS rats, increase the contents of monoamine neurotransmitters including NE, DA and 5-HT in PFC, AM, ST and HIP brain regions.

Objective To discuss the nursing intervention of Rey syndrome in children patients.so as to search effective nursing measures.Methods 12 children patients with Rey syndrome received comprehensive nursing treatment with reducing intracranial pressure and were under continuous close observation.Slightest changes were feeded back timely,then effective nursing measures were taken to stabilize their illness,patients also received dietary therapy,medication nursing and rehabilitation training,etc.Results All patients ameliorated after 3 to 7 days,and achieved clinical recovery after 20 to 30 days without sequelae.Conclusions Early diagnosis and correct effective nursing care can improve curative rate and avoid the occurrence of complications and sequelae.

Objective To explore the role of histone H3 acetylation modification of brain derived neurotrophic factor (BDNF) in the pathogenesis of Alzheimer's disease (AD).Methods 2 months and 8 months SAMP8 mice were used as AD model.Morris water maze was used to detect the impairment of learning and memory.Western blot was used to detect BDNF protein expression in the hippocampus,and chromatin immunoprecipitation (CHIP) was applied to study the changes of histone H3 acetylation in different BDNF promoters.Results The results of water maze test showed that the time across the target quadrant in 8 months SAMP8 mice(0.9±0.4) was significant declined compared with that of 2 months SAMP8 mice(3.7 ± ±0.9) and 8 months SAMR1 mice (3.3±0.6)(all P＜0.05).Meanwhile,compared with 2 months SAMP8 mice ((23.9±4.0) s) and 8 months SAMR1 mice ((21.5± 2.3) s),target quadrant time in the 8 months SAMP8 mice((11.7±2.8) s) was also significantly reduced(both P＜0.05).The western blot showed the expression of BDNF in the hippocampus of 8 months SAMP8 mice was significantly decreased compared with that of 2 months SAMP8 mice and 8 months SAMR1 mice(P＜0.05).Lastly,CHIP assays showed that histone H3 acetylation of BDNF exon Ⅳ and Ⅵ in the hippocampus of 8 months SAMP8 mice were remarkably decreased(P＜0.05) compared with that of 2 months SAMP8 mice and 8 months SAMR1 mice.There was no significant change of histone H3 acetylation of BDNF exon Ⅰ and Ⅲ among all groups(P＞0.05).Conclusion Histone H3 acetylation of BDNF exon Ⅳ and Ⅵ is reduced during the development of AD,which may be the mechanism underlying the impairment of learning and memory in AD.